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What material fills the synaptic cleft? Is it water?
The synaptic cleft is the gap between the pre-synaptic and post-synaptic neurons, and neurotransmitters are transferred between the neurons within this region. What substance exits in this space, is it water? If so, what force makes the neurotransmitters move toward the receptors despite colliding with water molecules?

@Ali Lavasani I updated my answer with additional reference.

There are two types of synapses namely Electrical synapse and Chemical synapse. In electrical synapse there is physical contact between two cells through gap junctions. In chemical synapse there is a small gap between two cells which is termed as synaptic cleft.
The presynaptic and postsynaptic membranes at chemical synapses are separated by a synaptic cleft that is 20–50 nm wide, 10 times the width of the separation at gap junctions. The cleft is filled with a matrix of fibrous extracellular protein. One function of this matrix is to serve as a “glue” that binds the pre- and postsynaptic membranes together.(reference 1)
The same reference also states Water is the main ingredient of both the fluid inside the neuron, the intracellular fluid or cytosol, and the outside fluid that bathes the neuron, the extracellular fluid. Electrically charged atoms, ions that are dissolved in this water are responsible for the resting and action potentials.
Reference 2 mentions, The synaptic cleft is not simply an empty space, but is the site of extracellular proteins that influence the diffusion, binding, and degradation of the molecules, including neurotransmitters and other factors, secreted by the presynaptic terminal
If we think in this direction, of course holding together two neurons at synapse position is important. Moreover, the presence of several dissolved ions (in water) are necessary. If you remember, for the release of neurotransmitters into the synaptic cleft, influx of Ca2+ ions through voltage gated ion channels is essential.Thus, from above all points we can conclude that, the extracellular fluid in synaptic cleft is mainly aqueous in its composition with several ions, released neurotransmitters and several proteins that constitute a matrix.
What force makes the neurotransmitters move toward the receptors?
An essential role of astrocytes is regulating the chemical content of this extracellular space. For example, astrocytes envelop synaptic junctions in the brain, thereby restricting the spread of neurotransmitter molecules that have been released.(reference 1).Thus, it helps to confine the neurotransmitters in the small region, thereby increasing the probability of getting in touch with the target receptor.Also, as reference 2 says, there are several proteins present in the synaptic cleft which influence the diffusion.It means movement of neurotransmitter is by diffusion and above mentioned various factors can influence their movement towards receptor efficiently.
References:

Bear et.al, Neuroscience, exploring the brain, 2015
Neuroscience, textbook by Dale Purves.

The components of the inter-stitial fluid will be dependent on where the synapse is though yes it will be aqueous.  Good old fashioned diffusion over a concentration gradient will be responsible for ensuring sufficient neurotransmitter reaches the receptors on the other side of the synaptic cleft.  Tough to find something you can easily reference online for yourself independently to verify my answer.  I would say that there will be whole chapters on this in any basic pharmacology textbook.  Pharmacology by Rang and Dale is the most easily found in a university library and readable without  a lot of biology knowledge.

Welcome to SE Biology. Your answer may well be correct, but you need to support it with evidence so the poster and others can judge it. That's the way the site works. A quotation from a book or a link to a reputable web site will do.


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How random is genetic recombination?
Two parents can have a very large number of different potential offsprings, and it's common knowledge that the daughter chromosomes in meiosis are produced randomly, i.e. in crossover, the exact spots where the parent chromosomes are "cut" and genes are exchanged are random, with a larger probability at recombination hotspots.
I can't understand how the crossover process can just be completely random, what is exactly different in each trial that leads to different outcomes? Is there something at the molecular level that actually determines the outcome (e.g. the exact positioning and the orientation of the chromosomes or other cells/molecules involved in the process)?

possible duplicate https://biology.stackexchange.com/questions/28243/how-does-the-molecular-machinery-choose-where-to-cut-a-chromosome-for-recombinat?rq=1

Overall, the crossover locations within a chromosome can be seen as random. More specifically, hot-spots depend on population (Fig 1) and sex (Fig S2) (in human) and can be predicted [1].

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What makes protein binding to the DNA random?
We know that the genetic recombination process in known as a random process. On the other hand, it has also been discovered that certain proteins (such as PRDM9) determine what recombination hotspots are used in the crossover process (i.e. DNA is cut and exchanged at those points) by binding a DNA sequence motif encoded in their zinc finger domain.
MY question is, why is genetic recombination still a random process with different outcomes in every trial, if all the hotspots have a potential PRDM9 variant that can activate them? I'm trying to understand why some hotspots get bound to a by a matching protein variant that recognizes them, and some don't.
Is it just due to the random motion of the proteins and that only some of them happen to find a matching hotspot, or only some protein variants have a matching hotspot and the rest go unused, or another reason?

I suspect your disconnect is in the meaning of randomness - random is not a synonym for "arbitrary".

Aren't there many hotspots on a chromosome?  How does a PRDM9 molecule choose a hotspot to attach to?  Could that process be... random?

@BryanKrause it's indeed not arbitrary because not every recombination is allowed (there's certain hotspots) but there are still a large number of possible recombinations and which one happens is kind of random, I'm trying to figure out how that's determined

The term random, is often used in the context of a “random variable” in a probabilistic so-called “random process”. This by itself does not mean that the process is not constrained to certain interactions and boundaries. Could it be that you possibly misinterpreted the term random? A biological process can be random but still under constraints.

@al-Hwarizmi I'm not trying to argue what the term "random" means, even if there are constraints and underlying causes to the process as you are saying, my question is what those are. In this question, why most hotspots are not bound to by a protein (e.g. do very few proteins succeed in finding their hotspots, or matching proteins don't exist for some hotspots in a certain meiosis event, etc).

@AlexL What I meant was that the overarching process of gen. recomb. is random, even though there are constraints by the fact that all hotspots (in human) have a potential PDRM9 variant. There are other factors that randomize the process such e.g. chromatin structure, epigenetic modifications, and the availability of the recombination machinery, random assortment of chromosomes, possible combinatoric multiplicity of hotspots etc. -- while there is deterministic constraint the overall process remains random.

@al-Hwarizmi Thanks. I'd like to know more specifically about the PRDM9 binding and hotspot usage, the average number of crossover recombination events per hotspot is only one per 1,300 meiosis events (even though they're "hotspots"), why is that? I know the PRDM9 finds it's matching hotspot by a random brownian motion, is it that only a small percentage of PRDM9 molecules will come across their matching spot in this search?

Crossovers during Meiosis are not random in human beings.  Its an interesting question as to whether there are organisms that are completely random but the reasons we will discuss here, that is pretty unlikely.
Selfish Gene Theory is based upon the pretty substantiated idea the genes on the genome themselves compete with each other.  Some genes create strong leverage by being indispensable - if they are disabled by a mutation the organism is not viable.  Others genes participate in meiosis directly to game the system in their favor.
This study of sequencing individual sperm is an illustration of the preferences of the meiosis process:
"In many species, recombination events occur mainly in narrow regions of the genome called recombination hotspots. In humans, mice, cattle, and likely many other vertebrates, an early step in recombination is the binding of DNA by the histone methyl transferase PRDM9. A subset of PRDM9 binding sites are subject to the formation of programmed double-strand breaks (DSBs). These breaks are repaired by a specialized pathway, which involves the meiosis-specific protein DMC1, and uses the homologous chromosome as the template for repairing the break. How the correct homologous sequence is located efficiently amongst the bulk of chromatin-embedded nuclear DNA remains unclear. A subset of the breaks repaired via the homologue become crossovers, whilst the majority resolve without a crossover. Any remaining DSBs are likely repaired using the sister chromatid as template. Despite its fundamental importance, critical aspects of the meiotic recombination process remain poorly understood.
Most mammals make only a few crossovers per chromosome, even though the number of DSBs is substantially greater. This raises the question of how the cell determines which DSBs will be repaired as crossovers. While it is clear that not all DSBs are equally likely to resolve as a crossover, the factors affecting this decision remain largely unknown. Improper crossing-over leads to aneuploidy, which affects 20-30% of human eggs and 1-8% of human sperm."

Crossover events are random in humans. Not arbitrary, but random.

I should have expected that completely random crossovers could occur in any place.  what are 'hotspots' in random crossovers?

I think my use of term "random" has created some confusion, by "random" I don't mean that every arbitrary crossover is possible, however, there are numerous possible outcomes depending on which hotspots are actually used in a specific meiosis event. My question is, what on a molecular level determines which set of hotspots are used, for example the random motion or availability of PRDM9 molecules, or the evolution of PRDM9 over time, or something else.

As @BryanKrause hints, this is confusion about randomness. Even above you say, "I know the PRDM9 finds...by a random Brownian motion" and so your knowledge (and question) needs refinement. Brownian motion is a type of unbiased, thermal-driven movement. It's not the only kind of stochastic search for a binding site. So, if something appears random in this context, it means the factors that determine the outcome are unknown or cannot be specified. So, a literature consensus that a biological process gives "random" outcomes ensures (in a near tautology) that you cannot learn here why it is random

here's a gallary of some protein:DNA dynamics in the context of finding DNA motifs. much can be done with no Brownian dynamics (whole molecule, rigid body diffusion) http://www.weizmann.ac.il/CSB/Levy/video-gallery

maybe this is some deep nomenclature.  not clear to me.  Sure the specific place is not predictable, but crossover deserts of millions of bases do help us avoid the wrong impression.  I think that works well to avoid the confusion mentioned.  just trying to be clear and answer the question as asked.

