text:
Do fruits have fingerprints: Can a fruit (say mango) be identified uniquely by some characteristics?
I am not a biology/botany person, so pls excuse me.
Context as asked in comments.
I want to track a fruit from the time it was plucked out of tree to the time it reaches in the hands of customer. Can customer ensure it is the same fruit what the seller claims it to be. Intermediaries can be cheaters and can also replace one with other.
Questions:
Can a fruit (say mango/kiwi) be identified uniquely by some of its characteristics? Do they have some fingerprint / facial recognition / retina scan / or some other similar way through which they can be identified uniquely?
Physical characteristics? I am not sure, but I think not: most of the kiwis look exactly same!!
Veins structure (using microscopy)? If yes, are there some mobile apps which a normal person like student use?
Similarly, can eggs be identified in some way?

Curious question, I'm imagining a "usual suspects" style lineup. Could you tell us a bit about the context, why you're expecting the science of (individual) fruit IDing might have developed, what sort of answer you're expecting here. Remember the site's requirement of showing your research when posting. There are for example ways of detecting ripe fruit, used by automatic picking systems in commercial groweries, is that what you're thinking of?

Sure. I have updated the question with context.

Please edit the question to limit it to a specific problem with enough detail to identify an adequate answer.


text:
(NSAA 2023 Section 1 Q80) Does a haploid blood cell exist?
I recently worked through the NSAA 2023 paper (the admissions test for those who wish to study Natural Sciences at the University of Cambridge) with my students and encountered the following question:

NSAA 2023 Section 1 Q80
Four blood cells were taken from a human:

one that was about to start cytokinesis
one actively producing antibodies
two that cannot use oxygen for respiration

What is the total number of chromosomes present in all of the cells mentioned above?
(Ignore mitochondrial DNA.)
A     92
B     115
C     138
D     161
E     184
F     207

My Workings
Four blood cells were taken from a human:

one that was about to start cytokinesis
[a diploid haematopoietic stem cells, with 2 copies of the 46 chromosomes]
one actively producing antibodies
[a diploid B-lymphocyte, with 1 copy of the 46 chromosomes]
two that cannot use oxygen for respiration
[two diploid anucleate red blood cells, each with 0 copies of the 46 chromosomes]

What is the total number of chromosomes present in all of the cells mentioned above?
(Ignore mitochondrial DNA.)
[1×(2×46)+1×(1×46)+2×(0×46) = 138 chromosomes]
A     92
B     115
C     138   ⟵ My Answer
D     161   ⟵ Answer Key
E     184
F     207

It turns out my answer does not match what is given in the answer key, but I cannot yet find a mistake in my workings. Since this is an important exam and the paper, as well as the answer key, probably went through multiple revisions before it became publicly available, I believe mistakes from the examiners' side are quite unlikely.
The fact that the given answer 161 (= 138+23) is an odd number suggests that one of the four cells could be haploid. However, this cannot be the case, for these are all somatic cells and not gametes.
Therefore, I wonder if I have missed anything here.

Source: https://esat-tmua.ac.uk/esat-preparation-materials/

https://uat-wp.s3.eu-west-2.amazonaws.com/wp-content/uploads/2024/05/07120523/NSAA_2023_S1_QuestionPaper.pdf
https://uat-wp.s3.eu-west-2.amazonaws.com/wp-content/uploads/2024/05/07120531/NSAA_2023_S1_AnswerKey.pdf

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

sort: votes


text:
What are the factors to consider when determining the sample size for a given study?
Say I'm designing a retrospective study (where I'd collect data from various schools for the last 5 years) to see if consuming milk can contribute to childhood obesity.  How do I decide on how many schools to visit? If I remember my stats correctly, in general, the goal is to achieve 95% confidence in our results, right?  So how many schools would I have to collect data from so that I will have 95% confidence in the outcome of the study?

Related Question

this is a question of statistical experiment design.  The statistical power of the experiment must include all the factors you are controlling for - age, geographical region, family income etc etc.  So this really depends.  not sure this can be answered here without a lot more information.

You might consider posting this on Cross Validated, but as shigeta mentioned, you'd need to provide more details.

Thanks...actually that's the kind of information I was hoping to hear. The age is 5-10 years, geographical region is US, and family income is irrelevant (randomized).

Maybe this isn't the answer you're looking for... nobody who has ever done a study like this has wanted to have fewer subjects than they could get.  I'd say the answer to your question could just be 'funding'

That's a good point...

I think it depends on what type of analysis you are going to do, but I know for at least an ANOVA you can calculate the smallest sample size for a given power, but in that case you have to have an idea of how big difference you are looking to find-.

About experimental design and is a purely statistical question.

I'm voting to close this question as off-topic because this question is about statistics, not biology.

@Remi.b Agreed, it is also far too broad for here or Cross Validated. There is an entire tag (although unfortunately populated mostly with other poor questions with no answers): https://stats.stackexchange.com/questions/tagged/sample-size

Could be as much as possible – using multistage sampling. But it all depends on how much you are willing to spend, and your time constraint.

Welcome to Biology.SE! This does not seem to answer the question. Please add some more details and references to your answer.

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text:
When can I assume individuals marrying into a pedigree are non-carriers?
If I'm not told that they're non carriers, and if I don't have proof of their geneotype based off of progeny, when can I assume they're non carriers for a trait?

All the time.
Unless you are specifically told/shown they are carriers, they are assumed to be Wild Type and do not carry the mutation.

You can only rely on statistics in this case. Check the population the person is coming from for statistical probability to be carriers.

Usually you assume neither situation. You are given some probability that they carry the trait based on measured allele frequency in the population. Then you use that probability in any downstream application, such as calculating the probability the children are carriers or affected with the genetic condition.

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text:
What determined the evolution of different faces in humans?
The most distinctive characteristic of a human is it's face - it is unique among each individual (with the exception of identical twins). It is uncertain to me if whether we best identify other humans by their face due to special brain parts developed for this (there are people with disease that cannot recognize faces) or for actual very distinctive physical face forms; maybe it is a combination of this.
Anyway, the question is about evolution. Why would distinct faces (or ability to recognize distinct faces) be something useful that would be retained by evolution? How is this better at survival?

I've read that penguins are also pretty good at identifying family members(visually and/or vocally) amongst hundreds of other similar looking birds.

Given the prevalance of myopia in humans I would have thought that facial recognition was secondary to other indicators such as gait recognition which is also unique to individuals though can be copied to an extent. Voice and shape are also used to identify people.
Being able to recognise individuals would allow the formation of groups, allow for structures of trust, reciprocal altruism to develop as well as punishing transgressors. Repeat interactions with other people require some kind of identification, but I dunno if facial recognition is the only/primary one.


text:
How can the child and the mother have different blood types?
As far as I know the fetus is fed by the umbilical cord which basically connects his/her circulatory system with the mother's in order to supply oxygen and nutrients. But how is this possible if they (the mother and the fetus) have different incompatible blood types?
It is possible that the father has A blood type, the mother B and the child A and thus incompatible with the mother's.

The fetus makes its own erythrocytes from a combination of the father's and mother's genome. If the mother is B and the father is A, the child will be AB as they are co-dominant. Only 'O' is recessive. This may be a too-basic question for this site...

If the mother is BB and the father is AA. In practice, the kid could be AB, B, A, or even O, if the mother and father are both heterozygous. BO/AO.

The blood of the fetus does not mix with the blood of the mother.  Instead, the placenta provides a system where the two separate blood streams flow past each other with thin separation allowing nutrients to flow between the two streams but the not the blood cells and other large components.

what's more, fetuses use a different set of hemoglobin genes, designed to take oxygen from the hemoglobin in mother's blood stream by diffusion through the placenta.


text:
What causes XYY Syndrome?
It's obvious how a misdisjunction can result in klinefelter's syndrome (XXY) but I don't see how this can result in XYY syndrome. Your parents have a collective total of only one Y chromosome so how can any misdisjunction result in a child with two Y chromosomes?

It comes from a Y nondisjunction in the father. Anaphase nondisjunction of the Y yields a YY, which goes with one X from the mother to give XYY.

http://en.wikipedia.org/wiki/XYY_syndrome#Cause  during sperm generation


text:
Help me understand how the thyroid secretes
Please have a look at this close up light microscopic image of a thyroid gland:

So I'm guessing the cubic epithelial cells surrounding this big red pulp are the secreting cells...? If so, is the red pulp a blood vessel that they are secreting into?
Am I misunderstanding?

Please do open any physiology/histology text and find the answer better explained than any of us could do it here. When you have read and have further specific questions, you are welcome to ask them here. BTW, no these are not blood vessels.

Do not believe that this is a HW question and if it is, he has made an attempt to answer it so I am fine with it.

