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What happens if there is a blood incompatibility during pregnancy?
There are possible combinations of blood types with the rH factors:

Rh factors are genetically determined. A baby may have the blood type and Rh factor of either parent, or a combination of both parents. Rh factors follow a common pattern of genetic inheritance. The Rh-positive gene is dominant (stronger) and even when paired with an Rh-negative gene, the positive gene takes over.
If a person has the genes + +, the Rh factor in the blood will be positive.
If a person has the genes + -, the Rh factor will also be positive.
If a person has the genes - -, the Rh factor will be negative.

I am aware that an infant receives one gene from the father and one from the mother, but what happens when the mother's Rh factor is negative and the newborn's is positive? What happens if the mother is O and the infant is A or B?
What happens within the placenta and to the maternal blood poles which are connected by open ended arterioles into intervillous spaces? Will the chorionic villi be "demolished" and exchange of materials isn't as possible?

Search erythroblastosis foetalis on Wikipedia

Little harm comes from ABO incompatibility (that would have been a major problem with reproduction.) Rh incompatibility is more dangerous, though.
If a fetus is Rh+ and the mother is Rh-, when there is mixing of maternal-fetal blood (at birth, but sometimes before that), the mother will form antibodies to the blood cell surface antigen. It doesn't usually affect the first baby (not sufficient antibodies), but if a subsequent baby is Rh+, there can be major consequences, which are multiplied with repeated exposure. Those maternal antibodies - which cross the placenta - can attack the fetal red blood cells and cause destruction of many of them (called hemolytic anemia) which, if severe enough, can be fatal to the fetus. It was a not-uncommon cause of fetal demise before Rhogam (Rh immune globulin) injections.
The immune globulin shots are given to women who are Rh- with Rh+ mates at a period before birth (before blood mixing), and immediately after birth if the child is Rh+. The antibodies bind with Rh+ antigens and "mask" the antigen from the mother's immune detection, so to speak, preventing the mother from making antibodies that can be used against subsequent pregnancies.
The major risk is to the fetal blood cells, not the placenta. The placenta isn't attacked. But with anemia, the fetus struggles, for example, without enough blood, the fetus can go into congestive heart failure and die.
It's also possible to form anti-Rh antibodies from blood transfusions. If an Rh- female has had a blood transfusion prior to her first pregnancy, maternal antibody levels will be drawn earlier during the pregnancy.
What Is Rh Incompatibility?

Thank you for your answer, the details you posed are very interesting. As a follow up question, is the Rh immune globulin injection affected by maternal sensitization? Would it be possible for anyone to be impervious to the Rh Shots?

I'm sure there are cases where the usual Rhogam shots were insufficient to protect against the formation of maternal antibodies, but that usually involves massive amounts of maternal-fetal blood mixing, not what would be the case with the vast majority of pregnancies. Rhogam has changed the outcome of literally countless pregnancies and is very, very effective, so I would not say anyone is "impervious". It's more a case of "has the mother enough antibodies to cover all the antigens she has been exposed to?"


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What are the carbohydrates that are found in white rice?
From this Wikipedia page on rice, it is mentioned that 100g of rice contains 80 g of carbohydrates, of which 0.12 g is "sugar" and 1.3 g is "fibre". I believe the "fibre" refers to dietary fibres that are not absorbed by the body and are just passed out of the body. However, I understand "carbohydrates" to be almost the same as "sugar" so what is the difference between the two terms as used in this context. I am guessing that "sugar" refers to simple monomeric units of carbohydrates while the rest of the "carbohydrates", excluding "sugar" and "fibre", is in the form of starch polymers, namely amylose and amylopectin. Could someone help to verify my understanding?

Fibre is contained in a particular form of starch, called resistant starch. Fibre, like sugars and starches, is a type of carbohydrate. However, fibre is different because it is not digested by the human body in the same way as sugars and starches. this is a good read from the 4th paragraph: https://www.researchgate.net/publication/305890780_Rice_as_a_Source_of_Fibre

The word carbohydrate is most common in biochemistry, where it is a synonym of saccharide, a group that includes sugars, starch, and cellulose. Starch (a polymer of glucose) is used as a storage polysaccharide in plants, being found in the form of both amylose and the branched amylopectin. In animals, the structurally similar glucose polymer is the more densely branched glycogen, sometimes called "animal starch".

@aliential you might consider putting your comments as answers instead, as they seem to actually answer the question rather than comment upon it.

Thanks, its just copy paste research...

source: Stack Exchange

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How do cells become differentiated using epigenetics despite having the same genome?
How is epigenetics used in the differentiation of cells and is this the only thing that is used? I've seen that transcription factors play a role but are these simply proteins that initially write the epigenetic code or something different altogether?
I've written this explanation of how I understand it currently. Please tell me if this is right or wrong.
How do our cells become specialised if they have the same genome? The answer lies in the fact that gametes have most of their epigenetic information taken off at fertilisation, (apart from small sections like at IAP retrotransposons) so it’s like a clean slate. The zygote cells divide to form many identical cells that have the capacity to become any cell in the body.
Proteins in the egg then bind to certain genes and regulate their expression by adding epigenetic markers like methyl groups and histone modifications. The proteins created from these genes then go to control the regulation of other genes and so on, until all the cells have different epigenetic markers put on them that mean they produce different proteins in different quantities to serve different functions in the body.

Have you had a look at wikpedia > Cellular differentiation?

@Remi.b Yes I have and that's how how I wrote that explanation but I don't know if it's correct

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Why is the body cooled during cardiac surgery?
When undergoing cardiac surgery, the heart is disconnected from the blood circulation and blood is passed through a heart-lung machine and cooled so that the body temperature of the patient is reduced.
I understand that this would slow down metabolic processes but how exactly does slowing down these processes benefit the patient?
Thanks for answering!

As you mention, hypothermia is routinely induced during cardiac surgery. There is a blog post including a photo of a heart being cooled with ice chips here: https://www.heart-valve-surgery.com/heart-surgery-blog/2010/10/17/ice-cardioplegia-open-heart-surgery/

The primary therapeutic benefit of deliberate hypothermia was long thought to be, as you say, the slowing-down metabolic processes, which reduces the amount of oxygen needed by the brain and other vital organs (source). Cooling the blood during open heart surgery therefore allows the operation to be performed more slowly (2-4 hours).
However, according to this open-access article on the benefits of therapeutic hypothermia for cardiac surgery:

the widely held notion that hypothermia protects because lower
  temperatures slow metabolism is not completely accurate. Recent
  research has shown that hypothermia can alter a plethora of cell death
  and cell survival pathways including gene regulation resulting in the
  inhibition of apoptosis and inflammation and the up-regulation of
  anti-apoptotic or trophic factors.

So basically it does slow down the metabolic processes but it also reduces inflammation and cell death.
After surgery, rewarming needs to be done slowly to maximise the chances of recovery (source).

Does the lowered amount of oxygen used by organs other than the heart really matter? Surely they have a good supply of oxygen due to the heart-lung machine.

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Is protein production doubled if you have homozygous dominant genes as opposed to heterozygous genes?
At school we were taught in quite simplistic terms. We were told that there is a dominant and recessive type of every gene and that if the dominant gene was present, the protein is produced and if it isn't, then a protein is not produced. We were just told that dominance was just an intrinsic property of some genes.
However, upon researching a little, I see that some genes are dominant because their corresponding allele simply doesn't make the protein but the dominant one does (please correct me if I'm wrong).
Does this mean that if someone is homozygous dominant for a particular gene, they produce double the amount of that certain protein as someone who has heterozgous genes or is there a mechanism that suppresses the expression of one of the dominant genes?

Dominance is defined based on the phenotype
Dominance is defined based on a phenotype of interest. Pick a phenotype, say coat color for example. If genotypes AA and Aa have the same coat color while aa has another coat color, then A is domiant over a.
The concept hold even for sequence that do not produce proteins
The concept of dominance can be applied to any locus which variance explains phenotypic variance, whether this locus codes for a protein or not.
Most sequences that affect the phenotype are regulatory sequences that do no produce any protein. In such case, your intuition that dominance is the allele that produce more proteins really does not make much sense.
Mechanism
A whole lot of mechanism can yield to such dominance relationship. It is not uncommon that the recessive allele comes from a loss-of-function mutation. In such case, yes it is likely that the AA genotype produce twice as many proteins as the Aa genotypes. But this is definitely not the only possible mechanism. Note that whether the number of proteins produced of the AA genotype is twice the number of protein produced of the Aa genotype, won't change anything to the phenotype of interest by definition of what dominant mean.
Dominance is actually pretty unusual
Most phenotypic traits actually result from the influence of several loci and allelic relationship at these loci are rarely perfectly dominant. Perfect dominance exist in reality but is definitely over represented in intro classes as they are simple to understand study cases.
Fitness
Note that there is a positive correlation between how recessive an allele is and how deleterious it is. It does not mean that the recessive allele is necessarily deleterious but there is a tendency.

Suppose that the allele for a curled tail is dominant (A). So if you had Aa for particular phenotype, does that mean that the loci and protein coding genes associated with the "a" allele are expressed as well as the ones associated with "A" but only the effects of the "A" gene is seen on the outside? Or does it mean that the expression of the genes to do with "a" is suppressed, possibly epigenetically?

There are many possible mechanisms of dominance. It is not because a is recessive that it necessarily does not express anything (but it is possible). It can be, but not necessarily. The notion "seen on the outside" is a bit misleading. It could be possible that A is dominant but Ao individuals (individuals that have lost one copy of the gene on one haplotype) differ from the Aa individuals. So really, the mechanisms are multiple, the only that matters to the definition is that AA and Aa have the phenotype while aa has a different phenotype.