I feel like you all are kinda making up nomenclature and terms on the spot. in biased systems randomness is not the term used.... randomness implies a flat distribution of out comes.  weighted dice are not random. ;p

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Why does centipede keep running into my hair and bite me?
After I moved into a new house in the suburban area, I was bitten by an unknown creature near my spine at mid-night. I felt painful and dizzy. However, after 15 mins, I no longer felt dizzy and the pain faded, so I did not see a doctor.
Serveral months later, the same thing happened again at mid-night, the creature ran into my hair (I have long hair) and bit the back of my neck. This time we figured out that it was probably a centipede, as it was red, had many legs, and ran fast.
Yesterday, a centipede ran into my hair again in the morning. Luckily, I felt something was in my hair and I manged to shake off the centipede, so it did not bite me.
Why does centipede keep running into my hair and bite me and what should I do?

It could be useful to first identify the centipede. Did you catch it? The more common centipede in houses is [https://en.wikipedia.org/wiki/Scutigera_coleoptrata], I have seen it in my house but it never tried to bite us.

@heracho Yes, we caught it but sadly we didn't take any photo of it. It looks like https://en.wikipedia.org/wiki/Geophilus_flavus (brownish red & long)


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Difference between KEGG Pathway and Module (from KO mapping)
At the KEGG otholog mapping query page I can map pathways and modules. I can't seem to find an extremely low level description of the difference between the two. I think I understand what a pathway is. I can't seem to find any definition or description of what a module is.

A pathway shows all the reactions required for the synthesis / metabolism of a given product.  A module is a functional unit that can be utilized in a pathway, and some modules are common to many pathways.  For example, look at the tetracycline biosynthesis pathway 00253.  This pathway has a description at the top that includes this excerpt:

Tetracyclines contain a linear tetracyclic skeleton, which is formed from a malonamate starter unit and malonyl-CoA extender units through a common polyketide pathway [MD:M00778].

Confusingly, that "common polyketide pathway" is actually a module, Type II polyketide backbone biosynthesis, acyl-CoA + malonyl-CoA => polyketide or M00778.
Note that this module is included in other pathways:

map01056 map00253 map01100 map01130

Looking at the drop down menu at the bottom of the module page, we see that the Reference Module contains multiple different KEGG Orthologs that perform the same function in different systems.

Choosing an organism from the drop down menu, the specific Orthologs used by that species are highlighted.

So, you can see how separating pathways into modules can help in identification of these components in other organisms, even if the full pathway does not exist.


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Are there autotrophic fungi?
Are there any completely autotrophic species of fungus?
If so, what species are they? What ecosystem do they live in? Some answers from Quora state that a fungus can never be autotrophic, but why is that?
Thanks for your time!

There are some radiotrophic fungi in Chernobyl. Not sure if you would consider that as an example of autotrophy.

no none of the fungi in the nature is  autotrophic.
they are dependent mostly upon dead and decayed matter.
the reason that they are not autotrophic is that they lack any type of photopigment to carry out photosynthesis.
photopigments are necessary because the are the only components that can trap the solar energy and use it to extract the electrons from the inorganic source such as h2s or h2o by splitting them which are further used to prepare ATP and NADPHH+. these 2 are the assimilatory powers for the further dark reaction. so if these are not there then the processes of photosynthesis would not be there and therefore the organism will not be able to produce its own food in turn it would depend on other autotorphs for food (in case of fungi dead and decade matter).


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What is the most detailed living-tissue scan available
There are a lot of ways to scan living tissue. What is the most detailed one to date? What kinds of resolutions can it produce? Is there a different answer for 2D vs 3D?

I assume you are asking what is the most high-resolution in vivo imaging that science has performed to date?
I think the best way to answer such questions is to explain the nature of the question.
This depends a lot on what kind of sample you are interested in for the question to address. It also depends on whether we are talking about time (temporal) or space (spatial) resolution, because there is usually a trade-off for imaging methods. Some things we can image with femtosecond resolution, and other things we can with femtometer precision.
What property do you want to look at? Is it a certain staining, such as a fluorescent marker? The topography of a molecule sitting on a membrane? The force generated by a motor protein?
Do you consider a reconstructed image (in 3D) from 2D slices to be a fair comparison with techniques that aim to directly image in 3D? Microscopy and imaging are quite advanced fields and we're only beginning to scratch the surface.
Some more considerations for the questioner: is your sample moving? Are we talking about imaging insects hovering near flowers, or anesthetized flatworms? What scale of the sample is being imaged? What are the requirements for keeping it alive during imaging? For instance, perfusing nutrients or imaging a microbe growing on a substrate normally requires the modification of your microscope in such a way that may limit your optical resolution. Imaging some things necessarily requires long working distance objectives, while other specimen may be visualized at short working distances. These have tremendous impact on resolution!
As a case study: let's say we are interested in looking at the human brain with high resolution. You can do this with high temporal resolution (using EEG) or with high spatial resolution using magnetic resonance! Or are you interested in the resolution of real time activity of the brain, as measured via oxygen delivery to regions? This is not possible with either of the above; you have to rely on functional imaging, e.g. fMRI!

Whew. That is a lot more complex than I had thought. I think you have given me enough info to construct a much better question, though. I may open another one here or perhaps take this over to Quora, since my inquiry may be a bit loose for stack.

Also please know I was a little pendantic in my response, I was hoping others would cover the basics. My two cents: live imaging of cells can go down to single-molecule resolution, if it's a fluorophore. Here's a review for single-molecule imaging methods in neurons. You have stuff like atomic force microscopy which are also feasible for living tissues. Notice that the 'best' spatial resolutions are achieved with electron microscopy and x-crystallography, but these are not performed on living specimen. Good luck! :-)


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What virus properties affect their airborne contagiousness?
What properties of a virus affect it's ability to be transmitted by air? I assume it must be able to withstand different temperatures and be smallish in size?
For example why is influenza very easily transmitted by air but the ebola virus is not?

Your question is very broad. There are multiple factors that determine the infectivity of a virus.


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How do NSAID's work and what are the differnces between COX-1 and COX-2?
NSAID's work by slowing down the COX enzym, but how do does enzymes cause pain? because I've read that they're also needed for the body and do "good" things.

NSAIDs work by inhibiting COX-1 and/or COX-2. These are the key enzymes in prostaglandin biosynthesis. Prostaglandins act as messenger molecules in the process of inflammation and therefore can cause pain and other inflammatory symptoms. Source
COX-1 is normally present in different tissues of the human body and is for example important for maintaining the stomach lining. By contrast COX-2 mediated prostaglandin synthesis is only induced by injuries and inflammation. The analgesic effect of NSAIDs is therefore mainly based on the inhibition of COX-2.
There are to different classes of NSAIDs, non-selective (aspirin, naproxen, ibuprofen, ...) and COX-2 selective (celecoxib, parecoxib, ...-coxib). Due to the different roles of COX-1 and COX-2 these different drug classes have different adverse effects and differ in their analgesic effect depending on the dose. E.g. use of aspirin can lead to ulcers of the stomach or duodenum while COX-2 selective drugs do not cause gastric problems (but others).


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How valid is Schwartz's criticism of molecular phylogenetics?
A proponent of the human-orangutan clade, Jeffrey Schwartz argues, in this paper [1], that molecular phylogenetics is largely based on a baseless assumption.
To sum up, according to him:

this type of phylogenetics relies on overall similarity, rather than cladistic considerations, to infer relationships. He claims that even parsimony algorithms (albeit traditionally contrasted with distance-based methods) group taxa on the basis of overall similarity.
this reliance on overall similarity is based on the baseless and questionable assumption that sequence evolution is gradual and continuous.

Could you tell me if his objections and paper hold water, and how valid they are?
[1] Schwartz & Maresca, 2006, "Do Molecular Clocks Run at All? A Critique of Molecular Systematics", Biological Theory, Springer.

Heaven preserve us from phylogenetic flame wars! As was said by Lord Palmerston about the Schleswig-Holstein question, only three people understand it, the Prince Consort who is dead, a German professor who has gone mad, and he himself who had forgotten all about it. I don’t fancy your chances of resolving it here.


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Can you find the amount of heterozygotes in a pop. from the phenotypes shown in the pop
I know the hardy Weinberg equation but that is for the amount of alleles not the amount of phenotypes. So if there are 600 black(dominant) organisms in the population and 400 green(recessive) organisms. Can you figure out how many of the blacks are actually heterozygous?

No one want to do your homework for you.  You will get far better answer if you show what you think the answer is and why.

In short, you would need to know the genetic architecture underlying your trait. How many loci? How does each allele contribute? In your question, you seem to assume that there is a single bi-allelic locus with a simple dominance relationship (where black is dominant). Then yes, you can. What have you tried? You will find the answer in the post Solving Hardy Weinberg problems

Number, not amount. If you need help with your English you may find the following example useful: “amount of sugar, but number of lumps. This is not pedantry — in science precision of expression matters.


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Why are worms, centipedes and snakes long?
Some animals have mostly distinct, non-repeating body parts, each performing a particular function. However, some kinds of animals, such as worms, centipedes and snakes, have a long body that appears to be longitudinally uniform in most of its length. What is the evolutionary sense to that? For instance, what advantage does having a hundred of limbs convey to a centipede, while a spider is happy with a tenfold less?