That "red pulp" spaces you're referring are not blood vessels but, in fact, thyroid follicles that selectively absorb iodine from the blood for production of thyroid hormones and storage of thyroglobuline. So, they act as a reservoir of the materials used by the thyroid's epithelial cells, also called follicular cells, to produce thyroid hormones (T3 and T4).


text:
Why is oxygen and CO2 measured in pressure instead of mmoles/L like other ions?
Na, K, Cl...All measured in mmol/L in plasma. Why is oxygen and CO2 measured in pressure (mmHg)? (I guess it has something to do with them being bound to RBC but I don't know why the difference).

By the ideal gas law, PV = nRT, you can find pressure by dividing both sides by volume, P = nRT/V. Since R is a constant, and you can usually assume T isn't changing very quickly for biological systems, you can pretend P = n/V, which is moles per unit volume, analogous to concentration. The reason the units are written in pressure is probably because gases are hard to weigh, but measuring pressure is easy. This also accounts for the affect of temperature, which shouldn't affect the soluble ions you mentioned, but would affect the "concentration" of gases.

@user137 Good answer. Could you make it into an official answer

As you suspected, hemoglobin is the reason why O$_2$ and CO$_2$ in blood are expressed as a pressure (mmHg) and not a concentration. Most of the oxygen in blood is bound to hemoglobin; the concentration of free oxygen in plasma is low because oxygen does not dissolve well in water (which is of course the reason why hemoglobin exists in the first place).
When the oxygen content of blood is given as a pressure, it refers to the partial pressure that a gas (air) must have in order to be in equilibrium with the blood. This might seem a bit roundabout, but it captures the effects of both solubility and hemoglobin. In essence, this pressure describes how much oxygen the blood can release, which is the critical parameter for oxygenation of tissues.
The molar concentration of free O$_2$ in plasma is proportional to the partial pressure over the liquid, a fact known as Henry's law. The proportionality constant is the solubility of oxygen in the liquid, about 1.3 10$^{-6}$ M / mmHg for plasma. So at 100mmHg, the plasma O$_2$ concentration is about 130 $\mu$M. For comparison, the O$_2$ concentration in an ideal gas at 100 mmHg is 9 mM, or 70-fold higher.
See for example this book chapter for more information.

By the ideal gas law, PV = nRT, you can find pressure by dividing both sides by volume, P = nRT/V. Since R is a constant, and you can usually assume T isn't changing very quickly for biological systems, you can pretend P = n/V, which is moles per unit volume, analogous to concentration. The reason the units are written in pressure is probably because gases are hard to weigh, but measuring pressure is easy. This also accounts for the affect of temperature, which shouldn't affect the soluble ions you mentioned, but would affect the "concentration" of gases.

No, this is not correct. The ideal gas law is not applicable here, since blood plasma is not a gas! Blood gas (partial) pressure refers to the pressure over a gas in equilibrium with the liquid. To find the concentration in blood, you must take in account O2 solubility in plasma and also the effects of hemoglobin. The actual plasma concentration is much smaller than the concentration P / RT in air. (And also you cannot pretend P = n/V; there is proportionality, but not equality.)

@Roland I don't think OP was looking for a lecture in physical chemistry, but rather why the concentration of dissolved gases are expressed as pressure rather than a molarity. The ideal gas law should be a "close enough" demonstration that pressure is analogous to molarity, especially considering the practical aspects of taking measurements 100+ years ago when these unit conventions were put in place. If OP wanted to know how to determine the affinity of O2 for hemoglobin, that would be different, and the ideal gas law would be insufficient.

Well, solubility is not a minor detail here, the concentration I get from the ideal gas law is 70x higher than the plasma concentration.  And solubility + hemoglobin is the reason why concentrations are given in pressure, I think.  See my answer.


text:
Why doesn't the body optimize how many fatty acids it burns?
Ketone bodies are produced due to an excess of fatty acids being burned (accumulation of acetyl-CoA) so my question is: Why doesn't the body simply regulate how many fats it burns so it doesn't have to produce ketone bodies?

Under which conditions does the body burn preferrably fats? What makes you think that this process is not optimized (in fact, most biochemical processes are)?

At about 65% VO2 in a trained individual or during fasting.
I still don't understand your point, but I assume that it is optimized it just doesn't seem so to me.

When there is not enough fast disposable energy like carbohydrates around. He does this to maintain the support of certain critical tissues, while producing more energy by breaking down fatty acids. If he had glucose (or other sugars) available, this wouldn't happen. Fatty acids cannot be used directly but need to go through beta-oxidation to make the energy available.

I understand that. But I've read that Ketone bodies are supposedly the end-product of beta oxidation, which is not true if I look at the exact process of beta oxidation. Ketone bodies seem to synthesize because an excess of Acetyl-CoA accumulates when fats are burned, so ketone bodies seem to be an unwanted side-effect of too much fat being burned. I'm asking why the body burns so much fat that it gets an excess of acetyl-coa instead of regulating it.

Can you provide a reference for you statement that ketone bodies results from "excess" fatty oxidiation? In my view, ketone bodies are not an unwanted side product, they are deliberately synthesized (mainly by the liver) to support other tissues like the brain when glucose is scarce, as Chris mentioned. Also, I don't think it likely that acetyl-Coa accumulates to high concentrations, since this is limited by the amount of CoA available.


text:
Is there a way to examine amount of red/white muscle fibers without biopsy?
I want to conduct some research on red and white muscle fibers, why do some people tire during certain movements while others do not. Obviously I can't get a biopsy on the subjects so I wanted to hear if anyone here maybe had a suggestion to a reliable method to test for amount of red vs. white muscle fibers?
Maybe some strength measurements, endurance tests etc. I'm looking for something that is documented to work.

Indeed, a paper was published in 2011 regarding the same for humans by using a magnetic resonance spectroscopy to measure carnosine content.

A significant positive correlation was found between muscle carnosine, measured by 1H-MRS, and percentage area occupied by type II fibers. Explosive athletes had ∼30% higher carnosine levels compared to a reference population, whereas it was ∼20% lower than normal in typical endurance athletes.
Muscle carnosine content shows a good reflection of the disciplines of elite track-and-field athletes and is able to distinguish between individual track running distances. The differences between endurance and sprint muscle types is also observed in young talents and former athletes, suggesting this characteristic is genetically determined and can be applied in early talent identification. This quick method provides a valid alternative for the muscle biopsy method. In addition, this technique may also contribute to the diagnosis and monitoring of many conditions and diseases that are characterized by an altered muscle fiber type composition.

Baguet, Audrey, et al. "A new method for non-invasive estimation of human muscle fiber type composition." PLoS One 6.7 (2011): e21956.

Sounds great but not very helpful, logistically speaking. I don't have access to the kind of equipment needed. But definitely a good answer.

@Paze Anything preventing you from using model animals instead of humans?


text:
Cholesterol's role in lipid uptake
I'm studying the digestion of fats and I understand that our dietary fats mostly consist of triglycerides. We absorb the fats and eventually they end up in a muscle/adipose cell for storage (as triglycerides) or for oxidation for energy.
However I don't understand exactly where cholesterol plays in? I read about lipids being synthesized by the liver being exported by VLDL and then taken up by cells. We're moving closer to cholesterol here but I still don't see the connection.

Can you be a bit more specific? Are you asking about the role of cholesterol in cells in general, or its function in lipoproteins, specifially in VLDL, or ... ?


text:
Dynamic mutation and huntington's
I read that Huntington's is a disorder caused by dynamic mutations in the DNA, which means that a triplet sequence of DNA changes from generation to generation. Say we have the sequence ATGATGATGATG. The child of this person with have ATTATGATGATG and the grandchild will have ATTATTATGATG etc.
This means that Huntington's will be worse (debut earlier) the longer the generation lasts.
My questions are: Is my understanding of dynamic mutation correct? Is there no MINIMUM age where Huntington's will debut? In other words, if a generation is very long and has Huntington's, can a baby have symptoms at birth?

In triplet repeat diseases it's a probabilistic addition of more repeats. 30 repeats goes to 32, or maybe to 30, or maybe less. The longer the repeat section, the more likely it is to gain or lose repeats due to duplication errors. You're not guaranteed to get just one each generation. There is likely to be a minimum age of onset where more severely affected individuals do not develop normally or die before developing chorea.

At the moment, the youngest diagnosed Huntington's case was 2 years of age. This paper appears to discuss not only this boy's onset, but also the diagnosis of symptoms in the early-onset disease.
Here they research a link between age-of-onset and the length at which the repeats are.
The thing is that these repeats won't just constantly get longer. There is "slippage" during replication which causes the repeats to get longer, but it also causes the repeats to get shorter. It's possible that mom's bad chromosome may have been inherited but because of the slippage, it no longer produces Huntington's symptoms.
This image doesn't show actual mechanics of it happening, but it shows how the repeats can be added and subtracted.