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why do sodium channels close with excessive extracellular potassium ions in cardiac myocytes?
When there is an excessive concentration of potassium ions outside cardiac myocytes, the membrane potential surely goes up. I would have thought that this would make it easier for the membrane potential to go up past the threshold level, opening sodium ion channels and causing an action potential like at a synapse.
However, I understand that as the high concentration of extracellular potassium ions actually deactivates voltage gated sodium ion channels as opposed to opening them. Why does this happen?
Sorry if this question is pretty basic. We haven't covered anything nearly as complicated at school, especially not about cardiac cells.
Thanks for answering!

Short Answer
Depolarization block keeps sodium channels in a different state where they aren't available to open.
Longer Answer
The answer here applies equally to cardiac myocytes and neurons, and has to do with the gating properties of sodium channels (calcium channels have some similar behavior, which is also important).
Voltage-gated sodium channels at rest are pretty much all in a 'closed' state. The probability of a channel switching to an 'open' state increases with increasing voltage. However, those channels don't simply stay open indefinitely: they transition to third, 'inactivated' state. 'Inactivated' channels can't reopen. This helps keep sodium-mediated excitation brief and saves a lot of metabolic energy versus 'forcing' a cell to repolarize by only overwhelming the sodium conductance with potassium conductance.
Channels will stay in the inactivated state if the membrane remains depolarized. The probability of a channel switching from 'inactivated' to 'closed' (and therefore 'ready to open') increases with decreasing voltage. If a cell does not repolarize sufficiently, many sodium channels will stay in the 'inactivated' state. Further, channels that do switch to the 'closed' state could open, but not in synchrony. The eventual result is an equilibrium with a mix of sodium channels in open, closed, and inactivated states. There aren't enough 'closed' channels around to switch to open, there aren't enough 'open' channels to depolarize the membrane more, and as 'inactivated' channels switch to 'closed' there are other channels switching from 'open' to 'inactivated'.
This whole condition is referred to as 'depolarization block.'
Here's a helpful review on voltage-gated sodium channels that contains information covering what I discussed in my answer:
Catterall, W. A. (2000). From ionic currents to molecular mechanisms: the structure and function of voltage-gated sodium channels. Neuron, 26(1), 13-25.
You can also find lots more information in textbooks and elsewhere if you look for the term 'depolarization block.' Note also that I have simplified the gating transitions for voltage-gated sodium channels for the purpose of this answer, so some sources might explain a more complicated system; the general principles still apply to the question, though.


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Is prion a term used to describe the normal form of the protein as well as the disease causing form?
I've been reading my textbook and it refers to prions as a normal protein with a helpful function but it can turn into a disease causing form. However, I look in my other textbook and it refers to the word prion as solely being a disease causing protein.
I'd like to know which is the correct definition. Ie. Would I be correct in saying "The prion protein is normally involved in synaptic transmission but can turn into a disease causing form"?
Thanks in advance!

If we are considering prions in general, I disagree with the answer supplied by Gerardo Furtado.
Here is a definition taken from an article by Susan Lindquist:

[Prions are]...self-perpetuating and heritable protein conformations that cause multiple phenotypes,
  represent an unusual mechanism of information transfer that occurs via protein instead of nucleic acid.

Compare Wikipedia:

Prions are infectious agents...

If a prion is self-perpetuating or infectious then the normal form of such a protein is not a prion. In yeast the term prion is used to refer to the infectious form of a protein in a formal genetic sense. For example the [PSI+] prion was discovered as a genetic element and  then subsequently found to be associated with the translation termination factor Sup35, a protein with a known cellular role. All yeast strains have Sup35 protein but only certain strains contain and transmit the prion form of this protein. So [PSI+] is referred to as the prion form of the protein.
The problem with interpreting the language used to describe the TSE prions is that they were discovered because of their prion activity so the normal form is referred to as prion protein (as far as I am aware the function of the normal form isn't known). This doesn't mean that this form of the protein IS a prion, merely that this protein is associated with the original prion phenomenon so is called 'prion protein'.

If you didn't truncate your Wikipedia quote: "Prions are infectious agents composed entirely of a protein material that can fold in multiple, structurally abstract ways"

And if you didn't truncate your Lindquist quote: "Prion proteins can assume at least two conformations"

I don't understand why you think that makes a difference. If a prion is the infectious form ('infectious agent') of a protein that can fold in different ways, that doesn't mean that the non-infectious form is a prion. A cell which contains only the normal form of a prion-forming protein doesn't contain any prions since it contains no infectious agents.

Yes, Lindquist refers to proteins that can form prions as 'prion proteins' but not as prions. Just like the cellular form  of the TSE agent is called 'prion protein'. But please, write your own answer.

I don't need to. I just need to upvote the correct answer and downvote the wrong one.

@OrangeDog I don't know why you're so emphatic that this answer is incorrect. The original definition from Prusiner states ...a new term "prion" is proposed to denote a small proteinaceous infectious particle.... Clearly that definition precludes its use for referring to normal proteins, especially since it predates any linkage between the infectious particle and it's normal, non-infectious variant. As Alan Boyd said, there is a distinction between prion and prion protein.

@GerardoFurtado The title also poses the following question (which is the one you answered yes to): Is prion a term used to describe the normal form of the protein as well as the disease causing form? The answer to this question should be no, which is presumably where the disagreement arises (though I can only speak for myself). Again, there is a distinction between a prion and what was later called the prion protein.

@GerardoFurtado There are two explicit questions and it seems that you answered one and this post the other. Anyways, you've got my upvote after your edit.

@canadianer is correct in referencing Prusiner, as he is credited with the nomenclature and usage.

The Wikipedia definition of prions is quite clear I think:

Prions are infectious agents composed entirely of a protein material
  that can fold in multiple, structurally abstract ways, at least one of
  which is transmissible to other prion proteins, leading to disease in
  a manner that is epidemiologically comparable to the spread of viral
  infection.

Your definition: "The prion protein is normally involved in synaptic transmission but can turn into a disease causing form" it is misleading. First, it sounds like there is a protein called prion that is involved in synaptic transmission, which is not true. Prions are a subset of the group proteins. Moreover, not all the prions are derived from proteins involved in the synaptic transmission. Prions have been found in other organisms like bacteria and fungi, so there is little to do with synaptic transmission there. The wiki page I have linked is full of links to the related literature, start there your journey!


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During interphase, is DNA wrapped around histones?
Are histone proteins present around DNA in the nucleus during all of interphase (including G1) or do histone proteins only form later on when chromosomes are condensing into chromatids?
Thanks in advance!

Yes, DNA is always wrapped around histones.
DNA condensation using histones is not only meant to form the chromatids for mitosis/meiosis, but also one of the factors that control gene expression. Tightly packed heterochromatin is not being expressed, whereas unpacked euchromatin is transcriptionally active. The process of condensation is controlled by enzymes such as histone actelytransferase (HAT) and deacetylase (HDAC) that change the electrostatic properties of the histone proteins. Positively charged lysine in heterochromatin histones allows condensation with negatively charged DNA. By acetylation of these lysines, they become neutral and the heterochromatin turns into euchromatin, which, provided the necessary activators etc., can now be translated. To silence gene expression, the process is reversed.
Gene expression control is very complex and histone acetylation is only one factor out of many. Nonetheless, you see that histones are a crucial part of the chromosomes and are not only formed during mitosis or meiosis.
3.0.jpg
Source: https://en.wikipedia.org/wiki/File:Histone_acetylation_and_deacetylation.jpg


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What sort of biofiltration is best for a small, portable, biofiltration unit?
I've been exploring the idea of a system to allow re-use (drinking) of RV greywater, or at least the freedom to dump in storm drains (I think the requirements are looser about this, but it still has to be somewhat purified)
Greywater is wastewater that does not contain feces. The primary contaminants would be food waste, various soaps (probably only biodegradable or non-antibacterial), and used shower water. I would also probably add urine, after sterilization to remove pathogens.
I was thinking of pre-filtration to remove larger fragments and detritus. Probably with the highest grade of this
-Processing rate would have to be 10 liters per day absolute minimum. 2x to 3x that would be best.
-Weight and volume are both at premium

How are you testing the purity or cleanliness of your filtrate (the water thats been filtered)?

why portable considering shower? any aquarium filter generates a heap of bacteria that process all useable impurities in the water to grow a mat. the bigger aquarium filter the better. it's ultra simple question to me having worked with many dank water ecologies and aquaria. it's only a function of bacterial medium substrate (sponges) temps and wather throughput in a given surface are of sponge. aquarium filters are designed fo rthat, soaps are mostly phosphate.

Any kind of sponge and pump filters will breed nitro bacteria to remove organic content. Added to a drip filter made from pure mineral sands and clays, you'd have a bacterial sponge and plant aquarium plus a sand filter.
You can make you own activated carbon too.
Urine requires at heavy plant growth to purify. You already have a tank, volume not given so I'll say it's 125 L. Here's a two stage bio filter: one with an incoming and circular bacterial filter to filter incoming water in graded sponges up to about .05 - 1 mm finest incoming particles for foods and stuff.  Use 2 divisions in the tank, one of 100 L, one of 25 L that you can prepare 10 L from every day.
Use 2 fish filters AC of 7 - 20 watts (?) or 12 V (DC) pumps similar to fish ones. Use 500 ml - 1L volume of filter sponges with fast access so you can squeeze out the bacterisl mats periodically because they will fill with nitrogen and phosphate and oxygen based pond organisms.
If you can fill the 100 liter tank with algea, it's ideal.
Put a valve to keep 2nd 25 L tank separate. Filter final 10 L drawn daily through mountain mineral sand from places with great spring water, i.e. dolomites / chalky to add trace elements. It's recommended you use sunlight and lots of plants in the first tank.