We have an ontogenetic answer (the Oct4 gene is responsible for the continued growth of snakes), but it doesn't look like we yet have any good explanation for why it has happened. My take would be for the way snakes have been feeding. It helps them by having longer stomachs that can accumulate more preys in one hunt, then they can rest for a while.


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What kind melanin do fair or light skinned black or mixed people have, eumelanin of pheomelanin?
I am doing a study on melanin and conductivity but I cannot find the answer to this question anywhere. Do light complected black or biracial people have eumelanin or pheomelanin? or both?

Race is not a biological construct, which is why asking this question from a racial perspective is not productive. All major variants associated with pigmentation (including the production of eumelanin and pheomelanin) had evolved a very long time ago and were selected upon as humans migrated from Africa. People of African descent, being the most genetically diverse group of humans on the planet, vary greatly in pigmentation, because they represent that initial pool of variants https://science.sciencemag.org/content/358/6365/eaan8433

Pheomelanin is associated with paler skin, while eumelanin predomominates in people with darker skin — this is influenced by alleles of the MC1R gene Swope and Abdel-Malek, 2018, NIH article on MC1R.


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Why is an antibiotic-resistance gene required during transformation of recombinant plasmid?
In my biology textbook, it said that in transformation, the recombinant plasmid containing an antibiotic-resistance gene act as a 'selective marker'. That means that plasmid in transformed bacteria must have taken up the gene of interest and is able to grow in an antibiotic culture medium.
However, will there be a chance that the plasmid doesn't contain the gene of interest but only the resistance gene? How can those plasmids be identified and removed? And how can the resistance gene act as a 'selective marker'?
Thank you very much.

What research have you done to answer this question yourself? Have you even searched past questions on this site? This general topic comes up repeatedly. Please read the Help on asking a good question.

Suppose I pass out notes at your school. Some notes are coupons for a tanning salon.  A few say "You are the chosen.  Wear a green ribbon in your hair tomorrow.  This note is your ticket to the awesome concert".
The next day you wonder who will be coming to the concert.  You look for people with the green ribbon.  That means they got the concert ticket.
Your plasmid has a gene of interest and a marker.  The marker is antibiotic resistance.  If you got it, then you fail to die when the antibiotics come.  If you fail to die that means you have the gene of interest too.  Antibiotic resistance is a marker for having got the plasmid, just like green ribbon is a marker for having got the concert ticket.
To get the ticket but not notification about the ribbon, or ribbon without ticket the note must have been torn or damaged.  To get a plasmid with gene of interest but not antibiotic resistance means the plasmid must have been damaged.  If the plasmids were good when you added them there is not much time for them to have been damaged by random events.  It could definitely happen but odds of that happening increase with time, and in the short term odds are against a damaged plasmid or a torn note.


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What is the use of having a surrogate mother in animal cloning?
In animal cloning, an ovum is collected by an animal and processed to form an embryo after fusion, which is going to be inserted to a surrogate mother. So my question is that why can't the embryo be inserted the animal that gives the ovum as they are both maternal?

Seems trivially obvious, doesn't it?  Presumably the goal of cloning would be to produce many identical copies of the cloned individual, therefore you need many surrogate mothers.

It would make the result at least a little ambiguous. How would you establish with high confidence that the offspring was the results of your implanted cloned ovum and not a naturally fertilized one? DNA testing would have to be quite extensive to establish that offspring was a clone and not the result of an ordinary pregnancy. If you use a surrogate mother, the offspring will have DNA quite distinct from the surrogate.


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Why does glomerulus don't allow white blood cells to leave?
The glomerulus in nephrons are just a ball of capillaries, so why can't it allow the white blood cells to squeeze though the epithelial cells into Bowman's capsule just like the formation of tissue fluid in other capillaries by filtration?

Red blood cells, White blood cells, platelets and proteins with large molecular weight cannot pass through the podocyte and fenestrations in glomerular capillary, but small molecules like water, salts and sugars are filtered out as part of urine.
As these cells and proteins are large to cross through this filter, they remain in the capillary and create osmotic pressure within the capillary. Bowman’s space has osmotic pressure approximately zero. So, only hydrostatic pressure works in this state and help in movement of fluid across the capillary wall.
Via:  https://opentextbc.ca/anatomyandphysiology/chapter/25-5-physiology-of-urine-formation/

So it means that the epithelial cells (podocyte) in the glomerulus are more closely packed so they don't allow the filtration of white blood cells like other capillaries in the human body? Thank you very much

Yes, in association with endothelial capillaries and basement membrane they form filtration barrier in glomerulus.


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Why do chromosomes uncoil back to chromatin after cell divisions?
At the telophase of meiotic and mitotic cell divisions, the chromosomes of daughter cells uncoil back to chromatin, but after interphase, it coils up again to form visible chromosomes. Why do this happen? Isn't it simpler and more convenient for the chromosomes of the cells coil up in 1 cell cycle?

Isn't it simpler and more convenient for the chromosomes of the cells coil up in 1 cell cycle? -- please clarify.  Are you asking why chromosomes uncoil at all, considering they just need to condense again before the next cell division?

@Dirigible Yes, I don't know why this happens since it sounds redundant. Thank you

The condensed form of DNA that exists during cell division is tightly wound and therefore unavailable to the enzymes and transcription factors that interact with and read DNA.  So, if chromosomes are constitutively condensed, the cell will not be able to transcribe RNA, and thus will not be able to make new proteins, and thus will not be able to grow and divide.  The process of selectively condensing certain regions of DNA to prevent binding of transcription factors and RNA polymerase is actually a conserved method of epigenetic transcriptional regulation in eukaryotes.
You may be thinking Then why condense DNA at all?
Uncondensed chromosomes are difficult to separate, and failure to properly segregate homologous chromosomes during mitosis (a phenomenon called nondisjunction) can lead to aneuploidy.  Aneuploidy in germ cells is often lethal, and aneuploidy in somatic cells is a characteristic of cancer.

It’s happening because genetic information from DNA can be read only if it’s in the chromatin form, it can’t be read from chromosomes and so the cell can’t fulfill its functions. But if it’s need to take apart cell’s genetic material, the form of chromosomes makes it easier

Would you please edit your post and add a reference to back-up your statement?


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How can parentage test be accurately done even though crossing over occurs?
As crossing over occurs when gametes are secreted, so when a zygote is formed after fertilization, the base pairs of DNA in the child should be different from that of the parents. So when gel electrophoresis occurs, the position of DNA fragments of the child shouldn't be the same as half of their father and mother. But why is this statement wrong? sorry for bad English.

Crossing over is an event that occurs during meiosis, which produces the gametes. This crossing over occurs between 2 homologous chromosomes, which are both from the parent. Hence, even though crossing over occurs, the recombinant chromosome that is passed down to the child will contain an allele that matches with the allele on one of the parent's chromosomes. Within the allele, the base pair sequence would not change.

So it means that the allele extracted from the child should be the same as the parents to attain the same base pair sequence? i.e. tandem repeat? Thank you very much

Yes, the same allele should be targeted in the child as in the parent. This would ensure that the size of the DNA fragments obtained are the same, so the position of the DNA bands on the gel would also be the same.


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Is one DNA molecule same as one chromosome
Is one DNA molecule = one chromosome or is one DNA molecule = all the chromosomes, ie, all the genetic material in our cells? I have googled it but  I am not getting clear answers ?

Considering the encyclopedic definition of a molecule...

Molecules are held together by shared electron pairs, or covalent bonds.

...one DNA molecule is one DNA strand.
Put another way, one DNA molecule is a polymer of nucleotides connected by phosphodiester bonds. This means that one intact double-stranded chromosome is composed of two molecules of DNA interacting by hydrogen bonds.
In practice, however, one piece of double-stranded DNA is commonly called a DNA molecule.
All of the chromosomes in a cell constitute a single genome.
To further add to the confusion, identical chromatids may be said to compose a single chromosome, such that one replicated chromosome composed of two chromatids may comprise four DNA molecules, by the definition outlined above.

Note, the same encyclopedia lists ionic bonds as being on the same "continuum" as covalent bonds...

Ionic and covalent bonding therefore can be regarded as constituting a continuum rather than as alternatives.

...so atoms held together in ionic interactions are also considered molecules, by this definition.


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Can citric acid be used as fungicide in banana based fly (Drosophila melanogaster) food?
I am experimenting with a banana based fly food for better larval synchronization. Instead of propionic acid, I am going to use (added) citric acid as fungicide. Is there any downside to this approach?

There is still some dispute over the exact cause of the antimicrobial effects seen with organic acid. One of the theories is that the protonized acid crosses the cell-membrane and destroys the pH-balance inside the cell.
This would explain why these acids are more effective at low pH (a higher fraction will be protonized).
Citric acid is a significantly stronger acid (pK = 3.1 for the most acid proton) than propionic acid (pK = 4.87), meaning that the pH of the food has to be around 2 units lower to obtain the same fraction of uncharged molecules.

I have no data on the fungicidal and insecticidal properties of citric acid at various concentrations (and you may be hard pressed to find a good study on this), but I have worked in some fly labs and I understand the composition of fly food only peripherally. The most commonly and most abundantly used fungicide in a lot of fly labs is methylparaben (trade names Tegosept or Nipagin in Europe). I imagine food recipe-makers have arrived at this solution through trial and error over the years; this is as much an art as it is a science, in balancing the ingredients with humidity, temperature, species and genotype with desired generation time. Methylparaben is used with and without propionic acid for Drosophila melanogaster. Do you have methylparaben in your fly food? Also, I think citric acid is not commonly used, again I imagine because technicians probably found it inferior to its alternatives.
The National Drosophila Species Stock Center at Cornell uses methylparaben with its banana food recipe.
Alternatively, please take a look at the variety of recipes Bloomington Drosophila Stock Center uses. To my knowledge they supply and stock the largest collection using the most recipes.