As it turns out Kayser et. al decided to look at chimps and humans to discover which of two proposed mechanisms are more likely. Their findings suggest the slippage is closest to the "heterozygote instability model".
The model suggests:

heterozygous loci might have a higher mutation rate due to mismatch repair events that occur during synapsis

To answer your question in short:
It appears that the "minimum age" so far is 2, however, that does not mean that it hasn't occurred earlier. Huntington's is characterised by a change in motor skills, and if the change occurs before birth it might not be noticed. In theory, it is possible that Huntington's symptoms can start pre-birth.


text:
Is the autonomic nervous system only activated by internal stimuli?
My professor claims that the autonomic nervous system is only activated by stimuli from organs but I really feel like I've read that it can be activated by outside stimuli, although I'm not sure what receptors that would be.
Is my professor right?

my bet is that you should examine specific pathway. Saying in general that ANS is excited only from within doesn't mean much, to my taste. ANS actions are mediated by CNS so one can say that environment does have influence on ANS

Short answer
External stimuli can drive autonomic responses.
Background
The autonomic nervous system is a visceral sensory and motor system. The viscera are the internal organs. Virtually all visceral reflexes are mediated by local circuits in the brain stem or spinal cord (Fig. 1). It is one of two major subdivisions of the nervous system; the other being the somatic (or voluntary) nervous system. The main distinction between the two is that the latter is involved in voluntary and conscious actions (e.g., movement, perception and cognition), while the autonomic nervous system is engaged in involuntary processes, such as regulating heart rate, breathing and bowel function (Fig. 1).

Fig. 1. Autonomic nervous system. Source: Austin Community College
Although by far most stimuli driving autonomous responses come from within (think muscle movements driving bowel movements, increased heart rates during physical exercise), outside stimuli do directly impinge on the autonomous system.
For example, the cilliary muscle in the iris is under the control of light coming into the retina. The pupillary light reflex test is based on this principle, and is routinely used to diagnose damage to the visual system. Also, production of saliva is controlled by external stimuli (smell and taste of food and see the striking example below from @anongoodnurse). And technically, the entire digestive tract can be considered to be outside the body, as it is continuous with the skin and lining of the mouth. Hence, the mechanical stimuli impinging on the intestines by a moving bolus of food that drives the waves of peristaltic movements can, arguably, be considered to be caused by external stimuli too. Lastly, the fight-flight-fright response involving the hypothalamic-pituitary-adrenal gland (HPA) axis is often initiated by external stimuli (loud sudden noises etc.).
The most important characteristic of the autonomic nervous system, as said, is that the autonomous responses are not voluntarily controlled. While you can decide to look or track a visual stimulus, you cannot decide to move the bolus of food back up to your stomach, or voluntarily constrict your pupil. The way the input is received may not be the best way to distinguish it from the voluntary nervous system.
Didactic answer
If you are left with questions, the first place to go to is your professor.
Reference
- Kandel et al. Principles of Neural Science 4th ed. (2000). Ch.49 The autonomic nervous system and hypothalamus. p.960-81

I wonder if the professor meant it on another level: that the autonomic nerve system does not have sensory neurons connected to the outside world. The examples you cite are ultimately caused by external stimuli, but as far as I remember, visual and olfactory perception is not part of the ANS. This is of course a nitpicking distinction and not meant to make your answer look bad (I liked and upvoted it), but for a student who is trying to find their way through complex material, easily delineated distinctions are good signposts, so it could be an explanation for why the prof used the statement.

@rumtscho - I have edited my answer to accommodate your comments. I agree that questioning your professor's words on SE may not be the best practice. In fact, my first short answer was always listen to your prof. I removed it, because lectures generate questions so it is logical to be left with questions. Further, there are always exceptions to the rule, that is fundamental to biological sciences. Please check my "didactic answer" and I hope that suffices your critique on a student's needs.

@AliceD - Hmm... good answer, but professors are often enough wrong that I think SE is a great place to double check. One fun trick (to which you alluded) is to cause saliva to flow by telling a patient to imagine biting into a lemon, because this has become a conditioned response in adults.  When there is a parotid duct obstruction, the parotid gland will swell before our very eyes., making the diagnosis obvious (and easy). Sensory nerves in the tongue for sour cause salivary production. There are other examples.

@anongoodnurse - Thanks for your comment and your interesting addition directly from medical experience. I made my answer stronger, and although leaving the didactic answer in place, I made it less binding. BTW: mod nominations at Bio are open :)

I saw that. You already have my vote!

@anongoodnurse - thank you :) But I was in fact hinting that you should nominate yourself!


text:
What reference genome was used to bootstrap the human genome?
As I understand it, when we map a genome, the process is much more complicated than say copying text out of a book.  The genetic sequence cannot be copied from a genetic sample in a single pass, so instead the sequence is split into many very small sub sequences called reads.  These reads are then assembled into the complete genome using De Bruijn graphs.  To accelerate this process, a reference genome is used to help figure out which subsequences connect to each other.
In the case of the human genome project, obviously no reference human genome existed.  Was some reference genome used?  If so, what was the reference genome?  If not, how were they able to assemble the human genome?
Based on my reading, constructing the final assembly from a De Bruijn graph is NP-Hard.  So, doing the assembly from scratch seems completely intractable.  The human genome is 3,000,000,000 letters, and an individual read is about 300 letters.  This means there are at least 30,000,000 subsequences, and probably many more than that given how redundant the sequencing process is.  NP-hard problems tend to become completely intractable with problem sizes in the hundreds, and this problem size is in the millions if not billions.  That's why it seems essential that the assembly process used some sort of reference to greatly speed things up, but some googling around hasn't identified the reference used.

This seems like it might be more suited to the [HSM.SE] site. The short answer is that the chromosomes aren't one single "string", but 23 separate strings. In addition, IIRC the problem was further simplified by doing (possibly multiple rounds of) sub-cloning. Have you tried searching for something like "history of human genome sequencing project" — I'm certain that you would find as much detail as you want.

The technology that you are speaking about isthe next generation sequencing, which is not the one that was used in the first human genome project. Also, de novo genome assembly (e.g., with de brujin graphs) and genome mapping are different things - the former is done when the reference sequence is not available. Not sure what the OP means by bootstrapping...

Note that, while we have a "complete" human genome, it is not an ungapped genome. Telomere-to-telomere assembly has only been completed for the human X chromosome and chromosome 8, I believe. The unresolved gaps are caused by regions that are hard to assemble like segmental duplications, ribosomal rRNA gene arrays, and satellite arrays. These gaps can only be closed by careful long-read sequencing.

The process that you describe is true in some cases for the problem of shotgun genome assembly, but it does not describe the strategy taken by the HGP. This resource may prove helpful for understanding how a highly iterative procedure leveraging information from many disparate sources (sub-assembly, BACs, physical mapping) was used by HGP to get around the computational issues: https://www.nature.com/scitable/topicpage/dna-sequencing-technologies-key-to-the-human-828/

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text:
Where should one start if they want to go about identifying phytoplankton and dinoflagellates?
I'm a first year university student and I really need help on how to identify and recognize the different organisms observed in my water samples. Are there any good references/tips on how to?


text:
Mitochondrial donation - why is the second woman needed?
Mitochondrial donation or the latest case procedure describes that an egg of the second woman is used as a host with healthy mtDNA.
Being a complete layman I'm interested in whether it is a restriction of the method or some fundamental requirement. Is it in principle possible to replace broken mtDNAs of a mother with mtDNAs of a father, which are mtDNAs of his mother?

It looks like the current techniques might better be described as "nuclear donation".  You take an ovum with healthy mitochondria, remove the nucleus, and insert the desired nucleus from the woman with bad mitochrondria.  So yes, currently, the mitochonrdria have to come from an ovum, and therefore a woman.

+1, a better term would be "cytoplasm donation"


text:
Do the eggs for larger litters come from the same meiosis events, or different ones?
There are some species of animals that give birth to more than one pup at a time. In these species, are the fertilized eggs all from one or a limited group of meiosis processes, or are they from different ones?
To illustrate the idea, take for example a case where some animal ends up with seven offspring in a litter. Do the original eggs come from different meiosis events?
Meiosis   Meiosis   Meiosis   Meiosis   Meiosis   Meiosis   Meiosis
   |         |         |         |         |         |         |
   V         V         V         V         V         V         V
   1         2         3         4         5         6         7

Or from a smaller set of events?
  Meiosis     Meiosis
 / |  | \     |  |  |
V  V  V  V    V  V  V
1  2  3  4    5  6  7

I am aware that, at least in mammals, that egg cells are actually produced long before they are used, and pooled for later use:
Meiosis  Meiosis  Meiosis
   \\\\    ||||    ////
    VVVV   VVVV   VVVV
    =====Egg Pool======
    |  |  |  |  |  |  |
    V  V  V  V  V  V  V
    1  2  3  4  5  6  7

I do not have any idea how this would work for other types of life though, like birds, reptiles, or fish. How does it work for those sorts of life?
I am mainly interested in this to understand how the mother's chromosomes are represented in the offspring. Are all of her chromosomes guaranteed to be represented in at least one offspring?