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College Genetics: Xist vs. transposon
I'm taking introduction to genetics and I'm trying to understand the following question: Lets say there is a male cat with blue ears, a single gene mutation called BLU.
We try to obtain pure bred blue-eared cats, mating the above cat we recieve:
*Males with a different colored ears
*Females with blue mosaic ears.
Now I'm trying to understand which is more likely. BLU being silenced by Xist or having non autonomous transposon on the BLU gene while only females have autonomous genes.
Thank you in advance!

Why do you think a transposon would cause this?


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Which trophic level has the highest population in a food chain?
The basic trophic levels in any food chain are the producers, the consumers and the decomposers. Most of the websites I've searched say they are the decomposers. But shouldn't it be the producers? In any given food chain, the number of individuals progressively decreases towards the higher trophic levels.

The concept of a trophic "level" really only applies within the category of consumers (and even there it's only a rough approximation).
This is because some consumers eat producers (e.g., herbivores eating plants), while others eat other consumers (e.g., carnivores).  So the notion of a "level" is basically counting how far something is from producers, which in turn creates the pyramid structure of bigger and badder predators eating smaller predators, and so on. This is really very specific to predatory animals because it is only in the context of predation that size goes up and numbers go down as photosynthesis becomes more remote.
With other types of interactions like parasitic worms infesting your gut or mosquitos sucking your blood, you could categorize the organism as a consumer and count it as another level removed from producers, but since it's only tapping a small amount of resources, rather than the more total interaction of predation, the ecological consequences are very different, and you can have a lot more mosquitos than people in a way that you can't have more wolves than deer.
So it is with decomposers as well, for yet another different reason. Decomposers don't need to be big (though they can be), since they aren't trying to hunt and kill something, they're extracting value from something that is already either dead or cast off. Thus, once again the concept of "level" doesn't really apply, and a vast number of flies can be born from the corpse of a single dead lion.


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Does DNA have 5 nitrogenous bases?
Does DNA have 5 nitrogenous bases? I believe they are 5 because Uracil is not the same thing as Guanine, because, first of all, uracil "replaces" thymine, not guanine. And second, uracil performs a range of functions that go far beyond "replacing" thymines at the time of transcription and translation. Am I right?

No. Uracil is present in RNA which is not the same as DNA.

The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site as are "homework" questions unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Under researched questions may be subject to down-voting and closure. In particular, I have a found KhanAcademy to be a very helpful introduction to unfamiliar subjects.

Thymine is 5-methyl-uracil, and one way of remembering this is that THYMinE and METHYl are (almost, but not quite) anagrams.

Uracil in DNA arises from the deamination of cytosine , and as such replaces C and not thymine. Thus a C-G base-pair is converted (by deamination) to a mutagenic U-G base-pair (and there are sophisticated repair mechanisms to fix this).  See Uracil in DNA – occurrence, consequences and repair, for example

It's a bit more complicated than that.
This wiki entry on nucleotides should help clarify things: Nucleotide
Diagram of chemical structure of bases, nucleosides, nucleotides, etc
I'm not sure what you mean by "...a range of functions..."

From How do I write a good answer? in the [help], Answer well-asked questions. Not all questions can or should be answered here. Please save your efforts for questions appropriate to this site. I also encourage you to delete your answers to  such questions (e.g. homework questions like this) as giving them answers encourages more undesirable posts. This is also destructive to the learning process by rewarding lack of thought and effort on the part of students. Thanks.

For "It's a bit more complicated than that", you could reference Uracil in DNA – occurrence, consequences and repair. (Uracil in DNA arises from the deamination of cytosine)

@user338907 I was attempting to provide a starting point for the questioner's research rather than a direct answer, as suggested by (at)tyersome (I may not have succeeded in doing so).


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What species left these underwater eggs?
While inspecting some plants planted about 1.5 ft underwater in my pond, I noticed what appeared to be eggs on many of the plants.
Note that the eggs are the white, oblong, opaque things. The clear perfect spheres in the picture are just water bubbles.
For scale, the branch is probably 1/8" thick. These are really tiny, maybe 1 mm across.
The location is the American southwest.
The eggs had to be at least 1 ft underwater, which rules out most kinds of flying insects, I think. What kind of animal lays an egg like that?


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Help identifying this Queen Ant
Could someone please help us identify this queen ant ?  We live in the North Island of New Zealand. So far our google image searches haven’t found a match. Any help would be appreciated.

Any chance of more photos? if you can, to count the teeth in the jaws at the front, number of segments in antennae, segments on abdomen etc. from above also.


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From an evolutionary standpoint, why don’t couples attempt to have as many kids as possible?
Many couples have 4 or 5 kids, but it is unusual for a couple to have 10 or 15. Shouldn’t humans have evolved to want as many kids as possible to maximize the chances that their genes are passed down?

Remember that until 100 years ago even in developed countries, conditions were very different than now -- women often died in or near childbirth, children often died of disease during childhood, hormonal birth control was not available, etc.

Because many humans are intelligent creatures. and place their personal well-being ahead of abstracts like evolution?  I mean, why on Earth would I give a damn about whether or not my genes are passed on?

There's strong cultural component to it. It is not uncommon in strongly religious communities to make as many children as possible. Also, baby-boom took place not so long ago, while average number of children in a modern European family is 1-2 (depending on the country).

Typical family sizes (especially in developed countries) are much smaller than they used to be, because cultural factors influence behaviour (do you want to have 10-15 kids if you can't afford to give them a good education?) From Kopf and Livni 2017:

More fundamentally, maximizing the number of offspring does not necessarily maximize reproductive fitness, because the amount of resources/care you give to each individual offspring matters; if you have too many offspring, maybe none of them will grow up to be high-quality/reproductively successful. This trade-off affects non-human organisms as well; there is an entire literature in evolutionary biology on optimal reproductive tactics that includes this issue (Pianka 2008).

Kopf, Ephrat, and Dan Livni. “The Decline of the Large US Family, in Charts.” Quartz, 2017. https://qz.com/1099800/average-size-of-a-us-family-from-1850-to-the-present/.
Pianka, E. R. “Optimal Reproductive Tactics.” In Encyclopedia of Ecology, edited by Sven Erik Jørgensen and Brian D. Fath, 2567–72. Oxford: Academic Press, 2008. https://doi.org/10.1016/B978-008045405-4.00841-7.

Wow. Great answer, thanks!


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Biology Experiment Algae pH & temperature help?
I am planning a Biology investigation for my IB IA on the impact of temperature and pH on algae growth. Does anyone have tips on how to measure the growth rate of algae? What algae is the most suited for such an experiment? Also, how do I change the pH of the water containing algae? I'm a beginner, any ideas would be a great help!

Welcome to the site - can you tell us what sort of equipment you have access to? In particular do you have access to pH meter, microscope, hemocytometer, low mass scales, drying oven,

Perhaps spirogyra? Make sure any tap water is left overnight to gas off the chlorine compounds.

i have access to a wide range of equipment, all those you listed I can use

In general is a good idea to check the scientific literature in the subject. In the section "materials and methods" you could find how people do stuff like measuring growth or controlling pH.
Of course, many of the methods described there could be out of reach, but you can get ideas and ask here more specific questions.
For this specific question a quick search lead me to this paper "Standard Methods for Measuring Growth of Algae and Their Composition"


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How to Find Ticks for Research
I am an amateur researcher looking for castor bean ticks for a science project. Where could I procure them the easiest? I am located in southern California.

Why castor bean ticks specifically? There are lots of USA native species that might work in their place rather than getting one largely found in Europe.

We want Ixodes ricinus specifically because we are experimenting with their reaction to static electric fields and that interaction has only been shown with Ixodes ricinus so far.

Where do you live? How you obtain them most easily vs. most economically depends in part on where you live.

Near Los Angeles.

I'll assume (danger!) that your Ixodes behaves like most Ixodes do. The way "questing" ticks (e.g. Ixodes scapularis) are collected is to go where they are common and use a white flannel cloth attached to a pole, the ends of which are tied to a rope, then dragged behind oneself and checked periodically for ticks and collected if present. This works wonderfully for a variety of applications. If that mostly European tick isn't common near to where you live, then you'll have to buy them. Sorry I don't have a better suggestion.

I should add that the cloth should be weighted. Here's a link in case of interest. You might try exposing Ixodes scapularis to a static electric field; they aren't very different ticks, and are probably abundant somewhere not too distant from your location. Where I live (a hotspot for Lyme), I could probably find a hundred in a couple of hours or less this time of year.


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What is the relation between Transpiration and Physiological support in plants
According to my information,When transpiration increases, The amount of water lost from the plant's leaves increases.So,Shall i assume That the relation is inverse according to this condition,or shall i put in consideration that when transpiration increases , The amount of absorbed water increases to compensate the lost water so the relation is direct?

What do you think - what would be the result if water uptake did not compensate for water loss?

@bob1. I Think that no physiological support occurs.

Why do you think that? What would be the consequence for a leaf if it lost water and didn't replace it? A hint - what happens to a cut flower if you don't put it in water?

When transpiration increases, the rate at which water evaporates from the plant's leaves also increases. This creates a negative pressure (tension) in the xylem, which helps to pull water up from the roots to replace the lost water. So, in this case, there is a direct relationship between transpiration and water absorption, as increased transpiration can lead to increased water uptake from the soil to maintain the water balance within the plant.
However, an excessive transpiration, such as during hot and dry conditions, can lead to water stress on the plant. If the rate of transpiration becomes too high and the water uptake from the soil doesn't compensate for the water loss, it can lead to wilting or even damage. So, in this case the relationship could be considered somewhat indirect, as high transpiration could potentially lead to reduced water availability and stress on the plant.