Fly foods
Alternative recipes

I have used methylparaben (with propionic) acid in past while preparing the corn flour based fly food. We used same preservatives for banana based fly food and larval growth was not satisfactory. That's why I was considering alternatives.


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Why do leeches lose septae due to parasitism?
So I found this piece of information in my textbook without a proper explanation, and I can't seem to find the relation between the two.

Welcome to Bio.SE! What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!

Please start by editing your post to include the source of your information (in other words, cite your textbook), and please provide a direct quote referencing your piece of information. After dong that, please indicate what other research you've attempted on your own and what you've found out. Thanks.


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Which trait does the given Pedigree chart show?
I have a doubt in this pedigree chart , according to me it should be autosomal dominant. But the ans given is X linked recessive , in the case of X linked recessive one daughter should be carrier and not affected , but in the chart it's shown the daughter is affected and not a carrier .
What should be  genotype of female parent ?

Please do not post questions as photos of text. It discriminates against people using screen readers and cannot be indexed.


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Insertional inactivation using pBR322
I have questions regarding "selection using insertional inactivation".
In a typical DNA recombination experiment using plasmid pBR322 where a new gene in inserted in the place of tet gene, it is said that entities with the recombinant plasmid can be selected by growing all the bacteria in two different medium: one with tetracycline and one with ampicillin.
I know that pBR322 contains two genes that make it resistant to both tetracycline and ampicillin, and also that the newly created plasmid will only be resistant to ampicillin, since its tet gene is no longer functional.
So in the plate with tetracycline, only entities with the original plasmid will grow. In the plate with ampicillin, however, entities with the original plasmid and the modified plasmid will grow.
How can this be a selection when two different types of entities are growing in one plate?
Am I misunderstanding the meaning of "selection" in this case?
My explanation above seems very immature, so it would be great if someone can provide me with deeper understanding.

Yes. I concur with canadianer.  As currently described, replica plating is the way to go.  IF: you had a drug that killed bacteria resistant to tetracycline, THEN: you could use that as a selection.

The ampicillin plate is selecting for bacteria transformed with the plasmid, either the original or recombinant, whereas the tetracycline plate is selecting only for bacteria transformed with the original plasmid. Since you are only interested in the recombinant plasmid, you need to do some form of replica plating and compare the two plates to infer which colonies contain the recombinant plasmid (those which grow on ampicillin but not on tetracycline).


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Which animals don't have pheromones?
Which animals are known to not have pheromones besides humans?
I can't find any research on this. There are examples of every class that uses pheromones. However nobody seems to answer conclusively that any particular species is not likely to have pheromones.

I'd guess none. If any chemical factor used in an organism's metabolism is volatile, it could be easily released and trigger a response in a nearby organism. And that's essentially a pheromone. Even bacteria do it.

Ok, does it get more complex if we limit it to sex pheromones?

Possibly. Approximately half of all animal species (including hammerhead sharks) can reproduce asexually, so it's possible they have less need for sex pheromones. But I'd say it would probably be difficult to show that an animal doesn't use any pheromones since there's often thousands of substances released by the animal that could plausibly trigger a response (and how would you test them all?).

But were there any that were extensively studied and none were found, as in humans?

I can't say with certainty. Someone else will have to weigh in on that one

Like for humans, this is not really an answerable question. Even for humans, the absence of pheromones is controversial. Failure to identify a single compound suggests pheromones are not as potent in humans as in certain animals, but cannot rule out their absence entirely.

Is it likely that all animals besides humans have pheromones? Is there a strong reason that there would be exceptions?


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The Evolutionary significance of Coelom
What is the evolutionary significance of coelom formation?

Welcome to Biology.SE! It is expected that you will demonstrate that you have done research on your own before asking questions here — for example you could start with this: https://en.wikipedia.org/wiki/Coelom …. –––––––– For details on how to use this site, please check out the tour: biology.stackexchange.com/tour and then the help pages on how to ask questions on this site: biology.stackexchange.com/help/how-to-ask. Thanks!


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Knee directions
art student with very little knowledge of biology here. I was thinking about the designs of mythical creatures and I got stuck on the topic of knee directions, and couldn't work out the appropriate terminology to do my own research.
Is there a term for legs that bend towards the head (eg primates and the front legs of horses, cows, goats, etc) or those that bend away (back legs of the above mentioned, dogs, cats, lizards, primate elbows, etc)? Is there a large practical difference in the way these two types work/are used that is more notable than the other differences between types of leg structure?

cats/horses walk on their toes. the part that bends backwards is the ankle, the knee points forward.

Hi @Robann, welcome to the site. If you could ask one question per post, that'd be appreciated. E.g. "what is the term for legs that bend forward" and "is there a practical difference".

Also, you should note that (as Frieke has pointed out) the joint in a cat's/dog's leg that looks like a backwards knee is actually its ankle. The knee is further up in the leg and they walk on their toes. See Line of Action: Digitigrade animals don’t have “backward knees”.


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Reducing Ammonia Levels in Body through Bowel Movements Only
Can high ammonia levels in body be reduced solely through repeated bowel movements (4-5 per day), i.e., WITHOUT the use of Lactulose?

Lactulose can decrease the blood amonia levels by either drawing some ammonia from the blood into the intestine (MedlinePlus) or by inhibiting ammonia production by the intestinal bacteria and hence its absorption into the blood (Digestive Diseases, Emedicine).
By having frequent bowel movements, you could theoretically give less time to intestinal bacteria to produce ammonia from the undigested food, but, without laxatives, it may not be realistic to just decide to have 4-5 bowel movements per day.


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Why does it take so long for the human brain to develop from an evolutionary point of view?

I have read that it takes about 25 years for the brain to be fully developed.
  Coincidentally, humans from the Neolithic and Bronze Age had a very short life expectancy, in fact most of their life their brain wasn't fully developed.

My question is:
from an evolutionary point of view, is there a reason why humans spend so much of their life not being fully developed even long after being sexually fully developed?

You are asking about the phenomenon of neoteny, the delay of development well into adulthood. You will not get a better answer than this comprehensive wiki on neoteny in humans. You will find a rather impressive list of reasons and arguments throughout the entire page, especially under the Human Evolution section.

We can say that brain and our nerve system is the first system in embryo that starts to develop and as you said this system is continuing to develop until after birth.
So here is a question that why our brain don't develop completely before the birth ?  Evolution has gone so far as to limit the development of the brain in the human embryonic phase and to allow it to continue into the postnatal phase. This helps the infant to be born and ease the birth both for mother and the new born because if the brain had fully grown, the size of the head would have made problem in birth. Now, after birth, the brain continues to grow and develop majorly between ages 2-3 and becomes more mature after that . The ability of the brain to grow over the years gives us the ability to adapt to different environments , learnings and new issues and other capabilities That happens with the subsequent creation and pruning of dendritic spines.

This partially explains why we're not born with fully mature brains, but doesn't at all answer the question of why it takes so long for the brain to fully mature, long past when the rest of our organs and systems are fully functioning.

At the end of the paragraph I mentioned the one point that why our brain developing takes too long

Being born with a fully-developed brain would still give us those same capabilities, although one could argue that language acquisition is uniquely easier during childhood (due to the characteristics of the brain during that time) than it is in adulthood. As it is, I'm not going to downvote the answer, but I'm not going to upvote it either. I think you could go a lot farther in explaining the evolutionary biology of neoteny.


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How long it takes medium size dog's corpse being decomposed?
I am not a Biology student or expert. Moved the post from Pets SE.
Around a month ago, my 12 years old dog passed away. And I buried her in our front yard (mostly soil, 1 meter depth, wrapped in some cloth fabric material). The thing is I have a plan to sell my house, but don't have nerve to move away if my dog's corpse have not completely decomposed. There is a hard feeling to leave her like that, you know, the family bond stuff. So it will be relieving if her body are completely decomposed when that happen.
Background I live in Yogyakarta, Indonesia, which has tropical climate. But from the past few month, we have pretty unusual cold temperature during night until around 9 am, because of Australian Cold Monsoon. I mention this in case it has logical factor of how decomposition works.

Maybe Medical Sciences Stack Exchange is more suitable. Vets can answer this question there.

That's a very warm climate, about 25'C year average, which causes very rapid decompostion. 1m deep is about the same temperature, according to graphs. The limiting factor for you will be the air in the soil. wet compact clay can be very low on oxygen, and sand has the highest oxygen. to be on the safe side, you can also ask the new owner if you can come back in 2 years to collect the bones and cover the garden, and give him some extra flowers. My guess is that there can still be some non-bone material there for 2-3 years, hairs for 3-4 years. recall your dog, he is in the sky, dont be guilty.

@com.prehensible “He is in the sky”? Read the question. The poster said the animal is rotting in the ground.