I'm not sure about the ubiquity of this but, in many animals, each primary oocyte that undergoes oogenesis only produces one mature egg. The other products of meiosis are polar bodies, which are not fertilised. These cells often degenerate but can sometimes play supportive roles in embryogenesis.

To answer your question, each mature egg is necessarily from a different meiosis event and so it is not guaranteed that all of the mother's chromosomes are represented in her offspring.

OK, thanks. This is exactly what I was looking for.

@canadianer why would all of mother's chromosomes not be represented in her offspring?

Do you mean to say all of the 2x chromosomes of a diploid species?

@CRags Each egg contains half of her chromosomes, independently assorted and recombined. It's unlikely in smaller numbers of offspring that every piece of every chromosome will have been passed on.

While your question asking about birds, reptiles and fish (oh my!) may be too broad, hopefully looking at frog oogenesis can show some differences in large offspring number v. small offspring number. Some frogs even give birth to live offspring (Iskandar et al. 2014).
Much of this explanation can be found in Developmental Biology, 6th edition by Gilbert SF.
In frogs, meiosis happens in stages (Developmental Biology):

This shows that different "cohorts" of oocytes form, develop, and are released, rather than a single group of mitotic events that are released gradually (as in humans). When the eggs have undergone vitellogenesis (yolk development), they are ready for fertilization.
As far as this question is concerned:

I am mainly interested in this to understand how the mother's chromosomes are represented in the offspring. Are all of her chromosomes guaranteed to be represented in at least one offspring?

If you're asking whether or not all of the mother's chromosomes will be represented in her total offspring, perhaps--with a large number of offspring (and a high ratio of fertilized eggs) the probability is very high.
No single offspring will contain all of its mother's chromosomes. Let's look at a diploid organism with two pairs of chromosomes: A and B. At the beginning of meiosis I, a cell will have one copy of both pairs:
A1 A2 B1 B2

Then comes synthesis, duplicating all chromosomes. Now we have two copies of each pair:
A1A1 A2A2 B1B1 B2B2

In prophase, chromosomes are condensed and the duplicated pairs connect in a process called synapsis:
A1A1-A2A2 B1B1-B2B2

In anaphase, the pairs are pulled apart so that each daughter cell has two copies of a single member of the pair:
daughter Y: A1A1 B2B2
daughter Z: A2A2 B1B1

Note that at this point it is not possible for either of the daughter cells to contain all of the mother's chromosomes.
With meiosis II, these copies are pulled apart, making four daughter cells:
daughter Y1: A1 B2
daughter Y2: A1 B2
daughter Z1: A2 B1
daughter Z2: A2 B1

These are now haploid, and await the male's sperm to make them diploid once more. Also note that daughters Y1/Y2 and Z1/Z2 are chromosomally identical (they can be different in practice with crossing over).
Here is a prettier representation of what I just described (Wikipedia):

The key is to remember that pairs of chromosomes and copies of chromosomes are different and to keep track of how they segregate during meiosis.
Edit: To address your clarification:

I am not talking about whether or not any of the daughter cells contains all of the mothers genetic material by itself, but rather whether every segment of genetic material is found in at least one offspring.

This is more of a probability question. If all oocytes mature, and are fertilized, the answer is clearly yes. However, not all oocytes are fertilized. Let's look at the same four daughter cells from my earlier example:
daughter Y1: A1 B2
daughter Y2: A1 B2
daughter Z1: A2 B1
daughter Z2: A2 B1

Let's say 2/4 (50%) are fertilized by the male frog. Going through all possible fertilizations, let's see how many combinations result in all of the mother's genetic material being passed down:
Y1, Y2 - No
Y1, Z1 - Yes
Y1, Z2 - Yes
Y2, Z1 - Yes
Y2, Z2 - Yes
Z1, Z2 - No

The answer to your question really depends on what proportion of oocytes make it to maturity, and what proportion of mature oocytes are fertilized. The probability of all the mother's genetic material being passed down increases with increasing fertilization ratio/egg number, so given the high number of offspring produced by many species of frog, I'd say that there is a good chance of all the mother's genetic material making it to the next generation, although it is not guaranteed.

I am not talking about whether or not any of the daughter cells contains all of the mothers genetic material by itself, but rather whether every segment of genetic material is found in at least one offspring.

@AJMansfield I addressed your clarification further in my recent edit


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How do animals lose heat?
I remember being told as a child that dogs stick their tongue out to stay cool, because they can't sweat like us. This made sense to me.
But only a couple of days ago I suddenly thought: What about all the other animals?! I mean, I don't see a cat or a horse putting their tongues out, and yet I don't see them sweating either. How do they lose heat? How do different kinds of animals lose heat?

There are a number of ways, which are briefly summarized here. I also recommend reading this nice Scitable article on thermoregulation. It is not too technical. Felines do pant when they get hot. Horses do sweat. Jackrabbits can enlarge the blood vessels in their large ears to eliminate excess heat. Bird use a process called gular flapping, which is similar to panting of dogs and cats.  Animals can move into shaded areas.  The possible mechanisms are many.


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How come only a handful of animals can do photosynthesis?
As far as I understand, all the energy that living beings rely on comes from the sun. It's processed by plants in photosynthesis. These plants are consumed by herbivores, which in turn are consumed by carnivores. Energy trickles down that way, with photosynthesis being the crucial basis for all the other layers.
A couple of days ago I was wondering, how come animals don't do photosynthesis? This story talks about a few exotic animals that can do photosynthesis, but they seem to be an edge case.
It seems like there's a rule of thumb: Iff a creature can do photosynthesis, it can't move. Why is this so? Wouldn't it be beneficial for a herbivore-like mammal to be able to create sugars directly from sunlight? They wouldn't have to graze at all, just find water and sunlight. It's possible they'd have an easier time avoiding predators and expanding into more territory.
Can you think of a good reason why such creatures never became mainstream?

This paper will be of help: https://academic.oup.com/jxb/article/59/5/1069/537020

It is all about energy.
It is estimated to take 5000 square meters of plants to feed the average person in the developed world, while the same source gives the lowest possible for a human under ideal conditions at 700 square meters.  In comparison, the average person covers less than 1 square meter.  While there is a lot of waste (animals are able to eat only a few percent of the energy the plant produces), the total energy available from photosynthesis is still orders of magnitude smaller than daily requirements for a typical animal.
Even in the case of the slug you linked (which you would expect would need about as little energy as possible for a mobile animal), it seems they obtain little or none of their actual energy from photosynthesis.
Hence you see photosynthesis restricted to life that has extraordinarily low energy requirements, which typically means being stationary (or moving very, very slowly as in the case some plants).  As soon as you adapt to a mobile, higher energy niche, you need access to a lot more energy than photosynthesis can provide.

I don’t think that completely answers the question though. Yes, photosynthesis alone is definitely not enough to sustain any animal with a non-trivial energy requirement, but what’s stopping animals from evolving photosynthesis anyway? Wouldn’t it be advantageous to have photosynthesis as a complement to energy from food? Besides, assuming photosynthesis in animals would also be chlorophyll-based, wouldn’t that give animals better camouflage in places like rain forests?

@Kal Nothing is stopping animals from using photosynthesis (some do), but even in the case of the low energy slug, the amount of energy they can get from photosynthesis is so small it cannot complement food intake (see link).

The amount of energy coming from the Sun is limited (about 750 W/m^2, perpendicular to the incoming light).  It takes a comparatively large amount of energy to move around, so a photosynthetic animal wouldn't be able to move much or very often.  (And in fact the known examples don't.)

The key issue isn't the lack of incident solar energy, but the inefficiency of photosynthesis. The average human power output is only about 100W, but photosynthesis can only harness about 5% of the Sun's power, so it's still not enough.

@Nuclear Hoagie: I thought the inefficiency was a given.  But note that even with much more efficient PV cells (over 20% for the commodity sort you'd put on your roof), electric motors, and nothing used for unrelated metabolic functions, it still requires wheels & very efficient aerodynamics to move things with solar power.