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How does positional memory in fibroblast cells work?
I have a question regarding how positional memory in fibroblasts work, specifically, where the memory comes from/how its made.
For example, the Salamander & other amphibians are able to regenerate almost perfect copies of decapitated limbs, but lets say we have a female Salamander who is effectively given hormone therapy to “masculinise” them, if a limb was severed, would it grow back according to the hormone profile? So essentially a bit smaller since males are typically smaller?
I’m very interested in the possibility of sex change through genetics, especially after bones have fused, effectively a reversal. It seems as though this may be a way forward though I am unsure.
Thank you for reading!

I don't have in depth knowledge about how amphibians are regenerate their limbs but in embryonic development all tissue's cells differentiate and come from stem cells according to tissue they inhibit or enhance the transcription of which genes that defines the attributes of tissue. Connective tissue such as fibroblasts differentiated from mesenchymal stem cells. So, in theory if you want to regnerate or in this case replace the "Feminine" muscle and bone alignment with "masculine" we need Embryonic STEM cells to generate it but also we need to broke down former ones. So just we need to utilize apoptosis and use gene therapy to do that. There is risks involved currently with recent gene theraphy techniques and also concentrations and conditions in vitro are affecting the differentiation process when using ste cells. In short every tissues fate decided by STEM cells. Ah I checked stem cells, I just googled sex change by stem cells and find some articles
Click first!  "They produce male and female stem cells from same person that have mosaicism"
And also second!"Tissue Engineering Neovagina for Vaginoplasty in Mayer–Rokitansky–Küster–Hauser Syndrome and Gender Dysphoria Patients: A Systematic Review"
And lastly!"Biotechnologies that empower transgender persons to self-actualize as individuals, partners, spouses, and parents are defining new ways to conceive a child: psychological considerations and ethical issues"

Thanks for the response! In the case of an adult having their muscular skeletal structure changed from feminine to masculine & vice versa, would the cells have to at least have the memory to create the post-pubescent human structures? So perhaps growing subject tissue under a sex hormone & transferring the relevant genetic information over to the main subject?


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Plants taxonomy: priority of names published in the same year
Article 11.3 of the International Code of Nomenclature for algae, fungi, and plants states that the earliest valid name with the same rank has the priority.
The question is: if two names (or more...) of the same species have been validly published exactly in the same year and, apparently, it seems impossible to ascertain which one was published earlier, how to decide which one is the name which has the priority?
Thanks

Is this a hypothetical? Because I can't see this actually happening unless it's a new species identified separately by two individuals unaware of the other's discovery.

Not hypothetical. It is something that happens.
It is a case of two binomials (referring to two distinct plants) but that are exactly homonymous and have been published exactly in the same year. So, I have the need to decide if one or another has the priority.
Unfortunately old works did not show the month of publication, so at the moment I cannot uscertain which one was published earlier in that year.

As you state, it's not just the year but any point earlier in time. Even though the publications may not indicate themselves exactly when they were published, I think this still holds. I know there are cases where folks have done a lot of extra research to establish when, or likely when, certain manuscripts were published in order to clear up questions like this.

@David, nomenclature is essential for talking about anything in biology, and the taxonomists who craft the various Codes are working biologists, so they may indeed frequent this site and know the answer. It's true that this question isn't about biological processes, but this site is "for biology researchers, academics, and students," and specifically covers "questions about techniques in a biological or biochemical laboratory," which I think pretty squarely includes taxonomic techniques.

@Darlingtonia - I could not agree more that this question, though it may not have an answer, belongs on this site. To the OP, is it possible to contact the publisher(s) for the date of publication? If you must write about it, you can give both names. For a good while after orexin/hypocretin was discovered by two separate groups pretty much simultaneously, it was referred to as "orexin/hypocretin". Now it's usually referred to as "[one], also known as [the other]". I have no idea when this will be resolved.

Please supply details of the case and provide a link to the International Code of Nomenclature.


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What's this mold? (With microscopic images)
So I (living in NRW, Germany) found an apparently quite homogenous mold colony at home, and would like to know what type of mold it is.
How I found the colony, where it grew:

I ate something, then took a little nap, then woke up later a little nauseous. I blamed it on the food (which still is a plausible possibility).
Then I noticed that my room smelled a little different from the stairwell (a little sour), and went searching for rotten stuff.
I then found a large bowl with a little food leftovers and a huge mold colony.
I remembered that some days prior, I removed a plate with food leftovers that was stacked on top that bowl, ironically because it had gotten moldy (with what looked like a different type of mold).
Given that there was lots of mold in the bowl and I had removed the plate only some days prior if I remember correctly, the mold probably already grew in the bowl with the plate stacked on top, shielding it from light, and severely limiting air exchange, until I removed the plate, of course.

I made several images of the mold, one of the colony, which had grown on two leftover noodles, and several of the mold's structure, including its fruitbodies, under the microscope. All but the last two microscopic shots were made with the light coming from below, the last two shots were made with the light coming from above, if I remember correctly.
The images:
Image 1:

Image 2:

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I'm no expert, but there's a key here - it has picture and text keys in links inside the page. I think possibly Rhizopus or Mucor.

Thanks for pointing me to the "key", I didn't know such things existed.
With the help of the key, I now managed to form my own hypothesis of what fungus this is, tough I won't mention it to see if others independently arrive at the same answer, to check its "plausibility".

Keys of this sort have existed for a long time - I think it was around the 1700's they were invented. Certainly Lamark used them, but I think they were around before him.


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A fully understood living organism
I have no background in biology but in the context of other research I am wondering if there is an organism, however simple it is, whose functions and structure is fully understood by biology or biochemistry. This would mean that all the functions and roles of all its genes are documented and all its internal procceses also. In other words is there an organism that can be fully analyzed in terms of its chemical processes and its RNA/DNA?

Welcome to Biology.SE! It depends on what you mean by fully. We don't know function of every gene present in any organism (we don't even know how many genes we have!). However, if you exclude some processes from your list, most probably E. coli or C. elegans might fit in.

No, there is not. Biological organisms are complex and have substances/interactions which have yet to be discovered. We are discovering new things about relatively simple organisms every day. However, the closest you will come is a "simple" bacteria like a ssp. of E.coli. Better yet, a virus, if one could classify it as an organism.

I was asking this question because I was trying to come up with examples of "strong emergence". The idea that there can be properties of very complex systems that are irreducible to the properties or even the interactions of its constituent parts. The property of conciusness is an example of strong emergence and I guess the emotional effects of music is another one. From your answers I can see that there are examples of strong emergence even in single cell organisms.


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What is this small black spider found in NY?
I found this small, black, spider with a yellow mark at the top of its abdomen, crawling on my desk in my office (located in the Lower Hudson valley in NY). I have never seen a spider like this before.

What is this spider, and is it native to NY, or is it an invasive species?

It is hard to see in the picture, but did the spider have 3 distinctive yellow marks in its abdomen. If so, it could be a jumping spider.

I did some searching on line, and see it looks like phidippus audax, but it didn't seem to do any jumping.

Jumping spiders are the largest family of spiders on Earth; now that you've seen one, I'm pretty sure you'll notice them around. And they almost all look like this, but with different coloring, sizing, and back leg modifications. And, yes, they can and do jump when they need to, though it's more like a hop. A scary hop, when they are trying to scare you off. They make me jump.

If one of the answers below have answered your query, consider accepting it by clicking the green checkmark, giving you and the other user some reputation points. This aids in closing the question as solved. There is no obligation to do it either.

It resembles a juvenile Phidippus audax, of the family Salticidae.

Image Source: SpiderZule
According to Wikipedia >>

They are typically black with a pattern of spots and stripes on their
  abdomen and legs. Often these spots are orange-tinted in juveniles,
  turning white as the spider matures.

Phidippus audax is a common jumping spider in North America and definitely not an invasive species.

Are the number of spots on the abdomen variable? I am sure the one in my picture had only one, not three like the one in the image you provided.

@lzam There are varying patterns for the distinctive markings, ranging from strokes to spots. Most commonly observed are a collection of 3 spots with one of them being bigger than the rest of them. I cannot be sure, but maybe the number and type of spots change during maturation - this guess can be made because the color of their  spots does change on maturation. Again, I could be wrong.

It is the Bold jumper, Phidippus audax. The “Bold Jumper” is one of the largest and  common species of jumping spider in North America. The spider is mostly black with a white, orange, or red triangular patch in the center of its abdomen.


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Prevention of disease spreading in animal kingdom
It's my first question on here, so I'm not sure If my question fits the theme. Please refer me to the appropriate one, If I have made a mistake.
So a question that I wanted to ask has to do with whether or not animals potentially try to avoid spreading diseases. So I was thinking... In an event that a really deadly disease emerges in a population, it would be really dangerous for animals that live in social groups, of any size really, not to have any instinctual behaviours that try and prevent the disease to spread. Animals that live in big heads, like wildebeests would just probably leave the diseased individuals behind, apes and monkey could potentially cast out individuals from the group, etc. Ants have separate sections in their tunnels that serve as graveyards, I presume for this exact purpose.
A lot of parasitic organisms have adaptations that specifically target animals with social behaviour, so why wouldn't animals adapt against that?
Something that also came to my mind is that this could possibly evolve not as a social behaviour of a group, but sometimes that individuals in a group would do, for example self isolation. However, I do not find this likely, I possibly requires higher cognitive understanding of disease spread.
Am I way of base here? If not, could you please provide some interesting examples you are familiar with.
Please consider that I AM NOT a biologist, nor have any experience in the field. I am a computer scientist, who enjoys biology. If any of my axioms or hypothesis have don't even come close to reality, please be kind, I am not educated in this field. Thank you for reading

Humans lived in tribe systems like animals and were protected from pandemics, until very big cities and the start of globalization... yersinia pestis was one of the first to arrive by boat in constantinople in 4AD, they were walking on dead "like pressing raisins under the feet"... American indians were protected because they lived in tribe structures, from old world illnesses. Generally, animals  often live more like tribes than pan regional societies.