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Why do we need to grow plants to make food?
Why can't we synthesize the nutrients that we need directly from chemical reactions, from energy and simple inorganic molecules found around us? If it's hard, why not try to copy how plants do it?
I feel like growing plants is very inefficient: it is consuming a lot of energy for intermediate steps that may not be required – growing roots or inedible parts, performing reproduction, consuming soil and space, requiring constant light and irrigation... And huge amounts of energy is invested to slightly compensate for these caveats and increase productivity, while it still looks like an inefficient way of doing synthesis of nutrients and other compounds we need to eat.
Is there a reason that such resources are not directed to building processes to perform such synthesis via other – hopefully more efficient – means than growing plants/animals?
Note that I found a partial answer there, however I was not satisfied by an unexplained "photosynthesis is the only viable way to create material that can yield those nutrients".
Is photosynthesis that hard? If that so, why?
If it's so hard using organic chemistry, why cannot we simply extract/mimic the biological reactions happening in the plants to generate nutrients? (we still don't need to grow whole plants)
If we are not able to do that, what does it means about our current understanding/mastery of chemistry and biology ?

I'm voting to close this question as off-topic because it is about logistics of industrial chemically-synthesized food production.

Is there another stackexchange I could move it to?

I am not sure (perhaps [worldbuilding.se]). In any stackexchange, this would be a broad question.

Why are so many "why" questions accepted here? Everything is turning into phylosophy instead of biology. Why does everyone question everything when there is no major problem with it? Also, many nutrients, mainly sugars and sugar alcohols, are already artificially produced and they are mainly associated with - problems.

Even if we could synthesize "food" reasonably efficiently, we don't know everything that is needed for a healthy diet. 2) Growing plants provide many other services - from replenishing oxygen to soil stabilization to just being pleasant to be around.  Since you have them for all those other reasons, why not use them for food too, rather than resorting to industrial chemistry?

I'm simply curious, and I find it hard to find good answers to these questions. 1) seems to make sense ! 2) we could go back to having forests everywhere instead of fields, which seems like it would have lots of benefits

@palkeo: Plenty of things to eat in forests, and then there are grasslands.  WRT #1, you might reflect on the fact that (AFAIK, anyway) we really don't synthesize any significant amounts of organic chemicals from scratch (that is, starting with CO2, H2O, nitrates, and a few minerals, as plants do) .  Most things start from organic feedstocks, either plant-derived, or petrochemicals.

We are part of a biological system, and we evolved to be part of it. Plants are the base of that system, and the main means of capturing energy and inorganic compounds and converting them to nutrients which are bio-available, along with bacteria.  The further we move from the niche we evolved to occupy, and the further we change the environment of the rest of the system, the more likely we are to bring about our own extinction.
Edit: This answer is somewhat opinion based. We haven't finished the experiment that proves this thesis, yet.


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What are the various parts of an ant hill
How can I identify the parts of an ant hill structure from a casting?  Specifically, if there is no real commonality between species, I would like to identify the various parts of a fire ant mound in Florida


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Why can we sniff so much?
What was the point for us humans (or other mammals) to develop such a strong sense of smell? Depending on the source, we can distingiush from 10.000 to even trillions of smells. But how was the ability to sniff "artificial" smells (e.g. paint or burning rubber) being useful to our ancestors?

While the question combines a few points, an answer may be far from trivial (e.g.: when also considering the recent reduction in some animals such as humans, https://en.wikipedia.org/wiki/Evolution_of_olfaction#The_Olfaction_Tradeoff  , or considering the ancient non-olfactory role of olfactory receptors within early mammalian embryogenesis found by Dejosez et al. Science 2013, http://science.sciencemag.org/content/341/6153/1511 )

Smell samples the chemical composition of the environment, the groups of molecules you are sampling in those examples still exist in nature. It is like asking why being able to taste pizza would evolve, it doesn't, not by itself anyway, it is the inevitable result of being able to taste the things and conditions that make up pizza, carbohydrates, proteins, fats, oils, acids, bases, salts, etc. things that would be important for our ancestors to be able to detect.
With paint you are smelling volatile organic compounds, and many are important biological and/or hazard markers, some are related to rotting meat, others to infection, others to food sources, and others to natural toxic water sources. With burning rubber you have many different smell depending on the rubber, but in each case you are smelling a burning organic polymer which releases organic compounds which again would exist in nature.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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What are the small lumps in the mouth of the fish, and what is its function?

Today I was performing a fish head dissection to investigate the gas exchange process in biology. Then when I opened the mouth I noticed these small hard structures at the base, I assume they may be a form of teeth that allows the fish to grind hard shells of invertebrates and plant matter. Yet I was curious as to why some fish have this and others don't and what exactly it's function is. Also if you have a name I would highly appreciate it as I can label it in my lab book. Thank you so much for your time.

Yes those are teeth and some have them and some do not for the same reason some have sharp teeth wile others have flat scrapper teeth, it depends on their diet.
this kind of teeth are called molariform, and are used for crushing shellfish more than anything else. This slide show will help you, https://www.ru.ac.za/media/rhodesuniversity/content/ichthyology/documents/Anatomy%20Lecture%207.pdf

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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What is the precise mechanism by which exercise reduces chance of cancer?
Sources like this: http://www.cancerresearchuk.org/about-cancer/causes-of-cancer/physical-activity-and-cancer/how-physical-activity-prevents-cancer point out that we can reduce our risk of some cancers by exercising.
But it seems to just be hypothetical, like "scientists think insulin can turn on signals that tell cells to multiply", and
"This can lead to the cells multiplying much more frequently than usual, to replace dead and damaged cells, increasing the chances of mistakes that could lead to cancer"
But human metabolism significantly increases during and after exercise, implying high rate of cellular division! Therefore, these 'hypotheses' seem questionable in their attempt at saying, "cells don't divide as much". I believe that these may be contributing factors, but I don't believe they're the main cause of most cancers in general. I am deeply skeptical that muscle inflammation requires less cell division than colon inflammation.
I have a hypothesis that exercise simply reduces cancer in the following manner: increase cellular movement, which increases the probability of the following:
1) t-cells tag foreign pathogens
2) white blood-cells capture foreign pathogens
3) damaged cells are repaired/found/killed faster
Statistically, increasing the entropy of a system would allow the individual components to cover a larger area in a shorter amount of time. Since the number of pathogens introduced into the system remains relatively constant while the interal system speeds up, it's like running a high-pressure jet stream of water and soap through pipes to clean them out. The soap (t-cells) and pressure (contractions of heart/blood vessels) together help clean the system effectively.
I'm having trouble finding evidence/support for this hypothesis, so if someone could point out the flaws in my hypothesis or point me to some sources to find out more, I'd be deeply appreciative.

Check mTor downregulation during exercise.

I think the only answer here is "nobody really knows why, it's something that's been discovered through statistical studies".

Come on, comments aren't for answers, people...

No one knows, it's just a line of research

Can you cite any evidence at all that exercise does any of the list you have?

Vigorous exercise (even for five minutes) causes increased DNA damage http://www.ncbi.nlm.nih.gov/pubmed/20839226. The increased DNA damage would stimulate the defenses including the immune system (e.g. natural killer cells) http://www.ncbi.nlm.nih.gov/pubmed/16618710, and the boosted immune system would eliminate cancer cells, reducing cancers based on the immune suppression model of cancer http://www.ncbi.nlm.nih.gov/pubmed/27928220. The reduction of cancers with increased exercise (physical activity) has indeed been observed http://www.ncbi.nlm.nih.gov/pubmed/18506190.

You did notice that your last link offers a completely different MOA then the one you put together?

Welcome. It's good practice to give the full citations, just in case the link goes down. Nice referenced answer +1

This answer gives good information, but doesn't really answer the question because if individual organisms could just stimulate the immune system without an adverse effect, why would they need exercise to do it?


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How did genome replication first synchronise with cell division?
It is obvious that cell division in living organisms is now synchronised almost perfectly with DNA replication and, furthermore, the line of division has to intersect exactly the space between the two copies of all the DNA molecules in the cell.  I know that as otherwise, most cells would be either empty or have a lot of excess DNA strands, which would lead to an eventual termination of replication due to scarcity of resources and energy required to trigger it.
Some theories (https://www.ncbi.nlm.nih.gov/books/NBK26876/) suggest the first protocell might have formed by a liposome simply gobbling up a self-replicating molecule. However, how would the molecule then 'know':

when exactly it should replicate so that the replication coincides with the liposome diving and
where in the molecule it should be located at the time of division, so that its copy ends up in a different daughter cell to itself

?

I obviously don't know the answer as there isn't a proven hypothesis yet. It seems to me plausible that by chance alone (i.e. no molecular knowledge required), a small fraction of the early protocells ended up dividing with enough self-replicating material randomly spread among the two daughter cells for them to grow and repeat the duplication process until it became controlled and perfected giving those cells an evolutionary edge.

@cagliari2005 that would still be one division. In order for synchronisation to have developed, millions of synchronised replications must have taken place.

Agree, but if the number of protocells is sufficiently large at each duplication phases, then while the vast majority will fail at duplicating, the few that made it will slowly evolve to perfect the mechanism (i.e. think about a population of protocells rather than single individual cells). I also wouldn't be surprised if this mechanism didn't evolve linearly but rather made several evolutionary jumps. But again, this is mere speculations and while I found the question interesting, the answer is unfortunately bound to be speculative.

@cagliari2005 I am really not sure (in fact, pretty sure that the opposite is true) such a mechanism would have any evolutionary advantage over molecules outside of the cell, if only one in many could successfully reproduce. My own theory is that at first, many molecules were able sustain themselves in one protocell, which eventually ripped apart due to excessive tension exerted by the molecules. As it did, roughly half the molecules went into one daughter cell, and half went into the other. Then, as you say, perhaps a more efficient mechanism evolved in an evolutionary jump.