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What is the difference between a species tree, a gene tree and a phylogenetic tree?
I have found websites and text books disagreeing over this. For example,

Phylogenies are also known as “species trees”...

http://biologos.org/blogs/dennis-venema-letters-to-the-duchess/evolution-basics-species-trees-gene-trees-and-incomplete-lineage-sorting/
and

It is well known that a phylogenetic tree (gene tree) constructed from DNA sequences for a genetic locus does not necessarily agree with the tree that represents the actual evolutionary pathway of the species involved (species tree)...

http://mbe.oxfordjournals.org/content/5/5/568.abstract
Although the second source, being from a journal, would seem to be more reliable, my original thought was that phylogenetic trees do show the evolutionary relationships between species and thus are species trees as opposed to gene trees.
Any clarification on the issue would be much appreciated.

They are all distance trees where the nodes represent different things and the distance measures are different as well.  You can make a dendrogram using (1-correlation) as distance, or using euclidean distance.  You could also do it using nt specific distance measures like kmer distance.  In networks you can make trees from something called a topological overlap distance.  Whatever distance measures you create that satisfies the rules of a distance measure can be used. Also, they may use different clustering techniques too.

Phylogenetic tree
A phylogenetic tree is a tree showing relationship between lineages. These lineages might be computed for genome-wide DNA or from only a single gene. As such the term phylogenetic tree is general.
gene tree vs species tree
If you compute a phylogenetic tree, from genome-wide DNA, then you are computing a species tree (although some sister lineages might not perfectly fit the definition of species). If the phylogenetic tree is computed from data coming from a single gene, then we are talking of gene tree.
Why would a gene tree not match a species tree?
But a gene tree is not just a species tree with fewer data. There are reasons for why a gene tree may not match a gene tree. Genes may duplicate within a given genome. The two duplicated genes are free to evolve independently since the split. All descendants lineages will then inherit these two genes but if you map the two different copies of the gene (red and green below) in two sister clade, they will be much more different then the two same copies (say the green copy) in two distantly related species. Here is a picture to show that

Also, copies of genes can be deleted later on and there might have horizontal gene transfer. For all these reasons the phylogenetic tree of a gene might well be very different than the phylogenetic tree of species.
Below is a gene tree and the associated species at the tips. Take time to make sense of what is going on on the picture.

What is a species tree exactly?
One could call a species tree as some kind of average tree among all gene trees.


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How do detergents interfere with protein assays?
This has been getting me stuck. I've tried to understand what a detergent would do in an assay, but I can't figure out whether it would affect the protein or the reagent (say, in a Bradford assay).

Depending on the detergent, its concentration, and the exact assay being performed, it can affect both the protein and the assay reagent(s). Some detergents will bind the (usually colorimetric) reagent, or otherwise chemically react with it, giving high background to your assay and sometimes completely masking the specific signal of the assay itself. Many modern protein assays are tolerant of a fairly low level of various detergents, perhaps some but not others, and this underscores the necessity of running a buffer/diluent-only control to verify the background of your measurements. Other assays, like Bio-Rad's DC Protein Assay or the Pierce Detergent Compatible Bradford Assay Kit from ThermoFisher, are engineered to tolerate a certain (often fairly high) level of detergent without increasing the background of the assay.


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Do plants have cellulases?
I can't seem to find the answer to this. Not even Wikipedia could help- it mentioned bacteria and fungi that have cellulases but not plants. Using my own reasoning, I would think that

On the one hand it is better if plant cells do not have cellulases so that they do not break down the cell wall. Although maybe it doesn't matter because the cellulases would not reach the cell wall without being actively transported out of the plasma membrane.
Perhaps it might be useful for plants to have cellulase. I don't know if plants have any sort of immune system like humans, but plants also get bacterial and parasitic infections in their cells. Maybe plants should have some mechanism to destroy an unhealthy cell? In that case, the destroying cells would need to use cellulase, would they not?

https://www.ncbi.nlm.nih.gov/pubmed/16344110

@WYSIWYG Thank you for your reply! The article certainly answered my question, but the first sentence also confused me: "Many bacterial genomes contain a cellulose synthase operon together with a cellulase gene, indicating that cellulase is required for cellulose biosynthesis"        How does the fact that 'many bacterial genomes contain a cellulose synthase operon together with a cellulase gene' imply that 'cellulase is required for cellulose biosynthesis'? Would be grateful if anyone had any ideas about this!

I guess that these bacteria also produce cellulase for turnover of cellulose. Just the way all organisms have proteases to enable protein turnover. I did not get time to read that article in detail. I shall post an answer when I get time.

At least some plants have cellulases which can be used to cleave primers from mature cellulose chains.
Cellulose synthesis requires chain initiation and elongation (the two processes are separate). CesA glucosyltransferase initiates cellulose polymerization using a steroid primer and UDP-glucose. Cellulose synthase utilizes UDP-D-glucose precursors to elongate the growing cellulose chain. In some plants cellulase is then used to cleave the primer from the mature chain.
Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4119035/


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Is the signal peptide always cleaved during protein synthesis in the ER?
My university supervisor said that the signal sequence is always cleaved, however my text book differs.
What I gather from my text book (though it isn't very clearly stated so i'm not sure) is that:

A protein that is meant to be completely extracellular (or go into a membrane-bound organelle) will have only a signal sequence which will be cleaved by signal peptidase.

If there is a protein that is meant to have just one transmembrane domain, it can either:

a) have a single signal sequence, however this will not be at the start of the N terminus that is being translated. If there are more negatively charged amino acids before the signal sequence, then when the signal sequence binds into the translocon complex this beginning 'tail' will be threaded through as it is repelled from the more negatively charged cell interior. The amino acids following the sequence will be more positively charged to stay in the cytosol rather than passing through to the ER lumen. This will determine the directionality of this single-transmembrane-domain strand.
//Alternatively there can be one signal sequence and the amino acids before are more positively charged and after are more negatively charged, so you get the reverse situation where the already synthesised strand remains in the cytosol and the rest of the polypetide is threaded through as it is synthesised. Either way, this involves just one signal sequence.
b)The polypeptide can have one signal sequence and one stop-transfer sequence, with the charges on the surrounding amino acids determining directionailty, and then one of the signal sequcne or stop transfer sequence may be cleaved by signal peptidase.

Multipass proteins have a series of signal peptides/start-transfer and stop transfer.

But if my textbook (or rather what I understand from it!) is correct, then some but not all signal sequences are cleaved. So how does the signal peptidase know which to cleave?
I would really appreciate if someone could tell me answer this and also correct me where I have gone wrong in my understanding.

Would you mind providing a source/page number for the text so I could take a look at it? Having a multitude of transfer signals makes sense to me, but I don't understand the rationale for having multiple SRP-binding sequences.

@kingfishersfire I am using molecular biology of the cell 6th edition, Albert's et al (Garland Science). I do not know where one can get the 6th edition online-I have a hard copy- however I have found the corresponding chapter for the fourth edition https://www.ncbi.nlm.nih.gov/books/NBK26878/

I couldn't find the section you were talking about in that text, however I did find this http://www.zoology.ubc.ca/~berger/B200sample/unit_8_protein_processing/er_targeting/lect27.htm that looks like it might be helpful for you.

This is a rather long question, and I'm still not sure what exactly you're asking. Are you asking what makes a SP different to a TMH, or are there exceptions to SP cleavage? As far as I've understood the topic, signal peptides should be cleaved; it's part of their definition. If not, then there isn't too much distinguishing them from any other TMH post insertion. With a more specific question, I can provide a specific answer.


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What concentration of table salt is needed to kill bacteria in sweaty gym clothes?
My gym clothes retain an unpleasant musk even after washing them with warm water and detergent. I've experimented with soaking my gym clothes in salty water before washing them. My hypothesis is that the high salt concentration will cause plasmolysis in the cells of the bacteria. It has worked with mixed results; I'm never sure how much salt I should add or how long to soak the clothes.
I've looked for answers but I can only find papers with highly technical results.
(1) Can the odor-causing bacteria be killed with a salt treatment?
(2) If so, what concentration of table salt is needed?
(3) How long does the treatment need to last for plasmolysis to occur?

Lack of water and UV are great - Always let them hang outside right after use, never let them incubate in your sports bag and sunlight is devastating to microorganisms.

Specifically, hang them outside in the bright sun. You can soak your clothes is soap water or a mild perfumed disinfectant like dettol.

@WYSIWYG - is this question answerable without knowing the exact microfauna inhabiting OPs skin/clothes?

@AliceD Can be difficult because usually normal washing is sufficient unless the clothes have taken a long time to dry (rains etc). In such cases molds also start growing on clothes. In any case I am not sure if this salt method would be effective.

I just wanted to throw in, that if you are using fancy gym cloths (made out of those nice fabrics which are supposed to help air circulation and such, I am not an expert on what they actually can do), soaking them in salt water might actually destroy your expensive gym clothes in the long run.