If only we had an anthropology stack. Not an answer, as I can't find any references to the practice for this use-case, but I've heard tell of tribal practices/customs of abandoning the elderly/frail under times of hardship - the same may have extended to various forms of sickness.

Taking the evolution angle, some anti-transmission behavior may be hardwired (not requiring human-level intellect) e.g. an infection usually means symptoms like (high) fever, malaise, fatigue, lethargy (mental + physical) which, combined, leave the infected person bedridden and the less you can move around in the environment, the lower the chances of you spreading the infection. Sick leave? Modern, scientifically justified methods of breaking the transmission chain, e.g. isolation/quarantine/immunization, are ultimately extensions of natural behavior found also in nonhuman animals (in response to infections). The "objective", if we could call it that, of bodily response when under assault from a pathogen, is to immobilize (e.g. severe case of the flu) or die (ebola hemorrhagic fever), both being variations on quarantine.

I like the question, and it's an area I've given some thought to. My answer is "yes." Yes, animals have adapted behaviors to avoid getting sick from disease. There's not much motivation for an infected individual to avoid spreading it, except perhaps to avoid spreading it to closely-related individuals. Nor is there a mechanism for the behavior to evolve, since the sick individual isn't going to have as many (any) grandbabies.
That said, GROOMING is a great example of an evolved behavior that is almost universally done between mother mammals and their babies, and between close adult individuals in some species. It could be affectionate disease-prevention.


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Could a large constrictor kill a small animal?
According to this article there was a python whose body circumference was 85cm.  This means its diameter was 27cm.
Would it be possible for this snake to constrict animals that are about the same size as its diameter?  It is hard to imagine it having enough flexibility to constrict a swamp rat, for example, whose size is less than 27cm.  Could it kill such animals by another method, say with its jaws or by crushing them by rolling over them?  Or are such small animals simply off its target list?

Constrictors doesn't have uniform body circumference from head to tail. They coil around the prey accordingly. In your example, if the prey is very small, it just swallows. If its little big, it coils a little bit (check some videos like this) say two turn coil. This will only cover top half feet of constrictor's length which is of lesser diameter than the body.
So basically, they crush the prey and perform a kill. Its not a necessity for any constrictor to use its entire body to coil around a prey. They adjust their coil level to control the prey.


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Are all genetic instructions in DNA?
Wiki says

DNA is a molecule that carries most of the genetic instructions used
  in the growth, development, functioning and reproduction of all known
  living organisms and many viruses.

What bugs me is the "most" there, it implies some of the genetic instructions are elsewhere, but where?

Are all _____ instructions in DNA.. Genetic: yes. Inheritable: no.

Would you please expand on that, or give me a general direction on where to look for?

maybe you mean histone modification

Genetic information specifically means DNA or RNA in case of certain viruses. There are, however, other information that can be inherited which include cytoplasmic factors like mRNAs, proteins, vesicles etc. Check maternal inheritance.

Generally, in Biology it is better to use "most". Because we can't be sure that we have done a complete research about it. And about your question:
Yes. But note that the whole genetic instructions are NOT located in the Nucleus(of course, in eukaryotic cells like ours). Also note that some genes like Metabolic Enzymes's Genes are located in the Mitochondria(and the Chloroplast in Plant cells).

Food for thought: If you just have DNA, you can't set and forget a cell. The genes have all the information, but you have to borrow proteins that are already there from cells that already exist (and you get these during cell divisions, like DNA/RNA polymerases). This is a sort of cellular memory.

I don't know why it says "most". I think it is misleading and it should be written "all" (or "most" should be removed). Note though, that the genetic information of an individual is (in most species) is contained in more than a single DNA molecule, which makes the sentence even more confusing. Note also, that in eukaryotes (which includes plants, funghi, animals and some others but does not include bacteria and viruses), there are DNA in the nucleus and DNA in the mitochondrion (and other double-membrane organelles).

@Remi.b The statement is fair, especially if you are willing to consider RNA viruses as a form of life. Also, if you think about Maternal Effect in embryonic development, these are usually mRNA gradients that are established prior to fertilization and have a significant effect on embryonic patterning and axis formation. While the genes are expressed from DNA initially, they are not expressed by the organism that develops, so you can argue that these instructions are RNA-based, as they were expressed in the parent organism and not the resulting organism.

Genetic information is the heritable information used by organisms to guide their self-assembly. It's why traits can persist across generations. DNA is, by far, the primary material used (by life) to encode genetic information, but it's not the only one. RNA is a pretty common alternative to DNA.
If we're looking to Wikipedia, this is actually referred to (in passing) on many pages about genetics. They usually link to the page on the best known edge case, RNA viruses:

An RNA virus is a virus that has RNA (ribonucleic acid) as its genetic material. This nucleic acid is usually single-stranded RNA (ssRNA) but may be double-stranded RNA (dsRNA). Notable human diseases caused by RNA viruses include Ebola hemorrhoragic fever, SARS, influenza, hepatitis C, West Nile fever, polio, and measles.

While viruses fall into a weird middle ground between life and inanimacy, they still all need genes, and many of them use RNA for that. Side note: retroviruses get their name from the fact that they use reverse transcription to synthesize DNA from an RNA template.

I guess that's excluded where it says "many viruses" instead of "all viruses"

I'm not sure what you're referring to being excluded (too many pronouns), but 1) biology is full of exceptions, and 2) many viruses store their genes in DNA.

RNA is an alternative, not a complement, by using "many viruses" I think wiki rules out RNA viruses from that sentence. The use of "most" suggests that there is a complement. About mitochondrial DNA, it's still DNA. So it probably is just a wording mistake in wiki or a misinterpretation by me as so far I know of no such complement.

@erik Maternal effect genes during embryonic development are set up in the oocyte prior to fertilization on mRNA. Obviously these genes are found on maternal chromosomes (DNA), but they are not expressed by the oocyte or the embryo, so technically the instructions are stored on RNA and the RNA is heritable, They may also be referring to epigenetic modifications, though there is still a bit more controversy about whether or not those are heritable.


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How were the first genes isolated from genomic or cDNA libraries without already knowing a hybridization probe?
Let us go back in time to around 1975. It is my understanding that at that point (or at least by the end of the decade), both genomic and cDNA libraries had been created for a few organisms, e.g. rabbits. I'm interested in the logic of techniques that first used these libraries to isolate genes encoding for particular proteins. Note: I'm not interested in how we'd isolate a gene today; I want to understand the history.
First, consider the following thought experiment. Say it's around 1975. The one assignment for my Cal Tech biology class is a doozy: it goes as follows. The instructor (Tom Maniastis?) hands me a protein along with the cells from which the protein was isolated as well as genomic and cDNA libraries of the organism that makes the protein; the challenge is to isolate the gene encoding for the protein. I do not know anything about the protein except that the product I've been given is pure.
Of course, the basic idea is simple: isolate the gene by screening the libraries with a radioactive nucleic acid probe and using a hybridization assay. But alas, I do not have a complementary probe: all I have is the protein! What do I do?
Here is one solution I can imagine. (I don't know whether it was possible around 1975, much less whether it actually happened.) I could try to isolate the mRNA that codes for my protein (but how to do that?), then radiolabel it and use the radiolabelled mRNA as a probe in a hybridization assay on the cDNA library (not the genomic library, since the unprocessed DNA could have noncoding regions).

Would this have worked?
Did anyone actually do this?
If yes to either (1) or (2), how could one figure out which mRNA coded for the protein?

The question, in essence, is how to get to DNA, given only a protein, circa 1975.

I am curious as to why you posted here. If you really are at Caltech and just wanted to know the answer you should be smart enough to do a literature search and find the answer. However, again if you are at Caltech you presumably are bright enough to want to work it out by yourself, so you don't want those of us (me) who were around in 1975 gave you the answer (which I won't). As you, yourself admit, your proposal is flawed ("how to isolate the mRNA?"). Do you want a hint or discussion? That's not what SE Biology is for. Tell me why I shouldn't vote to close.

@David: I'm not at Cal Tech. I'm a math-trained grad student in the history and philosophy of science. I said explicitly it's a thought experiment. I don't know how to find the result in the literature. If you want a different way of asking the question: tell me how Maniatis et al 76 and 78 got mRNA rabbit insulin probes. I'm not trying to start a discussion: I want the answer. I find it cynical and unnecessary for you to assume I didn't want the answer.

Another possible solution: get the protein's amino acid sequence (using Sanger's technique), then synthesize a lot of RNA or DNA probes compatible with it (there will be a huge number, thanks to degeneracy of the genetic code). But was synthesis possible then? I don't know enough of the history to know which of these methods could've been done in the late 70s.

I wasn't being synical, just trying to find the context to your question (which nobody else had responded to). Your latest suggestion is a more logical use of the pure protein idea. You might think what else you can do with a pure protein, and also — as you mentioned cells — why proteins like insulin and globin were "low-hanging fruit". I'm a bit busy at the moment, but will respond in due course if nobody else does.

Thanks. I assume no one answered because others don't know the answer: it's a non-trivial problem, not Googleable or capable of being looked up easily. I know insulin and globin were overproduced by insulinomas and red blood cells, so their mRNAs were abundant. But how to isolate the mRNA responsible for insulin, say, in particular?

This paper seems to be the first to isolate the rat insulin gene. I'll convert it to an answer later if I find the time.

Many genes responsible for a given phenotype were discovered by forward screens using marked transposons or complementation mapping. I could also imagine a scenario where the protein sequence is used to create a degenerate oligonucleotide to probe a cDNA or gDNA library.

@canadianer: thanks for your comments. I don't know what "forward screens using marked transposons" and "complementation mapping" are. maybe I could google them, but a succinct high-level description of the idea could work nicely as an answer. I'll read the Ullrich et al rat paper in the meantime.