That is definitely a possible theory :)


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What causes the complementary copy of an RNA molecule to separate?
I have recently read an article which explains that, in the RNA World hypothesis, an RNA molecule gets 'scanned' by nucleic acid, catalysed by a different specifically-folded RNA molecule, to arrange itself complimentarily to the original molecule. However, what causes the new, complementary molecule to detach from the original molecule? I always hear people say that this complementary base pairing allows the RNA molecule to reproduce, but I never quite understood: how? If complementary bases tend to bind together, shouldn't the newly formed structure then be stable? What causes the actual reproduction?

Both complementary binding of RNA & DNA is dependent on temperature and salt concentrations (among other things), so if these factors change so does the stability of a double-strand complex

@Nicolai so both of those have to exactly spot on, or the bondings deform? Why, then, does an RNA copy itself completely most of the time? Why does it first have to scan itself completely and then detach (i.e. why can't some bases pair while the others will not due to a different temperature?)

There are many single-stranded RNA viruses in which the daughter strand must be released from the template. I imagine that this strand displacement is a feature of the action of the RNA-dependent RNA polymerase. How it works I have not been able to find from a brief search (hence comment, rather than answer), but it obviously does. So this is not a particular problem of the RNA world. I'd check the virology literature if you want more info.

@David I know it's not an issue with the hypotheses - it's my lack of understanding. So the RNA copy disentangles itself from the parent RNA because of a virus/polymerase? That seems logical, but then again, same problem: why can't it infect the RNA while it's being copied? Wouldn't it then create an incomplete copy, thus perhaps causing the whole system to malfunction? Or are these events rare because the copying stage is too quick?

The polymerase somehow starts synthesis at one end, the complementary NTP binds and the enzyme catalyses a phosphodiester bond, goes along the template strand one base so as to be able to catalyse the bond between the growing chain and the next NTP to bind, etc. etc. Your valid question is why the growing chain is released from the template rather than staying H-bonded to it. I assume that as the polymerase moves along it somehow destablizes the interaction (rather than just dissociating randomly). However I am unaware of the molecular mechanism.

Wow, what you described is very different to my current understanding of RNA synthesis. As I thought, surrounding nucleic components were somehow attracted to the RNA, and bond formation was catalyzed by other specifically-folded RNA molecules, which acted as physical shape-selective (sorry for unscientific vocabulary) enzymes and helped physically shape the bonds. I didn't know it was a polymerase that triggered the synthesis. That is very strange, because, especially if your assumption that the polymerase destabilises the bonds as it moves along is true, that would require it to have a

very particular function: it would first have to find the RNA molecule, then move along it, and while doing that it would catalyse the formation of a very specific bond, and it would also involve, as I understand, a complex negative feedback mechanism. How would such a molecule arise naturally? I know that you are right, but it just seems odd to me.

@David Sorry I forgot to tag you

First, I want to point out that the RNA world hypothesis is just that - an hypothesis. While it has been shown that it's possible for certain RNA molecules to make copies of itself, this is not a 'normal' function of any RNA.
Edit - to give a clearer answer to the question itself:
After replication of an RNA molecule it may form a stable structure together with its template or it may dissociate. Due to the various possibilities and complexity of RNA structures its almost impossible to predict this, since both the (exact) sequence itself and environmental conditions especially temperature are very important.
More background from the unedited answer:
Whether two complementary strands or RNA (or DNA) bind together is not something that can always be easily answered. For DNA of a given length (in a given environment / buffer) one can more or less predict the temperature at which complementary strands will separate (often called melting temperature), because DNA forms relatively stable helices.
RNA, however, often forms complicated 3-dimensional structures, often involving self-complementary and is not restricted to the typical helices seen in DNA. Trying to predict the resulting 3D structure of RNA molecules is still an ongoing field of research. Some of these structure are quite stable (e.g. in tRNA) but in other cases they can also be very dynamic and change quickly.
In the end it always depends on the RNA sequence, temperature and many other environmental factors.

So I assume this melting temperature is quite low, then? Seeing as (okay, I will switch to DNAs for now for simplicity) a DNA unwinds itself so often?

You mention various factors affecting base-pairing in RNA but you do not answer the poster's question, which is if the bases anneal to the template to allow polymerization in the first place, why does the product dissociate? Talking about RNA “liking to form complicated structures” won't do. It may have the potential to do so, but dsRNA viruses show that it has the potential to form duplexes.

@David I don't think it's possible to give another answer to the question than my last sentence (maybe I should make that clearer), because it will always depend on the RNA sequence and environment whether it dissociates after replication or not (even in the first place) - the fact that dsRNA viruses are possible is just another example to the ones I listed

I also remove the 'RNA likes to ...' which was indeed a bad way to describe this.


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What does this skull belong to?
I was cleaning out my pool with a leaf scoop the other day and found a small object, which I assume to be a sort of skull or cartilaginous structure of something that had died.
I live in Sydney, Australia and in the pool there were a large quantity of water boatmen and dragonfly nymphs.
What does this skull belong to, and what is the purpose of the hollow, bulbous mounds next to the eye sockets?


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Is this plant with very asymmetric leafes Aegopodium podagraria (aka ground elder)?
I found this plant in a city park in Germany. The leaves were about 20cm of height; the smell of the squeezed leaves was a bit like carrots. The stems were edged. So I guess it was Aegopodium podagraria (aka ground elder), but I'm not sure about it.

A man, collecting herbs, confirmed my suggestion about Aegopodium podagraria. Together with what I read about this plant, I can set my question as being answered with Yes.


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Is this a Enoki aka. velvet shank aka. Flammulina velutipes?
In December in southern Germany I found the following mushroom on a some remains of a tree. From what I read, saw and felt (sticky cap when wet), I am very sure it is a velvet shank, especially because in winter there are not many other types of mushrooms around to be confused with. However I would like to know if someone can confirm/debunk my assumption?

Please don't rely on any identification help given here to decide whether you should eat a mushroom you found.

I would agree with your identification of Flammulina velutipes based on the description in Mushrooms Demystified (David Arora, 1986) and the page on MushroomExpert.Com (Michael Kuo, 2013). Arora emphasizes the viscid yellow-orange to brownish cap, velvety dark-brown stalk, lack of a veil, white spores, and growth habit as diagnostic characteristics. Take a spore print and note the texture of the stem next time you come across them as additional tests. If the substrate is not too decomposed, also note if it is growing on a hardwood or softwood (F. velutipes only grows on hardwoods).

Fig. 1. Flammulina velutipes. source: MushroomExpert
I'm not familiar with European mushrooms, so I don't know if there are look-alikes where you are, but this mushroom does grow in Germany (see map at MushroomExpert).
And of course, heed Bryan Krause's advice.


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What are some features that do not make an individual better than others without this feature?
If a mutation occurs so that this allele gives a noticeable feature that is present in this individual but absent in every other individual and this feature is of no benefit or detriment to the individual, I was thinking that this mutation will not make the individual better soothed to the environment or worse and so the gene may not die out but be passed from one generation to the next generation.
If this is so, I thought, there should be many of such “useless” gene present in today’s world. Other than the appendix (which has no function in humans) and subtle differences like eye color, head shape ( not too severe ones but like the ones we see everyday - different heads), which other examples exist?

The human appendix does have a function: https://www.scientificamerican.com/article/what-is-the-function-of-the-human-appendix-did-it-once-have-a-purpose-that-has-since-been-lost/

Phenotypic effect of mutations
Most mutations have no phenotypic effect and therefore no fitness effect either (fitness is a function of both expected survival and expected number of offspring).
These mutations that have no phenotypic effects are therefore all neutral in terms of their fitness effect. Their probability to be passed on to at least one offpsring in a panmictic population of constant size $N$ is $\left(1-\frac{1}{2N}\right)^{2N} ≈ exp(-1) ≈ 0.36$. A mutation that is beneficial would have a greater probability and a deleterious mutations would have a lower probability. There are a whole bunch of equations for these but I don't want to get too "mathy" in this intro post.
Fitness effect of mutations
Among mutations that have phenotypic effects, some have no effect of fitness, some are deleterious, some are beneficial. The beneficial ones only represent a very small minorities of mutations.
Note that it is important to make the difference between a trait that seems to not be beneficial to you, while whether it actually is or is not beneficial. You cite things like eye color and head shape. Both of these traits can have very important on sexual selection. Try to date someone with a triangular head or with white iris! Also, if I am not mistaken, light colored eyes tend to let more light going through to the retina, hence light colored eyes are better adapted in environment where sunlight exposure is low. Head shape may have important impact too. For example, the jaw bones is an important contributor of the head shape and whether you have a strong or weak jaw is of importance (and the shape of the jaw is under sexual selection pressures).
Examples of neutral mutations
Most mutation that happen at non-coding, non-regulatory regions of the genome will be neutral.
Among the mutations that have phenotypic consequences but no fitness consequence, there are classical genetic markers (such as tongue rolling) that are likely free from any selection pressures. Note, that heritability for such trait is rarely 1.0 (see here for explanations). Maybe earlobes would be a good example, although there might have some sexual selection going one here.
Note also that as many mutations are recessive, the carrier of a single copy of the mutation may not be affected.
What is a gene?
You are using the term gene improperly. A gene is typically defined as a coding region. You might want to study a little the basis of genetics here. You should typically get used to the terms locus, allele and gene copy number. This answer can help you at this endeavour.
A small comment on the frequency of mutations

If a mutation occurs [..]