You should keep in mind that the odor is a mixture of stale sweat and chemicals produced by microorganisms, not necessarily the microorganisms themselves. Basically, by the time the odors appear, it's already too late. Thorough washing and immediate drying of your clothes after exercising can help mediate the accumulation of additional odors, but what's there is there. These aromatic organic compounds can bind very tightly to the fibers of the cloth, and are quite difficult to get rid of. Bleach may help, depending on the type of fabric (and color), but I doubt salt will do much of anything.

detergents containing benzalkonium chloride are very effective against bacteria in heightened concentrations or lengthened exposure time. they certainly work better than salt, plus they may also help clean your clothes of dirt, oil and sweat.

Short answer
Toxicity of salt depends on contact time. 50 g NaCl per liter kills nearly all bacteria in 2 days. 100 g NaCl/L may do a quite thorough job in 30 minutes.
Background
Body odor is caused by bacteria that feed on the fluids produced by the apocrine glands, mainly present under the arm pits and other areas with abundant hair follicles. Bacteria in the skin feed on the products of the apocrine glands and convert it into odorous compounds. Skin microfauna includes Staphylococcus, Micrococcus, Corynebacterium, Dermabacter and others. As pointed out by others in the comments, treating your cloths against bacterial growth may not be the most efficient approach, as the bacteria are residents of the skin. Nonetheless, the following studies addressed the antimicrobial effects of salt.
A study using the gut bacterium E.coli showed that survival in 5% NaCl (50 g NaCl per liter H2O) was <0.01%. In 2% NaCl survival survival was 8%. The contact time was 48 hours (Carlucci and Pramer, 1958).
Another study examined the effects of salinity on E. coli using a shorter contact time of 30 minutes, and concluded that 10% salinity killed 80% of organisms (Somani et al., 2011).
Sea water, which has a salinity of about 3.5% contains low numbers of bacteria (Carlucci and Pramer, 1958), suggestive of toxic concentrations of NaCl, the major salty constituent in sea water.
Although E. coli has been associated with skin fauna and body odor, I must note that Gram negative gut bacteria as used in the two studies above may not be representative of the mainly Gram positive microfauna found on the skin (Strauss & Kligman, 1956).
References
- Carlucci and Pramer, Am Soc Microbiol (1958)
- Somani et al., J Eng Res Studies (2011): 40-43
- Strauss & Kligman, J Invest Dermatol (1956); 27: 67–71

5% NaCl is 5g/100mL

well, approximately yes, but to be exact 5g/100mL is probably less than 5%, though the difference should be quite small.
@AliceD is it probable that skin flora have adaptations to make themselves more resistant to salt since they live on skin which easily gets sweaty?

@busukxuan good question!

@busukxuan Biologists often use w/v concentrations. 1% w/v is defined as 1 g / 100 mL. According to Wikipedia, the sodium concentration in sweat is around 15-65 mM (50 mM is ~0.3% w/v). Bacteria should easily tolerate this without special mechanisms.


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Leptin and fat mass?
I am interested in the relationship between blood leptin concentration and fat mass.  It is well known that as fat mass increases, leptin increases.
Have there been studies that look into whether the relationship is linear, or perhaps as fat mass increases, the level of leptin increases at a decreasing rate (e.g. logarithmic relationship) or an increasing rate (exponential) etc.
Furthermore, for two individuals with identical fat mass, is there a high variance of leptin concentration?

The obese gene (OB gene) secretes a protein that functions in the signaling pathway of adipose tissue and adipocytes (fat cells) produce the hormone leptin (reference).

When the amount of fat in the body increases, the amount of leptin
  released into the blood also increases and signals to the brain that
  the body has enough to eat (reference). Inversely, studies in rodents suggest
  that a reduction in leptin level during weight loss signals to the brain
  to increase feeding and decrease energy expenditure (reference).

Other molecules have a role to play in the ratio of BMI to leptin like the ghrelin hormone (reference). The genetic and environmental factors other than overall adiposity may also regulate leptin concentrations (reference) which is why individuals with the same weight may have different leptin concentrations.
A study has reported finding a strong exponential relationship for leptin levels with body mass index (BMI) (reference). Hope that answers both your questions.

The over-simplified answer to the question: "Have studies examined the linearity or non-linearity of leptin concentrations in the blood and body fat?" - is "yes".
Leptin (the product of the ob gene - that is, the obese gene) is typically thought of as being secreted in proportion to the amount of adipose (fat) tissue that an organism (mice, rats, primates, humans) has overall. Like most things in biology, though, it's likely not a perfect linear relationship across species or across a wide range of individual body weights within a particular species.
Even the plasma concentrations across individuals within a particular species with the exact (or very close) body weight is still different. In my own experience, when trying to "normalize" or "adjust" the estimated fat mass based on the leptin concentration there's still a good amount of variability between individuals. The leptin concentrations for a number of individuals at one specific body fat percentage are not identical - which could be due to some error in the measurement, but also due to biologic variability from other sources (for a example of this variability in animals matched for body weight see here). This is probably because there are a lot of other modifying factors or variables within the body that can affect leptin concentrations in the plasma (like other hormones or nutrients from the gastrointestinal tract). So yes, these other hormonal and/or nutrient signals probably contribute to the high variance of plasma leptin concentration for individuals with the same fat mass for all of the reasons listed above (I don't have any references that examine this specific question, though).
To my knowledge there are no studies that have examined leptin concentrations across multiple species or even within a large cohort of one species. Even though this might be interesting from a scientific perspective, it's not really necessary to be able to predict fat mass from leptin concentrations (or vice versa) for medical purposes, because we have 'good enough' methods for accurately determining fat mass in patients or animals.
Overall leptin is an adipose tissue hormone thought to be involved in control of body weight over long-term (weeks to months) time courses. For a good review of the long-term actions of leptin and other hormones controlling body weight see a great review on CNS control of body weight that discusses leptin and other factors that modify leptin and body weight regulation.
Additionally, Dr. Jeffrey Flier in Boston is a senior physician-scientist at Harvard Univeristy and has studied leptin biology and has some very nice articles on leptin including this review on leptin in energy balance and long term control of fat mass.


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How exactly does the carbon cycle work to transport nutrients?
In general, I know that the carbon cycle recycles carbon and transports it to various locations. However, in my biology class (I'm a freshman in high school), they gave us a diagram depicting the carbon cycle and I was confused on a few of the steps. Unfortunately, I wasn't able to download the diagram in the necessary format, so I will do my best to explain what it looked like. Essentially, in one step, it showed an arrow leading from detritivores (which also included soil microbes) to wood and fossil fuels. Basically, it was showing that there was a direct connection between detritivores breaking down detritus and the formation of wood and fossil fuels. Can anyone explain this connection? I haven't been able to find a source about it. If anyone has any sources or articles I can read to gain a better understanding, please post them as well. Thank you!

Welcome User. Remember we have a one question per post policy. Can you [edit] down. Any further questions should be posted in their own threads

Thank you for letting me know, I will edit it.

Thanks for the edit. The question is basically what, exactly, happens to decomposed carbon-containing matter;  how is it related to cellular respiration? What is the end product of respiration? Please read about it in the link provided, and a link with a quote including an explanation of exactly what confuses you (a requirement on this site) will help us identify the best starting point for helping you. Thanks.

I was wondering how decomposers release carbon into wood or fossil fuels (how carbon goes from the decomposer stage to the wood/fossil fuels stage), as that was what the diagram implied. I may be incorrect, and again I apologize for being unable to upload the diagram.


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What animal does this skull belong to? I found it in a cave buried in the dirt, with other bones

I did not find anything similar on Google.

You should include where in the world this was found (city/country/etc) and its length

Herbivore - something with large chewing muscles given the sagittal crest.

a shot of the teeth will tell you a lot more than a top veiw of the skull. teeth and their placment in the jaw will tell you a lot in mammals. Scale is also important, how long is it. Just from what i can see I am guessing some kind of canine.

@bob1 lots of carnivores have large sagitical crests.


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How to determine a gene based on the biological function of an organism?
I am studying genetic engineering.
I have a problem understanding how to find the necessary genes responsible for certain phenotypic traits.
Let's say plants have red petals. What methods are used to determine which genes provide this?
A biologist transfers a gene/genes from a spider to a silkworm. Now the silkworm produces spider web instead of silk.
How did this biologist determine which spider genes are responsible for producing the spider web?
How to identify a gene based on the biological function of an organism?
What methods?
It seems like we need to dig into transcriptomic technologies
Thanks!

This is very broad. I would expect an undergraduate-level course in Biology or Genetics would spend quite a bit of time on this.

This is hard to answer, I will try to explain why. For example "red petals". Are you interested in the genes for having a flower, genes for determining petal organ identity, genes for making red pigment, genes for not making purple or black or green pigment, genes for not transitioning away from sexual reproduction? All of these are needed to make the phenomenon "red petals". But we are now talking about maybe 5-10% of the total genes in the organism. Biology is complicated! "Gene for X" is usually not the best way to think about genetics. Try screening rather than transcriptomics.