The key sentence in the Ullrich paper is on the second page: "It seemed likely that the Hae III fragments were derived from insulin cDNA because of their prominence in the total cDNA preparation." So the answer to my question is that researchers exploited the overproduction of insulin in B cells to harvest all the mRNA, reverse transcriptase to cDNA, restriction digest, and then make an educated guess that the most prominent fragments contained the insulin gene, due to the high expression of insulin.

You can read this Wikipedia page for a start. In this case you don't start with a particular protein of interest but rather randomly mutate the genome and look for altered phenotypes. Then you look for the mutation that caused the new phenotype. If you used transposons for mutagenesis, you can include some kind of marker that allows you to quickly identify clones containing the mutated DNA.

@canadianer — If this question isn't taken off-topic, we should be providing proper answers. I've found a section of a book chapter I wrote last century on the topic, but it will take me time to condense it. Not before next week.

@David Agreed, I will write something soon hopefully. I look forward to your answer.

@David: can you just point me to your book chapter? Of course, you can answer here, when you get a chance, in order to close the question. But I'm very interested to hear that you wrote an entire chapter on this.

The following is based on a chapter on Cloning DNA in the 10th edition of The Biochemistry of the Nucleic Acids (RLP Adams et al.) published by Chapman & Hall in 1986. (This is probably more pertinent than the 11th and final edition, which was published in 1992 and had a more contemporary treatment.) Apologies for the fact that it will be difficult to find.  It should be available from some university libraries and through inter-library loan systems in certain countries. Section A.7.3 gives a taste of the methodology used at that time.
Protein properties that could be used as the basis of a cloning strategy
In attempting to clone DNA for a particular protein for which there were no pre-existing clones to use as hybridization probes, one had to consider the properties of the protein one is able to exploit. These might include:

Amino acid sequence
Antibodies to the protein
Biological activity
Particular physical properties, such as size

(Clearly if one had no such ‘handle’ to the protein one was not in a position to try to clone its cDNA or gene.)
Three general approaches
There seemed to be three general approaches:

No expression
Indirect expression
Direct expression

The approach that one might take was also governed by whether the protein is particularly abundant in a specific tissue, when one might expect less sophisticated more labour-intensive approaches to stand a chance of success.
Another point to emphasize is that, at least with eukaryotes, one would look for a cDNA clone first, and only try for a genomic clone after one had this to employ as a hybridization probe.
1. ‘No expression’ approaches
In the no expression approaches one relied on the amino acid sequence to identify the cloned DNA. One such approach was to use hybridization probes against stretches of amino acids, the codons of which had limited redundancy (Met and Trp have a single codon, and some other amino acids only two) using low stringency hybridization conditions. This required luck. Alternatively one could sequence random clones and hope to find one that correlated with the amino acid sequence. At that time DNA sequencing was slow and labour intensive, so that this was only applicable to proteins that were relatively abundant in the tissue from which the libarary was prepared.
2. Direct expression approaches
Direct expression generally entailed using a bacterial expression vector which produced a fusion of a bacterial protein with a part of the eukaryotic protein. (Statistically only one in six of clones would have the correct reading frame in a fusion protein.). This approach was favoured if one had an antibody, which did not require a complete protein.
3. Indirect expression approaches
By indirect expression was meant using immobilized cloned cDNA to select corresponding mRNAs (‘hybrid selection’) which could be expressed in a cell-free system. This was appropriate if the distinguishing characteristic required a full-length protein, as in the case of biological activity or size.

Specific to the insulin gene, the following paper is, as far as I can tell, the first to isolate it:
Ullrich A, Shine J, Chirgwin J, Pictet R, Tischer E, Rutter WJ, Goodman HM. 1977. Rat insulin genes: construction of plasmids containing the coding sequences. Science 196:1313-1319.
The took advantage of the fact that insulin is produced by β cells in the pancreas and so are enriched in insulin mRNA. After poly(A) RNA was isolated and reverse transcribed, the major band observed upon electrophoresis of the resulting cDNA was expected to belong to the insulin gene:

It seemed likely that the [major] fragments were derived from insulin cDNA because of their prominence in the total cDNA preparation. Therefore, these fragments as well as the complete cDNA preparations were used in the cloning experiments.

Thus they cloned this cDNA, sequenced it and discovered that it contained the entire proinsulin coding sequence:

Since the mRNA contains a terminal poly(A) sequence, the [cloned] DNA strand containing 3' terminal poly(dA) is of the same sense. This strand determines an amino acid sequence which exactly corresponds to the entire coding region for rat proinsulin I and 13 out of 23 amino acids of the prepeptide sequence.

With this sequence determined and because of its high degree of conservation, the homologous human gene could be isolated by hybridizing with rat insulin cDNA:
Bell GI, Swain WF, Pictet R, Cordell B, Goodman HM, Rutter WJ. 1979. Nucleotide sequence of a cDNA clone encoding human preproinsulin. Nature 282:525-527.


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Membrane resistance of a neuron
I am about to simulate a neuron activity with the "Leaky Integrate and Fire" neuron model. But for that I need the membrane resistance. I was really looking a lot online, but I just cant find a value. Does anybody know the measured resistance value, or the value usually used in this model?

Welcome to BiologySE - thanks for your question... do you think you could give some references to the "Leaky Integrate and Fire" model to help other individuals better understand your question? Also, you may want to check out the help center for pointers on how to ask a good question...http://biology.stackexchange.com/help


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Why can polar molecules like water pass aquaporin better than unpolar like H2 or CO2
We learned in our lecutre, that aquaporin lets Water pass, but blocks Ions like H+ and unpolar molecules like CO2 and H2. The reasons for the Ion blocking are comprehensible, but I dont get, why less-than-water-polar molecules are blocked. Our professor said, it has something to do with the water molecules are orient in the aquaporin towards the positively charged n-terminus of the alpha helix, but why is that an advantage compared to non polar not charged molecules?


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Evolution of the human Y chromosome
This recent news article suggests the number of genes in human male Y chromosome has steadily been reducing in the Y chromosome for a long time and is in danger of dying out all together.
What I want to know, is if this is a bad thing, why don't normal evolutionary forces act to prevent this? For example if some individual is born in the future with a further reduced gene count in their Y chromosome and this reduces or eliminates their fertility, they will will have less offspring and that trait will die out. Why would the human race evolve in a way that is disadvantages to reproduction, when that is the main driving force of evolution?

What I want to know, is if this is a bad thing, why don't normal evolutionary forces act to prevent this?

You seem to be attributing a moral value to an evolutionary process. So does the article you linked to your post (probably for sensationalism), which is not a scientific way of reasoning. I suggest you read the original article instead. In the abstract, you can read :

The results of our study suggest these forces are not exclusive to the Y chromosome, and chromosomal degeneration may have occurred throughout our evolutionary history. The reduction of recombination could additionally result in rapid fixation through isolation, of specialized functions resulting in a cost-benefit relationship during times of intense selective pressure.

Therefore, this trend is not specific to the Y chromosome, and there is no evidence that the reduction in the number of genes on the Y chromosome has been associated to a decrease in the fitness of humans.


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How to use karyotype notation?
I'm looking at two karyotypes, one for a person with Klinefelter's Syndrome and another with Patau's. What is the karyotype notation for them? I don't understand what I looked up online. Any help is appreciated. Thanks!

Welcome to Biology.SE. This is not simply an answer site, but instead a site that promotes self-learning with some expert help. Consequently, questions that show little or no prior research effort are off-topic on this site as are "homework" questions unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Please take the [tour] and consult the [help] starting with [ask] for details.

At a minimum, posting the notation that you found when you looked them up would be helpful.


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Using the law of independent assortment, why can't heterozygous parents make identical twins?
In a case where two parents are heterozygous, why can't any pairs of their children be identical twins? As the question asks, I tried to explain this using the law of independent assortment, which states that alleles a gamete receives for one gene do not affect alleles for the other. I don't get how this relates to identical twins. When I searched this up, I found that identical twins come from when an egg splits into two, but if it's one cell, why would the law of independent assortment matter? Same with the heterozygous part - why would that affect the formation of identical twins when it's copies of the same cell? Any help is appreciated, thanks!

They do it all the time, because identical twins come from one (fertilized) zygote splits into two embryos instead of remaining one. You and I understand this, but I don't understand the rest of your question. The independent assortment already happened before that split. :/

what do you mean when you "heterozygous" exactly? all humans are heterozygous (or rather, the probability of complete homozygosity of a human genome created by sex is astronomically small)

Are you sure the question is about twins? or just identical children from separate gestations? If the latter - then you can explain it using independent assortment. The former - as already mentioned - happens all the time for reasons already explained.


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Can GFP reporting be used to track localization of peptides in the ER, Golgi, and plasma membrane?
Suppose I want to study the trafficking of a peptide throughout the ER, Golgi, and plasma membrane. An idea I had was labeling a secreted or plasma membrane integral protein with GFP and using time-series live cell microscopy to track it through the secretory pathway.
However, I am concerned that by the time everything is set up, the cell will be at steady state, which means GFP signal would be present throughout the secretory pathway, preventing me from doing this tracking.
How might I overcome this, without changing the fundamental technology (GFP reporting)?

There are several well-established techniques for this kind of experiment ...

Historically speaking, the use of VSVG (Vesicular Stomatitis Virus G protein) labeled with GFP was indeed a practical method to define the secretory pathway. (@tyersome comment)

However, I am concerned that by the time everything is set up, the cell will be at steady state, which means GFP signal would be present throughout the secretory pathway, preventing me from doing this tracking.

Sec mutations in S.cerevisiae: Many biochemical pathways are initially identified owing to a particular mutation in the synthesis process. Recall Beadle and Tatum experiment and the logic they used to clarify the existence of 3 enzymes used in arginine metabolism.