Just to make sure you do not have a misconception about how frequent mutations are here, I would like to highlight that, in humans, at every reproduction event, the new born has about 10 to 100 new mutations that were not present in any of both parent. So, mutations are rather common!
Introduction to evolutionary biology
Your question is a very introductory question to evolutionary biology. You might want to have a look at a short introductory course such as evo101 by UC Berkeley.


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How is it possible for a new species to evolve?
Suppose a new species is created from a random mutation that happened during an instance of reproduction in an existing species. How can that new species survive and flourish if there only exists one of it's kind and therefore it's not able to reproduce? By definition a species can only reproduce with others of the same species, no? It seems to me the only way it could is if a mate is created due to a separate occurance of a similar mutation, and the chances of both mutations occurring at around the same point in timespace must be very close to zero. And even if it were to happen, it seems to me the offspring wouldn't be able to reproduce due to problems with inbreeding.

Your question implies some misunderstandings about what mutation and speciation mean. I recommend https://evolution.berkeley.edu/ - it contains a good short summary of the basics of evolution.

By definition a species can only reproduce with others of the same species, no? No, and this shows a profound misunderstanding of science in general and evolution in particular.  In any case, even if that was true, it applies to "species", not "incipient species". You should read the link that Armatus pointed to to begin to correct your misunderstandings.

Virtually all cats can interbreed. (Lions, Tigers...) So can almost all dogs. Interbreeding is an ancestral condition, lost on a case-by-case condition.

One single mutation won't create a species.  Suppose instead you have an initial population that is separated into groups by geographic barriers - say they're on the Galapagos Islands, for instance.  Then each group will experience random changes, different beneficial ones will be selected for given the different conditions on the islands, and eventually the populations will diverge enough to be considered new species.

"this shows a profound misunderstanding of science in general" thanks @iayork for the hasty generalization / just plain insult.

Suppose a new species is created from a random mutation that happened
  during an instance of reproduction in an existing species.

No honest informed person would define species in this manner.
This is a better analogy

So the key here is that a mutation that contributes to the evolution of a new species doesn't make the recipient of the mutation reproductively incompatible with it's immediate ancestors, but it may make the recipient reproductively incompatible with its ancestors farther up the line due to the cumulative effect of this and previous mutations of ancestors in-between?

Yes.  But also, speciation is not about individuals mutating.  It is about populations changing.  The population, due to mutations, changes so much from the ancestral population that we label it a new species.

When I saw your answer, with this ugly text posted as an image, I was getting ready to complain! Of course, then I read the answer. The analogy is good and simple enough. +1

@Jonah you are still confused about the difference between a definition and reality. There are many different definitions of "species"; you've chosen one of the dozens and are upset because it doesn't cover everything in biology. You're debating semantics that have little to do with science.

@Jonah For more information about the difficulties of the concept of species, you can have a look at this post.

@iayork I'm not upset about anything, I was just asking an honest question. I understand now that a species is not soley defined by reproductive compatibility. Really I already new that it's possible for two different species to have fertile offspring (e.g. Homo sapiens), I just gave an oversimplified definition as a postulate I guess. The confusion I had is more about what makes certain individuals reproductively compatible. My assumption that determining which two animals can reproduce with each other can be done with some hard-and-fast rules like chromosome count is wrong ...

I thought a single mutation would have to "make the jump" between reproductively incompatible groups of animals. Really my question should of asked how any two animals can be rep. comp. if mutating into a new species would always ensure 0 compatible mates. I understand now that reproductive boundaries are not so clear


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How do we see and/or detect neurons?
I'm curious as to how we "see" neurons, for lack of a better term. Is it the detection of the neuro-transmitters? Can we literally see the electricity firing and moving throughout the pathways? Is it a combination of both, or something completely different, like scanners?
What kind of technology is used to do these things?
thank you!

Google is a good technology to find answers to these questions. Did you try it? Please try doing some looking up from your side before posting a question. Questions with no effort from the asker are usually not very useful to anyone (unless the question itself is quite good). Plus, your question is broad. If you are interested in these topics then you can check out the first few chapters of Principles of Neural Science by Eric Kandel et al.

Currently, the big thing in Neuroscience is imaging in vivo Calcium release which correlates with neuron action potentials, seen here. Each white speck is a neuron, the black lines and circles are blood vessels. Using this method you can visualize distribution and activity of neurons in real time.


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What molecules does amylase enzyme work on?
I know that in the human body cellulose cannot be broken down by enzymes; however, I am confused as to which molecules amylase enzymes during fermentation.
I also looked at https://en.wikipedia.org/wiki/Amylase where it says that "All amylases are glycoside hydrolases and act on α-1,4-glycosidic bonds." so now I am confused.
Does amylase work to break down starch into glucose exclusively?
If not...
Does amylase enzyme break down corn cob extract which contains xylans, cellulose, lignin and some sugar for fermentation?
Does amylase enzyme break down corn stem which contains cellulose, hemicellulose and lignin for fermentation?

Your incomprehension is due to the fact that both starch and cellulose are polysaccharides.
As it is said in the wiki page. Amylase is active only on alpha linkage like starch or glycogen. If you want to break beta linkage like in cellulose you need a cellulase enzyme, which humans do not have.


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Do "real" human samples tend to return fewer protein identifications in Proteomics experiments?
I'm working with bottom-up (shotgun) mass spectrometry-based proteomics and have encountered an issue. If I do a run with a HeLa digest standard, the resulting data returns many protein IDs. When I do the same experiment with cultured human cells (TCells specifically), the number of IDs drops dramatically.
We've been racking our brains trying to determine why, and it doesn't seem to be an issue with the data itself. It's as if the database search can't find sequences that fit the data.
My boss also encountered a similar issue when dealing with a previous project; the system worked well on murine samples, but there was a huge drop off in IDs when looking at human cells (with a human database, not murine of course!)
Is there some kind of known issue when looking at human cells from patients/in vitro samples? Is there a high proportion of point mutations/non-canonical sequences that upset database searches?

What is the actual difference in protein IDs? 10%, 20%, 70%?  Assuming the same starting material amount was used on the same column on a clean instrument, there could be a number of reasons from alkylation/digestion differences to protein abundance differences (e.g. presence of high abundance ECM proteins) to the database used (e.g. Uniprot with or without isoforms).


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Is it safe to use an egg incubator to grow bacterial cultures?
I've been using a small egg incubator to grow environmental bacteria in petri dishes. I always wear gloves and glasses when I handle the plates and do Gram staining. How likely is it that bacteria grown on dish could become airborne when I open the incubator or the dishes themselves?

the type of egg incubator would be important that is a vast variety which produce very different risks.

if you keep the petri dishes covered there will be little or no contamination and there will be negligible e coli aerosol when you open the incubator. as mentioned by @MartinKivana don't open the plates, esp near the incubator.  In a sterile environment is better...
if you don't keep the petri dishes covered your experiment will be ruined.
you can wipe it down with bleach once in a while...
so that about covers it.


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Twins reproducing with each other ( just hypothetical)
If 2 twins (look exactly the same and also the genes which control their morphology, behaviour etc. are same and present at the same locus) produce an offspring , will their offspring be exact copy of their parents ?
Sorry . I know its not moral.

Aside from the fact that identical twins have the same gender and thus cannot reproduce, even if we ignored that issue the offspring would not necessarily be identical to their parents, because people are diploid (have two copies of each gene) and meiosis shuffles genes up somewhat. So for example if the twins are heterozygous for a gene (their two copies are different), with one copy being allele A and the other b, their offspring could be Ab (like their parents), or AA or bb (unlike their parents).
If the twins are monozygous for every gene then their children would indeed be genetically identical to their parents, stray mutations aside. That's what happens with some laboratory animals, that are inbred to the point they are pretty much all genetically identical, and they are monozygous for almost everything.

...and inbred individuals may suffer from inbreeding depression. There are several potential reasons for such inbreeding depression including the fact that deleterious alleles tend to be slightly recessive (see Evolution of dominance of alleles)

Monozygotic twins won't be able to reproduce (naturally), because they are of the same sex. Dizygotic twins may or may not be of the same sex, just as regular siblings; genetically speaking, they are just siblings, not twins, so this case is out of the scope of your question.

@SaraswatiSharma If you consider this answer answered your question, you can click on the checkmark next to the answer to mark the post as being answered.


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What's the lowest possible reaction time for the human brain?
I could not find an answer for this question out there so I thought it would be proper to ask it here.
Since our reaction time can be increased or decreased by ingesting certain drugs, I could not help but wonder: What would be limit for speed reaction and why is there such limit?
Furthermore, have we been able to quantify the delay between an event "actually" happening and our eyes seeing it and sending the corresponding signal to the brain?

It can probably be measured as eye perception to finger response speed, in tests... the lowest sober values are arond 70ms for very fast humans (computer games) top sportspeopke etc. and about 250ms average, you can certainly go beyond 1 second for very drunk, and those who are approaching an unconscious state, it may take several seconds.