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Medium-Small black beetle
Ive been seeing these types of beetles in my region ALOT and i really want to know which species they are.
The length is 1.5 cm, and the depth of this beetle is about 0.75 cm. There is open water, but its holes caused by cows stepping on them all the time, food sources have no droppings or chew-marks, thats all i have to say. Also, my region is Southern Brazil.


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Is infrared photosynthesis possible?
The post-apocalyptic science fiction novel Dark Universe by Daniel F. Galouye has some plants living inside bunkers that use infrared light for photosynthesis. There are speculations that extraterrestrial plants might use the same trick on planets orbiting red dwarfs and that their leaves would be totally black. Would this type of photosynthesis be possible and are there any plants on low-light environments from Earth that might do this already?

There is an algea that uses IR:
The newfound pigment, dubbed chlorophyll f, absorbs light most efficiently at a wavelength around 706 nanometers, just beyond the red end of the visible spectrum, researchers report online August 19 in Science. This unique absorbance appears to occur thanks to a chemical decoration known as a formyl group on the chlorophyll’s carbon number two. That chemical tweak probably allows the algaelike organism that makes chlorophyll f to conduct photosynthesis while living beneath other photosynthesizers that capture all the other usable light. https://www.wired.com/2010/08/infrared-chlorophyl/
Infra red can't directly disassociate CO2, it's too low in energy, so that it represents a relatively inefficient and complex chemical pathway for photosynthesis compared to conventional. Research shows that multiple IR photons can be converted to other photons using photon up-conversion, and then used for photosynthesis http://www.sciencedirect.com/science/article/pii/S0360319912001838
here is the most clear summary of why IR is absorbed as heat by water, visible light is gentle and goes through water and excites electrons to do chemical reactions, and UV is too energetic. https://www.reddit.com/r/askscience/comments/14jsms/can_plants_perform_photosynthesis_using_non/

I would hardly ever say never where biology is concerned.  In this case that utilizing red rather than blue light for a plant would require many of the basic assumptions of photosynthesis in terrestrial plants to be revised, but since we're talking about another planet, that might not really be an issue.
If we are asking only about how we could change our plants to work with IR light, I'd say that might take a few hundred million years of selection and it's harder to imagine.
Firstly photosynthesis in another planet doesn't have to fix carbon or produce oxygen - both of these chemical processes utilize the relatively greater energy produced in blue and red light photosynthesis we see in plants here.
Secondly using IR would have its particular questions associated with it.  In this case the energy quanta are very small and in fact in the same range as chemical bond vibrational energies.  Such energy might be hard to capture with any efficiency since simple heat would tend to compete with the photon, so this would work better if the entire system were at a relatively low temperature.
The leaves could be black or they could be completely clear by the way.

"utilizing red rather than blue light for a plant would require many of the basic assumptions of photosynthesis" Both answers to Are two colors (red + blue) necessary for LED grow lights, or would either color be sufficient? indicate that it's primarily red light that's useful in photosynthesis and blue light for phototropism. Yes blue light can excite chlorophyl as well, but all you need is circa 680 nm to make it work. That's already almost infrared if we used 700 nm as the boundary.

Several other answers provide actual examples where wavelengths longer than 700 nm are already in use by life on Earth for photosynthesis, so I think this needs some rewriting to align with actual facts. I noticed that you don't draw from any supporting sources for these assertions.

Photosynthetic bacteria can use infrared light down to 1050 nm (Blastochloris) for photosynthesis.
Oxygenic photosynthesis seems to have limit at about 750 nm.
I think there are organisms that can use longer wavelengths for both oxygenic and anoxygenic photosynthesis.  It is just they have not been looked for in the right way.
Here are some papers of mine.
92).    RITCHIE, R.J., LARKUM, A.W.D. and RIBAS, A. (2017) Could Photosynthesis function on Proxima Centauri b? International Journal of Astrobiology 0(0): 1 –30 doi: 10.1017/S1473550417000167.
93).    LARKUM, A.W.D., RITCHIE, R.J., and RAVEN, J.A. (2018). REVIEW: Living off the Sun: chlorophylls, bacteriochlorophylls and rhodopsins. Photosynthetica 56: 11–43, DOI: 10.1007/s11099-018-0792-x


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What's the biggest obligate anaerobic organism discovered till now?
Beside many anaerobic single cell organisms, there are some annelid worms that are obligate anaerobic at least in their early development stages. Probably, due to low concentration levels in nature, some of the other respiration methods (like uranium or iron reduction) can limit the maximum size an organism will grow. Given the lower energy level extracted compared to the oxygen respiration, what size limits enforces the sulfate, sulfur or methanogenesis respiration? What's the biggest discovered organism, extinct or alive, that is obligate anaerobic?

There are three worms which have been found in the sediment of the mediterranean seafloor, which not only live without oxygen but also do not tolerate the exposure to oxygen. They belong to the metazoans, for more details see either the report (reference 1) or the original article (reference 2). They reach a size og about 1mm.
References:

Scientists discover first multicellular life that doesn't need
oxygen
The first metazoa living in permanently anoxic conditions


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Is a double-yolk egg capable of producing two viable chicks?
As per title: If fertilized, is a double-yolk egg capable of producing two viable chicks (that could survive to adulthood)?
Have there been any reported cases of such (presumably) fraternal twins?

According to the discussion here they normally fail to hatch because the chicks cannot get enough leverage to break the shell.
Here is a video of an assisted hatching. It is claimed that these two survived.

I wonder then, if someone assisted to break the shell, or the shell was particularly thin, then perhaps they could survive. I was wondering if there would be enough physical room in one shell, although I have noticed that double yolk eggs are typically noticeably larger than normal.


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Is it possible to be (briefly) aware you had been decapitated?
If a person's head was cleanly and rapidly decapitated by a sharp blade slicing through the neck, such as would happen on the guillotine, could that person remain conscious? If so for how long? Long enough to be aware of (the head) falling down and hitting the ground?
Obviously it would be brief due to lack of blood supply, but it seems plausible that it could be a few seconds.
Or is there some inherent neurological shock due to the severing the top of the spinal cord that would cause near instantaneous loss of conciousness?
Could Marie Antoinette have seen her own severed neck from the basket below the blade?

According to this, in rats it takes about 17 seconds after decapitation for the EEG to become iso-electric. But there is no known correlation between EEG and consciousness. Also at 50-80 seconds after decapitation, EEG being iso-electric, a very slow, late wave appears on the EEG record.
The same article concludes that it takes about 3-4 seconds after decapitation for the animal to lose conscience and perceive no stress and pain.
Also, dr. Harold Hilman states in An unnatural way to die article from october 1983 issue of New Scientist, page 277 that:

Consciousness is probably lost within 2-3 seconds, due to a rapid fall of intracranial perfusion of blood.

So "yes", Marie could have looked up from the basket and seen her own severed neck. Whoa...

interaction with the head covered in extreme detail by this "classic"

I remember reading that during the French Revolution Antoine Lavoisier arranged with his assistant condemned to death to blink after the cut off if he still had conscience (Lavoisier was to call his name first to limit automatisms). He reported a possibility that the assistant did hear him (the blinking was apparently not that obvious)


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Advantages of bisexual reproduction over asexual one toward species promotion?
Are there any advantages of bisexual reproduction over asexual one towards species conservation and promotion? Do animals that have two or more sexes have more chances to reproduce?
Does anybody had a quantitative account of this fact?

Those are very good questions. Unfortunately answers are not easy and ask for writing a lot! But maybe someone else will give it a try and make it better than I can. Note that the evolution of recombination and of sexual reproduction are not quite the same thing. Also, evolution of sexual reproduction is not the same than evolution from various reproductive system. Finally there are also questions concerning the evolution of sexual determination system. You might have more chance to get useful answers  by splitting up your question and to ask for evolution between different reproductive system. Hermaphroditism vs Bisexual reproduction. Asexual vs sexual. And finally on another post you may add the "conservation" part of your question.
What do you mean "animals that have two or more sexes"? Do you mean hermaphrodites?
You may have a look to other posts on this sites that discuss the question. I don't think there is one post yet that really goes in depth though.
I think that would be great if someone could post an easy-to-read source of information on the subject. Here is one but it is in french only. This presentation by Sally Otto will probably interests you.
Some hints in very short: One issue with hermaphroditism is selfing and its associated concept inbreeding depression. For conservation purposes, note that if one beneficial mutation occurs (at any locus) before another beneficial mutation had time to reach fixation, then  the frequency of one of the two beneficial mutations will necessarily goes to zero. You may be interested in the two-fold cost of sex. Müller's ratchet is also a concept you may want to learn about. There are several very interesting quantitative models on the subject and it is still an ongoing debate. You may be interested in the work of S. Otto and B.& D. Charlesworth. You may be interested in E. Charnov's book although it is a bit old now.