(Image taken From https://www.chegg.com/homework-help/questions-and-answers/following-experiments-beadle-tatum-searching-mutations-disrupt-arginine-biosynthesis-pathw-q41797559)
A similar approach was taken back then to identify the distinct parts of the secretory pathway. Five different mutations in S.cerevisiae were identified named from A to E. Culturing all A to E mutated strains plus VSVG-GFP assay would clearly demonstrate the entire route.

(Image taken from https://slideplayer.com/slide/4382105/)
For example, even if the mutated class B, reaches the steady/equilibrated state, transport vesicles, Golgi, and the rest will not show the fluorescence activity (characteristic of VSVG-GFP) because all of the proteins have accumulated in the previous step(i.e budding from Rough ER)
Further Readings :
https://pubmed.ncbi.nlm.nih.gov/2188733/
https://www.sciencedirect.com/science/article/abs/pii/0092867481900647
MCB Lodish et al 8th edition chapter 14 section 14.1
https://www.nature.com/articles/35073068

Is this to say that it is indeed impossible to monitor localization without knocking out parts of the pathway and comparing?

@actinidia  Knocking out and comparing is usually the easiest way but, now that we know the basic fundamentals and characteristic features of each step in this pathway, other methods can also be employed but I haven't searched or seen any researches, to be honest. You can search for it on your own. Theoretically, we can use 1) Förster resonance energy transfer (FRET) Biosensors: As you know, there is a pH gradient from ER to cis Golgi and later to trans Golgi. (Later sections are more acidic) So one can use this feature to build a molecular environmental biosensor that assumes different ---

@actinidia ---conformations in the presence of different pHs, which in this case would colorize the pathway with 2 different colors(for example Yellow/Green if GFP and YFP are used in the construction of the biosensor protein.)
2)Pulse-Chase methods definitely could be used but it doesn’t use the fluorescence as you’ve asked, so it is off the table.


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Is it possible to exclude article types in a PubMed search?
I have a question about searching PubMed. I want to search for original research papers while omitting reviews. Is this possible in PubMed?
Example
If I am interested in the relation between Acute Renal Failure and Salt, I could use the following search string:

("Acute Kidney Injury"[Mesh]) AND ("Sodium Chloride"[Mesh])

Using the column on the left of the article overview list, you can select which article types you are interested in.
Question
But I wondered if it was also possible to exclude a specific article type (e.g., reviews) from the search?

I believe this will work:
((Acute Kidney Injury[MeSH Terms]) AND (Sodium Chloride[MeSH Terms])) NOT (Review[Publication Type])
Using the advanced search settings on PubMed it was easy enough to set up, here is the link in case you don't have it already:
https://pubmed.ncbi.nlm.nih.gov/advanced/


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How to correlate CNV with transcriptomic data?
I have a list of differentially expressed genes. I want to correlate these genes with CNVs. I have downloaded the data from both TCGA and FireBrowse. But I am not able to understand how to do the correlation? How should I analyze the CNV data. Do you have to do some processing to get a list of CNVs with a score or something to do the correlation? Please help

Might be better off moving this post to https://bioinformatics.stackexchange.com/

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. In particular, I'm voting to close this question because it better fits [Bioinformatics.SE], but please do not crosspost, instead request migration. ———— In addition, we encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Thanks!


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Difference between a phototroph and a photosynthetic organism?
A quick search on google about the topic and the page on wikipedia did not help understanding the difference between these two related terms.

Practically, 99% of the time there is no difference when using one term or another.
More strictly:
A phototroph ("a thing nourished by light") is according to your wiki page:

It is a common misconception that phototrophs are obligatorily photosynthetic. Many, but not all, phototrophs often photosynthesize: they anabolically convert carbon dioxide into organic material to be utilized structurally, functionally, or as a source for later catabolic processes (e.g. in the form of starches, sugars and fats). All phototrophs either use electron transport chains or direct proton pumping to establish an electrochemical gradient which is utilized by ATP synthase, to provide the molecular energy currency for the cell. Phototrophs can be either autotrophs or heterotrophs.

and

If their electron and hydrogen donors are inorganic compounds (e.g. $Na_2H_2SO_4$, as in some purple sulfur bacteria, or $H_2S$, as in some green sulfur bacteria) they can be also called lithotrophs, and so, some photoautotrophs are also called photolithoautotrophs.

So the difference resides in that some phototrophs do not carry out photosynthesis, which is a specific set of metabolic functions (those that do $CO_2$ --> organic compounds). An organism that carries out photosynthesis is then a photosynthetic organism.
In other words, photosynthetic organisms are a subset of phototrophs.


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Why doesn't the concentration of one ion affect the concentration gradient of another ion across a plasma membrane?
In the initial stages, some ion channels across the plasma membrane open to allow for ions to flow down their concentration gradient into or out of the cell. I understand that each ion's overall electrical potential across the membrane would affect the other ions', thus affecting their transport across the membrane. However, I don't understand why the concentration of ions aren't taken as an overall concentration because surely, if we are looking at diffusion of ions caused by Brownian motion, then all molecules on either side of the membrane would affect the other molecules on that respective side of the membrane?

Why do you think this about Brownian motion?

Because Brownian motion affects the random movement of the ions?

But, what aspect of Brownian motion makes you think the concentration of one ion affects the concentration of another?

Brownian motion is the random, uncontrolled movement of particles in a fluid as they constantly collide with other molecules (Mitchell and Kogure, 2006). Therefore, wouldn't the ions collide with one another and if there is a greater concentration of one ion outside a cell, it would increase the number of ions that can collide with the other ions, hence increasing the frequency of collisions, affecting the overall ion concentration gradient (is this a scientific term)?

No, it would not. I do not understand how you are going from frequency of collisions to a concentration gradient. In any case, the equations that are important are pretty well understood (Nernst, Goldman/GHK) - maybe best to start from those and try to understand what they say rather than speculation?

So is the point here that the concentrations of each ion only affect each other to the extent of their electrical potentials because the main thing that affects whether they can pass through the plasma membrane is the permeability of the leak channels/voltage-gated channels (in the case of diffusion).

Yes, that would be the main point evidenced by those equations.


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Do electron microscopy change the structure of the specimen due to the vacuum step?
Since specimens have to be prepared using the vacuum, would the pressure change affect the structures of the specimen?

What specimens ? It certainly does not bother  metallurgical samples.

You should specify the type of EM.  Transmission electron microscopy uses a tissue block not conceptually much different from paraffin-embedded sections for the light microscope.  Scanning EM often involves coating specimens with a conductive material, which in most cases probably changes their structure more than the vacuum, but there are other options... that answer would be more interesting.

I was thinking along the lines of biological specimens like Bowman's capsule, and this question popped up in my head when I was looking at an SEM, but I guess I was just curious about whether there would be any artefacts caused by the preparation stages of the vacuum.

There are several different ways to deal with the difficulties of imaging biological samples in vacuum. I'll go over the ones I'm familiar with.
TEM - plastic sections
The water in the specimen is gradually replaced with a resin which then solidifies, and slices about 100 nm thick are cut from the specimen and put into the TEM column at high vacuum. The chemical composition of the specimen is radically altered, but the shape of cells and even the arrangement of organelles inside can be preserved if the treatment is done well. Here's a representative image for this technique from http://www.cellimagelibrary.org/images/7722. You can see the endoplasmic reticulum with ribosomes and mitochondria.

TEM - CryoEM
The specimen is cooled so fast that the water in and around it solidifies without forming ice crystals, which would otherwise disrupt membranes, etc. The specimen is nearly identical to its natural state. These 'vitrified' specimens can be put directly into the microscope column, but they need to be maintained at liquid nitrogen temperatures. The size of specimen that can be cooled rapidly enough is limited to about 300 microns thick. A standard TEM beam doesn't penetrate well through samples more than about 200 nm thick; cryo specimens can be cut similar to plastic sections (though it's much harder than at room temperature), or by focused ion beam milling. Here's a representative image from https://www.pnas.org/content/117/16/8941 showing flagellar motors:

Environmental SEM
Larger specimens can be imaged without dehydration or coating in an environmental SEM (ESEM). This microscope has a high-vacuum chamber for the electron gun and lenses, and a low-vacuum chamber containing the specimen and detectors. This method can image larger samples, up to about 10 mm, close to their natural state, but isn't as high-resolution as the TEM methods. Here's an image from https://forschungsinfrastruktur.bmbwf.gv.at/en/fi/fei-esem-xl30-scanning-electron-microscopy_540 showing a small fish, you can judge for yourself how well the structure is preserved:

Love the images! And great answer


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What are examples of successful novel ecosystem integration?
The cultivation of novel ecosystems, while formerly disparaged due to being conceptually misappropriated by special interest groups, may be necessary in adapting to climate change or simply in innovating more sustainable farming practices.
What are successful contemporary examples of novel ecosystem development?

Could you share some sort of definition of a novel ecosystem? I assume you are not talking about pathological invasions or sub-pathological species introduction, as those are quite common, or e.g. Galapagos-style patchwork ecosystems made from periodic introductions. Can you link to some sort of resource explaining what exactly you mean? What time-scale, how many species, is it on top of an existing ecosystem?

It's quite possible I am referring to exactly what you suggest, though not limited to that example. I am referring to a certain circumstances wherein a new ecosystem emerges on its own as a result of climate change and possibly nonnative species which happen to either intentionally or unintentionally introduced while present in the process. I can't really be specific because the thing you are asking me for is what I am asking others for. It's just a theoretical concept but at this point in climate change it must be happening somewhere.

It might help if you could provide a few links (e.g. an example of "disparage[ment] due to being conceptually misappropriated by special interest groups"); I'm not skeptical of your claim, but I'm a little unclear what you mean.

