text:
What causes us to see white light?
Humans have three cones of color light, red, green and blue. If the region of the green cone is hit by his photons we will see green light. Now we don't really receive green light but our eyes and brains are 'making' it to look green. But if all the different cones are hit by their photons we will see white. Now the question is why is that white? Why isn't our brain just keeping these different colors, is this a kind of black out of our brain or an overwhelming of input making us blind etc?

Our brain doesn't really use cones to detect green light, and detect red light, and detect blue light. Each cone can be excited by many wavelengths; they're just most excited by green, red and blue wavelengths respectively. The brain then uses the different information it receives from all three cones to infer the wavelengths of the light it receives. It doesn't look at the absolute excitation of a cone so much as the relative amounts of excitation different cones get.
So for example, if the brain sees the green cones are very excited and neither the red or blue cones are, the light is green. If the green cones and red cones are equally excited but the blue ones aren't, then the wavelength may correspond to yellow (a wavelength that excites both red and green cones in the same middling way, and blue cones not much at all), or there could be a combination of green and red wavelengths; and in fact both are seen as the same thing by the brain. That's why colors can combine to make other colors.
This is OK insofar as the point isn't to calculate the exact wavelength of incoming light, but to tell the difference between certain wavelength compositions because that provides more information about the world.
So the reason we see white when hit with all wavelengths is the same reason we see any color when hit with any combination of wavelengths.
As for why "color" feels like a single unified perception and not a combination of three numbers, that's a general aspect of perception in general. We don't sense the raw data our brain gathers; we sense how the world is (as guessed at by the brain from the raw data it gathered).
As such, the colors we see aren't even strictly determined by the wavelengths of photons hitting the cones; because colors are a proxy for what the things we see are like, the brain will not only look at the light it receives, but also use its own assumptions about the world (is this thing in shadow, in bright light, mottled light, colored light, near, far...) to guess at what the color "really" is given the wavelengths it has received. This gives us a sense that color is inherent to objects and doesn't depend on lighting conditions, which is generally accurate (an apple's redness is a feature of the chemicals at the surface of its skin, and those don't change with the lighting conditions).
That's where illusions like that of the blue-black or white-gold dress come from: sometimes you get ambiguous stimuli, where the wavelengths hitting the eye could correspond to a black and blue dress in bright light, or they could correspond to a white and gold dress in shadow, and in that case the brain picks one, and you see the dress as the color your brain decided it must be. Except because the stimuli were ambiguous, different brains (or the same brain at different times) will make different guesses, resulting in very different perceptions. But the guessing is actually what happens all the time, it's just that usually the stimuli aren't as ambiguous so all brains agree on their guess, and the guess does correspond to reality, and so the illusion that we perceive the world directly with no filter remains unbroken.


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Shell-less Chick development - Incorporation of Calcium carbonate instead of Calcium lactate pentahydrate powder?
I'm a college undergrad biology student and currently studying developmental biology as part of my curriculum.
I've read a research journal titled, A Novel Shell-less culture system for chick embryo using a plastic film as culture vessels. by Yutakah Tahara and Katsuya Obara, and happened to be interested with this method but stumbled with a question that kept bugging me out of pure curiosity. While reading their journal I encountered a statement
"...250-300mg calcium lactate pentahydrate powder (Showa Chemical Co., Tokyo, Japan) was added to the culture vessels." and they also added distilled water.
The proponents seem to use Calcium lactate pentahydrate as a substitute for the chick's source of calcium. In dev bio class, I've learned that the chick embryo has two main sources of calcium - the yolk and the egg shell. The egg shell contains 94% Calcium carbonate (literally a major source of calcium). I've read that the Chorioallantoic membrane (CAM) is responsible for the mobilization or transport of calcium from egg shell to the chick's circulation -https://www.ncbi.nlm.nih.gov/pubmed/2955074 - and here is where my question starts:
I understand that the proponents used Calcium lactate pentahydrate powder because its soluble in water - making it easier for the chick to incorporate the dissolved  Calcium lactate. I also understand that Calcium carbonate is insoluble in water BUT If CAM is responsible for the mobilization of calcium from egg shell to the chick's circulation to form the skeletal structure of the bird, what difference does it make if I use sterilized powdered egg shells as the chick's 2nd major source of Calcium carbonate?
Thank you for taking the time to read and trying to answer my question! It means a lot