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Possibility and feasibility of producing designed antibodies with bacteria
As stated here it is possible to produce fragments of antibodies in bacteria and harvest them (from the medium, I guess, but I don't have access to the full article).
As it is possible to design antibodies, would it be possible and feasible to produce important antibodies large scale through bacteria like it is done for example with insulin?

Today, I fail at reading.

I'll preface this by saying that I'm talking about antibodies of mammalian/human origin, consisting of two identical heavy and two identical light chains disulfide-bonded into the classic antibody structure:

It is possible to produce antibody-like molecules known as single-chain antibodies, including single-chain variable fragments (scFv) in bacteria and viruses, where it is also known as phage display. These hosts can also produce a modified Fab fragment that is engineered as a single polypeptide chain, and multiple other single-chain antibody-like molecules as shown below. In the past, this has primarily been done in E. coli, as they are a common tool used in protein expression, and have many advantages as an experimental system in general. However, single-chain antibody production in E. coli is hampered by the fact that these exogenous proteins tend to form inclusion bodies instead of being secreted into the medium, where they can be collected and purified much more easily, without the need for lysing the host cells. The paper you linked to describes a method for producing scFvs in the Gram-positive bacterium Bacillus megaterium, which is becoming more common for the production of recombinant proteins.

So, it is possible to produce antibody-like molecules in bacteria. However, unlike insulin, full-length antibodies are made up of multiple polypeptide chains, and are both glycosylated and disulfide-bonded. While there is evidence that bacteria can accomplish both of these biochemical tasks, the processes seem to require additional chaperone, trafficking, and regulatory proteins that bacteria do not possess, and as far as I know scientists have so far not been successful in producing full "proper" antibody molecules in prokaryotes.
However, there are many mammalian/human expression systems for producing fully functional recombinant antibodies in very high yield, and a number of FDA-approved monoclonal antibody drugs are now on the market, with many more in various stages of development and clinical trials.

Great answer, but I'm not aware of evidence that bacteria can carry out mammalian-style glycosylation. Insulin is of course two polypeptides linked by disulphide bonds, but I believe that the A and B chains are produced in separate fermenters followed by assembly in vivo. Linking two Ig heavy and two Ig light chains in the same way just sounds like a step too far in view of all of the possible wrong pathways.

@AlanBoyd check out PubMed. I'm reading through this review now, and there is also evidence for N-linked glycosylation as well.

Thank you for the detailed answer, it really helped a lot!

@MattDMo hit the highlights, but I wanted to comment on the creation of libraries of anbitodies for screening in bacatera.  But there has been interest in nanobodies - the antibodies of camelids  (llamas and camels) have only one chain, which makes the idea of heterologous expression in bacteria even simpler.

.. on the other hand its easier to make a monoclonal antibody from a mouse than a llama!


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Would this mushroom make the basil dangerous to eat?
My sister is growing basil in a planter on her balcony. Recently this big mushroom started growing there. Obviously we're not going to take a bite of the mushroom, but would its existence make the basil dangerous to eat?

That could be a coprinus comatus / shaggy mane. If it is, the top will get pinkish then turn to black liquid . If that happens it was an edible mushroom.

@blacksmith37 I would say Leucocoprinus birnbaumii, which has a tendency to grow in pots.

@Ram Rachum From an academic perspective, I'm not aware of any cases where mushrooms caused toxicity in nearby plants. But consult a doctor for any medical advice.


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Why is it difficult for germs to jump species?
If you haven't watched CGP Grey's video Americapox: The Missing Plague, I suggest you watch it. It's an excellent video.
One assertion he makes is that "germs jumping species is extraordinarily rare [...] being the patient zero of a new animal-to-human plague is winning a terrible lottery."
Why is this true? Why is it so rare for a germ to move from a cow's body to a human's? Is it because it can't travel that distance while remaining alive? Is it because the human's immune system will kill it? More details will be appreciated.

A large part or the reason, especially with viruses, is that they target very specific cell-surface proteins in order to enter a cell.  So the virus is not only limited to species, it may attack only certain types of cells: https://www.genengnews.com/news/coronavirus-picks-on-some-cells-more-than-others/

Does this answer your question? Why are diseases generally specific to a particular species

The main reason is the biochemistry of two unrelated species are different. The more closely related two species the more similar things like the hormones and signaling molecules will be and inversely the more distantly related they are the more different those things will be. Even highly constrained molecules like hemoglobin may still pick of mutation that get carried on, and things like an immune system actually favor variation evolutionary speaking. Even within the same species these things vary, and this is often cited as a possible reason sexual reproduction exists at all, to make each individual slightly different, so there is less chance of catching disease or parasites from others.
Animals have many many barriers to infection, getting pass all of them is hard and tends to only occur with organisms that evolve alongside that animal and thus have been selected to get pass that specific combination of barriers. Getting past them all if you have not been evolving along side it is incredibly unlikely, some diseases manage it be cause there are billions of them, and if you run billion upon billion of random keys through a lock some may fit just due to chance. this is also why disease transfer is more likely the more closely related species are. SIV/HIV easily jumps between great apes because they are very closely related (and the insist on eating each other) the chances of a dog catching it are astronomically unlikely because the chances of the viruses surface proteins matching receptor proteins of a dog is basically only chance as there has been no evolutionary pressure to alter it.


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Cross-integration of puma subspecies populations
A major concern of conservationists  in south Florida is the population of native Pumas, the Florida Panther.
Until recently, it was thought that the Pumas were a genetically distinct subspecies, but some genetic studies have shown that they may not be, and so their subspecies status is disputed.
If the population of Pumas in Florida is genetically distinct from other populations in North America, is there any precedent for using a distinct subspecies to bolster populations of an endangered subspecies?
If the population of Pumas in Florida is not genetically distinct from other populations in North America, would there be any behavioral issues (hunting, etc.) in animals brought from other biomes to south Florida, either as adults or offspring of transplanted adults?

The study you are referring to is probably a study by Culver et al. (2000). They performed a genetic analysis of 315 individuals of the American Puma (Puma concolor), also known as the cougar. Their thorough analysis (especially for the late 1990s) showed that the Florida panther and the western North American pumas were the same subspecies, Puma concolor couguar (note the proper spelling of the subpecies). All individuals north of Nicaragua are this subspecies. From Nicaragua south into South America, they recognized five additional subspecies of American Puma.  The distribution of the subspecies, as well as the sample locations, are shown in the figure below, taken from Culver et al. (2000).

Notice in the figure above that the American Puma used to occupy most of North America but now is restricted to the the region west of the Rocky Mountains, except for the isolated Florida population. Because the genetics of the Florida Panther and the western American Puma are effectively the same, individuals from the western US can be introduced into southern Florida. This idea was first proposed (to my knowledge) by Hedrick (1995) as a conservation measure by introducing genetic variation and reduce the effects of inbreeding. In that same year, eight female pumas were transferred to Florida from Texas, which had the population of panthers closest to Florida. Introducing pumas from outside of Florida has pros and cons, reviewed by Pimm et al. (2005), from both a short-term conservation perspective as well as long-term evolutionary perspectives.
Several years after the Texas pumas were introduced, Johnson et al. (2010) performed a genetic analysis of the Florida population. They showed that the Texas females were indeed reproducing in Florida. The release of Texas panthers did introduce more genetic variation into the Florida population and reduce the effects of inbreeding. The net effect was that more Florida panthers were surviving. The downside is that habitat loss continues and the effective population size is still very small. That means that inbreeding is still very much an issue.
The studies to date have focused on genetic integration and overall recovery due to the introduction of genetic variation but I did not find any studies that reported any behavioral changes since the 1995 introduction. Given that it was only 8 females, I would not expect any significantly different behaviors to be introduced into the Florida population.
Introducing more genetic variation from Texas (and perhaps populations farther west) may be helpful but ultimately preservation of habitat and improving ability of individuals to move among available habitat fragments via corridors is necessary to protect the species long term.
Citations
Culver, M. et al. 2000. Genetic ancestry of the American Puma (Puma concolor). Journal of Heredity 91: 186-197. (open access)
Hedrick, P.W. 1995. Gene flow and genetic restoration: The Florida panther as a case study. Journal of Conservation Biology 9: 996-1007.
Johnson, W.E. et al. 2010. Genetic restoration of the Florida Panther. Science 329: 1641-1645.
Pimm, S.L. et al. 2005. The genetic rescue of the Florida panther. Animal Conservatation 9: 115-122. This issue of Animal Conservation has a few articles dedicated to the Florida Panther.