I am still not 100% sure of what the intent is here, but I think that you should look into community assembly rules. The basic (not universally or even generally accepted) idea is that there is some set of "rules" that makes a "successful" or stable ecological community. You can use those rules to design communities accordingly, goes the logic. Here is a short blog post that has some handy refs and simple language.
You could also look into microcosm + mesocosm research, where people have designed small self-sufficient communities, sometimes sealed off from e.g. gas exchange with the outside environments. Sometimes these collapse, and sometimes they work. Occasionally it has to do with randomness, and at other points it seems to follow a deterministic path.
All of these are under the heading of "community ecology", which I would strongly recommend looking into if you are interested.
I would also strongly recommend looking into invasion research, which is the most prominent example of getting a "new" community by just adding a few species to an existing community and seeing what happens. As I suggested in the comments, looking at communities on islands that have been invaded or have recruited species from elsewhere could be handy- e.g. Galapagos, Oceania, are examples to look into, how they have dealt with biological invasions and what has worked and what hasn't. This subfield is called "island biogeography", I do not know how many people still take it seriously but there are at least a lot of empirical observations about what happens when you add species.

Thank you for this more general information, I'll look into it.


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Do wolves mate with siblings?
I have just watched a "documentary" on a female wolf raising her cubs in the Alps. I found various aspects of the programme less than convincing, but one in particular puzzled me. The alpha male of the pack is killed, and his eldest son takes over as alpha. Whilst the alpha female remains with her dying mate, the programme stated she could not rejoin her pack, as her place had been taken by her daughter. This would mean a brother-sister mating - the female became pregnant very soon - which I find highly unlikely, although perhaps not impossible.
Wikipedia simply states:

Wolves are monogamous, mated pairs usually remaining together for life. Should one of the pair die, another mate is found quickly. With wolves in the wild, inbreeding does not occur where outbreeding is possible.

Wondering if there are any wolf experts on here?
https://en.wikipedia.org/wiki/Wolf

Do you have a link to this "documentary"?

@MattDMo - yes, it's this one, it does say it was "dramatised", which was fairly obvious, but still wondering how true to the facts it was. Thanks.  "BBC Two - The Snow Wolf: A Winter's Tale" https://www.bbc.co.uk/programmes/b0bwqdbg

I'm in the US, so unfortunately I can't watch the program. Usually the BBC is pretty good about trying to get the facts right, but seeing as they heavily emphasize the "dramatised" part, they may have played fast and loose with a few key details. OTOH, I'm an immunologist, not a wolf expert, so I can't really answer your main question. I hope it was at least a good show.

@MattDMo - thanks for looking, anyway. I have a feeling I've seen it before, but the last showing had a disclaimer at the end, saying it was filmed using a variety of wild and captive wolves. That disclaimer was not shown this time, if it was the same programme. But, yes, the scenery and film work were spectacular!

Mating with siblings or incestuous relationships (breeding within blood relatives) enhances the chance of expression of disadvantageous characteristics (mostly recessive alleles). Therefore, natural selection for complex animals occurred in such a way they avoid close relation mating. Wolves are no different. One study by Smith et al. 1997 with the samples from 16 wolf pairs showed that wolves rarely mate with their close relatives. However, inbreeding does happen on infrequent occasions. For example, a pair of wolves migrated to Isle Royale through an ice bridge in 1948. They are the first wolf pair on the island (founder population). The ice bridge doesn't happen again. Through the help of inbreeding (population bottleneck), the pack survived, and the population became 50 individuals [Inbreeding Causes Isle Royale Wolf Population Crash]. However, genetic diseases started expressing, and morphological deformity became very common in that wolf population. Therefore it is clear that nature support variation by avoiding inbreeding. And though billions of years of permutations combinations, biological organisms avoid inbreeding in ideal conditions.

Thank you, a very informative answer. I do  know most animals - including humans - avoid incestuous mating, although it is not unknown. Being more comfortable and with history, I know that brother-sister mating is thought to be responsible for the end of Tutankhamen's line, with two stil-born infants found in his  tomb. I did just find the email whole scenario in the programme unlikely.

I am not a wolf expert, unfortunately, but was able to find an article focused on just this question with grey wolf packs (1). The article studies relatedness via microsatellite locations in the DNA of mated pairs, and found that incest is seemingly avoided when possible, which supports your Wikipedia finding. Another article on Ethiopian wolves came to similar conclusions- wolves avoid inbreeding where possible, and resort to extra-pack matings when necessary (2).
Reference: (1) Smith, Deborah, et al. "Is incest common in gray wolf packs?." Behavioral Ecology 8.4 (1997): 384-391.
(2) Sillero-Zubiri, Claudio, Dada Gottelli, and David W. Macdonald. "Male philopatry, extra-pack copulations and inbreeding avoidance in Ethiopian wolves (Canis simensis)." Behavioral Ecology and Sociobiology 38.5 (1996): 331-340.

wow! Great find, thank you :-)


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Strange Onion and i don't know what it's
Today i cutting my onion and i saw so many verbs like this in it.  I searched about it through google lens and manually also but unable to find the reason of this. I doubt is it serious case ?

What you have there is the unripe flowering parts of an onion that's bolted, this can occur if the weather's been hot:

Copyright through: Greensideup.ie 2021, fair usage.
This would be more what it's like when the flowers open:

Copyright through: asergeev.com 2021, fair usage.
As you see, they come in a variety of colours, the ones in my garden are purple and red. They're edible and tasty in salads.

Ok so my one is also safe and it's normal.  Right ?

Assuming that what you had in the first place was an onion, then yes. But to be sure, check out hyacinths, they can look similar. Be assured that only the onion family (inc. garlic, chives, ornamental onions) smell like themselves. If it whiffs like an onion, then it's safe to eat. If it's an ornamental onion, it's safe, but not as tasty. @AmitMittal

Ohkey , thank you so much for all the details


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Is there an evolutionary advantage to bees to becoming docile when exposed to smoke?
I have not seen other research on this on line, it occurred to me though that this physiological behavior / stimulus-response of bees (calm down when exposed to smoke) might be a subject for original research, and understanding how benefits of this behavior may be applicable to human group psychology as well is another possible avenue of research.
An initial thought, perhaps the colony would better weather forest fires docile and hunkered down in a hive/ground/tree than reacting aggressively, or it may be a matter of another mechanism piggybacked on this response to sensory stimuli that is beneficial to the colony...or worker bee.
I'm just throwing this question out there, in the event that there is a theory or "answer".

There has been research done on this, and it's easy to find. Have you googled, "Why does smoke make bees docile"? If you have, please edit your question to improve it, because I can't see any application for it to human behavior.

You also might wonder what kind of Q&A site this is, getting such feedback. Aren't we supposed to just answer your question? Actually, no. We're expected to help if we so choose. We're scientists or people interested in science, a lot of us teach, practice, or research some aspect of Biology. We expect some meaningful degree of research; not a ton, but not nothing, either. Biology students need to learn how to find information. Consider this kind of like a classroom, not a chat room. You'll get a better response to your question with a better effort.


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How are spacer sequences created in a prokaryotic genome?
The CRISPR/Cas defense mechanism uses spacer sequences between palindromic repeats to search for the sequence to cut by an endonuclease. But how are these spacers created?
Let's take Bacteriophages, for example, which insert and integrate their genome into the prokaryotic genome. How does this infected cell get rid of the viral genome so that only a piece of the virus remains between palindromic repeats?

https://academic.oup.com/nar/article/50/3/1661/6511979


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CRISPR/Cas9: How can inserted DNA be used as a donor for the homology-directed repair if Cas9 only creates blunt ends?
The CRISPR/Cas9 method allows new genes to be inserted. After Cas9 cuts the Target-DNA, it can use a homologous piece of DNA as a donor template for homology-directed repair. But HDR only occurs when there are sticky ends, and Cas9's cuts end in blunt ends.
What did I miss?

According to this Addgene blog:

There are four different HDR pathways to repair DSBs. Here are  three
central steps of the HDR pathways:

The 5’-ended DNA strand is resected at the break to create a 3’ overhang. This will serve as both a substrate for proteins required for strand invasion and a primer for DNA repair synthesis.

...

Essentially, this resection process generates the required overhangs through partial degradation of one of the strands.
To understand the mechanism of resection a bit better, this is a good read:

Huertas, Pablo. "DNA resection in eukaryotes: deciding how to fix the break." Nature structural & molecular biology 17.1 (2010): 11-16.


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What insect/invertebrate species evolves fastest?
I am starting an experiment in which I will be forcing evolution in a moderately complex species of insect or invertebrate. I am prepared for the possible longevity of this experiment, but i have no clue what species i should use. I would prefer a species that can easily respond to biotic challengers. Reason being, every abiotic factor will be promoting the growth and prosperity of the target species, however every biotic factor will be trying to kill the target species. The species can be aquatic, amphibious or terrestrial.

Drosophila melanogaster. (fruit-fly, pomice-fly)

Image, public domain, via Wikipedia 2022.
Development time is under ideal conditions 8.5 days (at 25 Celsius, 77 Fahrenheit), the females produce perhaps 500 eggs per generation which can hatch in 12-15 hours - from the point of view of turnover, you should be able to observe many generations in a short-ish period at one generation per ten days in reasonable conditions.
Their diet is fruit, fungi - both preferably decomposing and are able to be anaesthetised with ether or carbon dioxide.
They have acted as a model organism (eukaryote) for the study of genetics and there are many known mutations, and established ways to produce them (ethyl methane sulfonate, ionising radiation).

A classic example

Thank you very much, you gave me all the info I needed.

@Astrophysicsteen You're welcome. Feel free to "click the tick" if you find this appropriate as an accepted answer.