I don't know if it helps, but calcium carbonate is not insoluble in water. It doesn't dissolve very well, but insoluble is something different.

source: Stack Exchange

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

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Could there be latent infections in the human population that we don't know of?
Herpes simplex 1 virus and toxoplasmosis are common infections that that many of use have (65% and 10% of americans, respectively). Both of these are chronic, latent infections that can occasionally cause problems (i.e. in HIV patients) but most of the time don't.
Could there by many other such common, latent infections in the human population that we don't know of? Do we have any idea of how many there would be?

Given the right (or wrong, depending on the perspective) circumstances, even your body's own microbiome can turn against you - a human body cultivates thousands of bacterial colonies that, if something disturbs their balance (e.g. antibiotics), can cause severe metabolic disturbances

@Sty: The micro-biome normally doesn't infect people, i.e. it's technically "outside" of the body.

@KevinKostlan From wikipedia Gastroenteritis, also known as infectious diarrhea, is inflammation of the gastrointestinal tract [..] Gastroenteritis can be due to infections by viruses, bacteria, parasites, and fungus.

@Remi: Key word "normally". Gastroenteritis seems to be a more "typical" infectious disease, which represents pathological conditions (unless most people who are actually "infected" show minimal symptoms and "don't" have the disease, where "infection" means infiltration into tissue).

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


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Serial dilutions
A student wants to make serial dilution of a sample. She starts with a 1mg/ml sample and 10 tubes, (labelled 1-10) each containing 2 ml buffer.
The student puts 1ml of sample solution into tube 1
Repeating the process.
What is the concentration of the sample in tube 4?
Give your answer to 2 decimal places and in µg/ml
I've started this question and I assume I would do 1/2^4 which would give me 0.0625
But i'm stuck if this is right?

I think 1/3^4 is the right factor which gives 12.3 microgm/ml
step #1 consists in adding 1ml of the sample to 2 ml of buffer in tube #1
which then contains 1mg in 1+2=3 ml's i.e  has concentration 1/3 mg/ml.Repeating we get 1/3^2  in tube #2 and  ...1/3^k in the kth tube.
for k=4 we get 1/81 mg/ml=1000/81 microgram/ml
As @xusr remarked this line of reasoning is a good first order approximation based on the additivity of volumes.If one needs a more exact answer in general
e.g for mixtures of organic and aqueous buffers etc one must consider the partial molar volumes of the components involved which will be be dependent both on their chemical nature and the thermodynamic state parameters of the
experiment leading to nonadditivity of the volumes mixed or in worst case to
phase separations(i.e solute is present only in one portion of the resultant
solution)

I think you are correct, could you please show your work for the serial dilutions. I think it would be beneficial for @user135629 to have your work shown

OK @xusr.Of cource if  one wants to be very exact one has to consider the

@xusr.I have discussed the matter completely in principle by adding to my answer what has to be considered in general when the first approximation I


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What is the difference between tissue engineering and 3D bioprinting?
3D bioprinting is the modified version of the tissue engineering but when we want to describe the both terms, what are the basic criteria or points to make difference between these?

Tissue engineering is research into ways of organizing cells and cell droplet/matrix structures into a useful form, usually for medical applications. In the near future, tissue engineering could refer to rewriting or genetically modifying cells for a new purpose or to enhance their existing function. Even more into the future and tissue engineering could mean custom-building multi-cell structures from scratch on a computer.
3D bioprinting is the practical or laboratory deployment of the first technology mentioned above - a subset of tissue engineering.
In a nutshell:
Tissue engineering = "Come up with a creative way to arrange these cells and cell structures into something useful".
3D bioprinting = "Use the above-mentioned technology to build part of a synthetic organ".