That is not easy to answer because it can be difficult to agree on what is meant by "reaction time" of the brain.  If you're thinking of the time between receiving a stimulus (e.g. a flash of light) and a major physical response (e.g., stepping on the brakes), the time really depends on the length of the signal chain from the retina of your eye to the activation of your leg muscles. That tends to be around 0.275 second.
To quote from Sourakov (2009):

The fastest tactile reflex time belongs to the star-nosed mole, Condylura cristata L., which uses 22 nasal appendages to navigate through soil and can react in just 120 ms, when one of these appendages comes in contact with food (Catania & Remple 2004). Here, I would like to report the startle reflex time in skipper butterflies, which is among the fastest recorded for the animal kingdom and which is at least twice as fast as startle eye-blink reflex of humans.
Startle reflexes have evolved as fast defensive (usually escape) responses in animals, engaging subcortical reflex mechanism that bypasses cerebral processing and voluntary movement. Because circuits involved are shorter, the latencies of the startle reactions are much shorter than those of voluntary reactions. In terms of electromyographic responses recorded in vitro, acoustic startle reflexes tend to be very short. In rats, for example, electromyographic responses can be as fast as 5–10 ms, and in humans as fast as 14 ms (Yeomans & Frankland 1995).

So the method of measuring reaction time has a strong influence on results, because it can amount to measuring reaction at different points in the signal chain.
Finally, it has been shown that task complexity, level of mental arousal, and conditioning can all affect reaction times. One hypothesis is that those influences can change the effective length of the signal chain going from stimulus to response. Drugs can affect any of several factors that contribute to the length of the signal path and the speed at which a signal propagates along the signal path.

Can you provide a source for That tends to be around 0.275 second.?

@vkehayas, Sure: [www.humanbenchmark.com] is a good source.  Different sources vary from about 215 ms to 285 ms.

S.McGrew you probably meant to tag @problemofficer


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Is this a real dinosaur species?
I recently got  and would like to know if this is a real species. It doesn’t look quite like a Styracosaurus, but is close. Can someone identify?

I'm pretty sure that's an Achelousaurus.
Two curved horns on top, plus hump on nose:
Front view:

Side view: (for nose)


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How can diving with 100% oxygen not destroy your lungs?
It is possible this should be moved to physics, depending on the nature of the answer (i.e. if the reason is physical). But I suspect the explanation is biological, so I posted it here.
Sometimes technical divers dive with 100% oxygen. I don't understand how can this not burn, oxidize or at least damage their lungs. To begin with, even if someone would breath 100% oxygen in atmospheric pressure, I'd suppose he'd damage his lungs, because the 79% of the volume that would normally be filled with inert nitrogen is now filled with oxidizing oxygen.
If, however, someone dives to, say, 30 meters, with pure oxygen, he'd have to fill his lungs with oxygen at 4 atmospheres to equalize the pressures. That means the pure oxygen filling his lungs is even more concentrated. How can this be? A friend of mine who dived with pure oxygen even says the breathing feels just normal. How is this possible? How are the lungs not damaged?

I think you might be misinformed about the gases that divers use. https://chemistry.stackexchange.com/questions/61406/why-would-breathing-pure-oxygen-be-a-bad-idea No one is really breathing 100% oxygen at depth, they are at most using a 100% oxygen supply. And yeah, the answers here aren't really based on biology. Maybe physics/chemistry, but you are probably going to get a better answer at a more specialized source for that particular niche of diving.

From what I recall, nitrox is at max 40% oxygen. Do people really dive with 100% oxygen? Can you please give a link that support this claim? Do they breath from it directly or do they use these tanks in a rebreather system?

@Remi.b It's a rebreather. They are recycling the nitrogen/other gases, scrubbing the CO2, and replacing the metabolic O2 from a 100% O2 tank to reduce mass.

I am VTC because I think the question is based upon OP's misunderstanding of diving equipment. Outdoor.SE might be of help to you to improve your understanding of diving equipment.


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Can predator-prey relationship be an example of negative feedback?
Predators eat their prey, prey population decreases. This results in the predator population to decrease, so less prey are consumed which causes the prey population to increase.
Therefore, if the reduction in prey population results in its increase then can this be described as negative feedback?

Somewhat related: What prevents predator overpopulation?

Yes, in the fields population dynamics/ecology, the standard predator-prey system is routinely described in terms of a negative feedback loop. See e.g. Lewontin & Levins, 2007 for an online exemple (the term is commonly found in articles and textbooks though).

From my experience, "negative feedback" is more often used in the context of processes in the body which attenuate themselves or in the context of stimuli and sensors. However predator-prey dynamics could fit the general definition of the term. In general, negative feedback is just when a process or output of a system leads back into the system to attenuate itself.

Negative Feedback:
"A feedback in which the system responds in an opposite direction to the perturbation. "
Source: biology-online.org, access date: 2018-04-06.

In a general case of a closed-loop (feedback) control system, you've got a stimulus that gets sensed by a sensor, which sends a signal to a controller. The signal is then passed on to an effector, which can change the original stimulus. In the case of negative feedback, the stimulus is attenuated. In positive feedback, it is potentiated.
$$\begin{array}{ccc}
\fbox{Stimulus}&\rightarrow&\fbox{Sensor}
\\
\uparrow&&\downarrow
\\
\fbox{Effector}&\leftarrow&\fbox{Controller}
\end{array}$$
A common example of this would be high body temperature being detected by neurons, which send a signal to the brain to cause the body to sweat more. In this case, the sweat glands are the effectors and can lower the body temperature.
$$\begin{array}{ccc}
\fbox{Change in body temp.}&\rightarrow&\fbox{Neurons}
\\
\uparrow&&\downarrow
\\
\fbox{Sweat Glands}&\leftarrow&\fbox{Brain}
\end{array}$$
In your case, I think you could describe it with an increase of prey population being the stimulus, which is detected by the predators as they see more prey. The predators would then choose to eat the prey (I suppose this could be the controller) and then act as the effector by eating the prey (and thus, reducing the prey population). Though I'm a little iffy on this since you'd have the predator acting as both the sensor, controller and the effector. Conversely, if the prey population were lowered, the opposite would be true.
$$\begin{array}{ccc}
\fbox{Change in prey pop.}&\rightarrow&\fbox{Predators sense prey}
\\
\uparrow&&\downarrow
\\
\fbox{Predators eat prey}&\leftarrow&\fbox{Predators choose to eat prey}
\end{array}$$


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Where do the protons in the mitochondrial intermembrane space originally come from?
I'm currently reviewing this concept in cellular respiration. The book which I'm using is Reece, Minorsky, Campbell's Biology and while it does a good job at explaining the process involved in the electron chain transport. I think it lacks of clearing out my doubts concerning initial protons.
Let me explain, the part where I'm stuck at is, where do originally the protons in the mitochondrial intermembrane space come from?. I understand that there is a proton gradient and the translocation of this protons in the proton pump is key during the electron shuttle process but, how did those initial protons come?. In other words, during the formation of the mitochondria in the cell, have they always been there? or are they part of some bigger molecule and that those protons are detached from them so that there is an initial gradient that triggers the process for the first time?. In other words, how does that initial spark or kick off begins?.
In most animations I've found, the explanations take for granted that the protons are freely moving in the intermembrane space such as here and also here but what do those videos lack is the explanation of how (as mentioned above) do those protons got there in the first place.
I'd like somebody could help me to clear out this doubt. I feel that as an addition to the answer, I'd like to know how does the mitochondria forms in the cell?. Since I believe there might be steps involved, I'd appreciate that the answer could explain those steps so I could easily understand, because as mentioned. I'm still confused on that part as well.

Well, proton gradient is set up by using protons of NADH2 and FADH2.Their proton is transported to the intermembrane space leaving behind NAD+ of FAD in matrix. Did I get your question correctly. You have asked about the source of protons I.e. which energy molecules provides them, haven't you?Also, the protons transported from NADH2 and FADH2 are more than what is coming out of F0-F1 particle so there is an excess of proton in intermembrane space.

@Abner Alfred Thompson Let me explain, I can understand that there might be protons due to water content in the cytosol from which during the formation of the organelles happens I believe in mitosis. But how does exactly there is an excess of protons so that a gradient is initially established in the intermembrane space?. I had believed that it was due to any terminal hydrogen from a peptide, aminoacid of protein contained in the intermembrane space and that when this gradient is held initially the process of electron chain can commence and go on in a cycle.

@Abner Alfred Thompson As I mentioned every explanation takes for granted that initially there is a surplus of protons taking this intermembrane space as a pool of protons. But as I mentioned before, where do they come from?. Is it due water, any peptide, protein, aminoacid initially present in the intermembrane space?. You mentioned that the transported protons from NADH2 and FADH2 are more than what comes out from F0-F1 particle, but again this is when the cycle is happening. But what it was that initial surplus source?. This is my question?. Can you help me to clear out this doubt?.

You can understand this if you consider the entire events of oxidative phosphorylation and electron transport chain.The amount of H+ from NADH2 and FADH2 going in is way more than what's coming out.This is what's the cause of proton gradient.You can see this video on YouTube to get your doubts clarified : https://youtu.be/wX7J2JtxM08 .Also,there is a minor error in this which is pinned in the comments section but it won't affect your understanding.Hope this helps

@Abner Alfred Thompson I understood the part that the amount of protons going in to be more than what is coming out but my question was more aimed at the ab-initio aspect. something more like Big Bang thing. I hope this makes clear my question. Probably this part isn't necessarily critical to understanding the process. But I felt that it is my general doubt. Come to think of it, if you put a sugar in a solution, you know there will be more oxigen due to its presence in the molecule, plus what it was in the water and probably from the air in the surroundings dissolved in that water.

@Abner Alfred Thompson In other words, is it possible to pin point when the process exactly begins?, i mean when the cycle isn't possible?. Maybe the precise moment when the first APT synthaze in the intermembrane space is created?.