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Is there any evidence of blue jays preying on other birds?
Are blue jays known to prey on other birds?  I've found that they are known to raid nests of eggs and young, but have not found any evidence of them actually preying on other birds.
Background:  A few years ago while raking leaves this time of year (late Oct/early Nov) the head of a house sparrow fell on me.  I looked around in the spruce tree I was under and saw a blue jay eating the rest of the house sparrow.  This was approximately 10 feet from my bird feeders.  I can't say that it wasn't dead beforehand, but it's proximity to the feeders made me wonder.

I know European Jays kill sparrows if they have an opportunity. So do crows. This is titled blue-jay but it's different than american blue jay. https://www.youtube.com/watch?v=VmeUcIxLTwk

@com.prehens.ible.  Thanks for the link.  It is pretty much exactly what I witnessed - including the decapitation.  Unfortunately it starts when it already has the other bird so we don't know if it was scavenged or actively caught.

Yes! This article gives an account of a Blue Jay killing and consuming a Cedar Waxwing, and further it clearly states that at times Blue Jays do predate on fledgling and adult birds, and gives a hefty amount of sources to back that up, if you're in the mood for further reading.

WOW.  Exactly what I was looking for.


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Distribution of the number of synapses per neuron
There is a mean number of synapses per neuron in the human brain which is not very well known, but is of order 10,000. (Some say, it's about 6,000, other say it's about 50,000.)

What is known about the distribution of the number of synapses - in a
  very rough sense?

The number is most certainly not distributed normally around one mean value of about 10,000 (because there are very different types of neurons).
More probable, there are some types of neurons with typical mean numbers of synapses (each distributed normally), which would give a distribution like this:

For the sake of simplicity I want to ask:

If we were to group numbers of synapses roughly into bins of powers of
  ten, how high would be the peaks, roughly?

You are correct, depending on the neuronal cell type or location in the brain (cerebellum versus a cortical layer for instance), the number of synapses will differ. I don't know if this has been systematically studied, cell type by cell type, region by region, so that the statistics you are looking for would be available... I imagine that work will be painstaking and difficult (particularly with the human brain) but the connectome project is making huge strides and is the likely source in the future for such information.

@LouisLeung: Do you accidently know a specific resource inside the connectome project which points into this direction?

The exquisite serial EM reconstruction of neurons with identifiable (and thus quantifiable) synapses has been demonstrated here: http://www.conte.harvard.edu/connectomics/. This paper at: https://www.ncbi.nlm.nih.gov/pubmed/26232230 has some synaptic statistics though it is volume- and not cell-specific which I believe is what you are after.


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Why glycosylation of a protein increases its non-specific binding properties?
This doubt arose while reading this website: https://www.thermofisher.com/cn/en/home/life-science/protein-biology/protein-biology-learning-center/protein-biology-resource-library/pierce-protein-methods/avidin-biotin-complex-method-ihc-detection.html

I think it has something to do with lectins binding to the glycosylated moiety.


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What are those patterns found on the surface of wooden furniture? Are those growth rings of trees?
This image can give a suitable example for the above question.

Which pattern the long lines are the separations between the individual boards.

*or; The streaks present on the top face of the table.

that is what I was talking about.

Just checking: you mean wood grain? As seen in https://commons.wikimedia.org/wiki/Category:Wood_grain#/media/File:16_wood_samples.jpg? (This shows a 4x4 grid of wood samples, each one shows a different wood grain pattern.)

Thees cut on any angle will reveal growth patterns; not all wood grows exactly the same. Some kinds grow straight and have a very even grain, at the other end is the "black gum", the grain of which seems to follow no organized pattern (it's almost impossible to split.)
Without a close up, it's hard to say exactly what's going on with your table.
Some woods, because of their grain and even density, take up stain very evenly and uniformly. An example would be oak. Some woods take up stain more irregularly, an example being maple.
Your table, though (all this is speculation since there's not a close up or head on view) looks like an example of blotchy stain uptake.
This is an example of blothcy staining wood:

If you look carefully at the grain, you can see that's not the only cause of uneven uptake. Some blotchiness is due to not sanding the table down finely enough. Some is due to the uneven density of the wood. See that diagonal scratch? It takes up color regardless of the grain. As do the ends of the boards.
Your table is made up of younger trees (you could see growth rings on the edge) which will give you more uneven uptake, plus it's a blotchy job. So, the answer is yes and no. Or, a qualified yes.


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What might a supposed “tree enzyme” be — injected into a Morton Bay Fig tree?
I was recently visiting Fremantle in Western Australia and noticed a large Morton Bay Fig tree in Kings square in the centre. Apparently the health of this tree had been declining, but they hope that recent treatment will lead to an improvement.
The notice by the tree said this was by “injection of a tree enzyme”. I also found the following quote on the City of Fremantle FB page:

To improve the tree’s absorption of nutrients which will help it grow stronger, the bioscientist has given it a ‘booster’ enzyme injection. This enzyme naturally occurs in trees and is an additional boost that will hopefully help the fig tree recover and flourish again this spring.

Well trees have enzymes like any other living thing, but I find it difficult to imagine what enzyme injected into a tree would get transported through its system and help it heal. Is there anyone in silviculture (or WA) who has any idea what this was?

Interesting question. Here is the sign, if anyone’s interested.

So eventually I decided to email the City of Fremantle, who put me in contact with their Parks Department, who gave me the name of the company who had handled the tree, who replied with a most informative letter.
And the answer is…

Glutathione

Most animal biochemists, like me, will be more familiar with the importance of glutathione (reducing sulphydryl group highlighted in yellow, above) as a reducing agent in erythrocytes, the constituents of which are subject to oxidation damage.
What was wrong with the tree?

“…the figs in Kings Square… had quite elevated levels of heavy metals Cd, Cr, and metalloids Hg and As.
We traced this back to the colonial past, where in the 1830s – 1840s, when gold had been discovered south east of Fremantle, a battery operated (by the Crown) in Fremantle. In those days, gold was commonly lixiviated using mercury. Kings Square had a pit cut earlier for mining limestone. A good place to dispose of battery mullock is a pit.The earliest gold deposits were mafic ores, so often contained Cd and Cr.”

Why use glutathione to treat the trees?

“Firstly, it stimulates the jasmonate pathway, thereby alters transpiration and root growth.
Secondly, it assists in the isolation and immobilisation of heavy metals.
Thirdly, if assists in the breakdown of triazine herbicides by ring cleavage…”

And my correspondent kindly provided a review by Hossain et al. in the Journal of Botany, which elaborates on the second point.
And why the “tree enzyme” business?
This did not come from the company that handled the treatment, but from someone (unknown or nameless) who was handling the public relations, and who wished to provide reassurance that the treatment was ‘natural’:

“I guess in the world of snake oil, “enzymes” are benign, natural things, rather than usually ephemeral catalytic proteins.”

I admit that, depending on a personal letter, the answer does not totally conform to the criteria of testability. (I did not think it appropriate to name my correspondent.) However the background details and the literature reference do provide strong support. In any case, as there had been some interest in the question, I thought I should do some work myself and then post an answer.

Interesting answer.


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Is it possible to use virus for genetic modification of embryos during the fetus stage
I know this probably sounds rather hypothetical and not very feasible but I would very like an answer telling why it is possible or not possible and why.
With the advancement of crispr and other dna technologies, I have been wondering whether it is possible for us to use a virus, which would easily pass through the gaps of the placenta and infect the developing fetus to alter its genomic materials for the creation of designer babies. Since Zika can alter the genome of a baby to cause deformities, is something opposite also possible, like using a similar virus to develop favourable genes in a fetus.
Also, what are the chances of the virus actually purposely acting under orders of genetic engineering to intentionally deliver the genes through transduction?
Putting all ethical and moral issues aside is such a principle feasible and if no, why not?

Zika doesn't alter the host genome at all.

Since Zika can alter the genome of a baby to cause deformities

Zika virus is incapable of altering the host genome. The exact mechanism by which Zika virus infection causes microcephaly is still unclear, but basically it depletes the neural stem cells at a point when the brain is developing, meaning brain development is more limited (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5516183/).
Some viruses do alter the host genome and are candidate technologies for gene therapy
Retroviruses are RNA viruses that copy their genetic material into DNA which is then integrated into a host genome. As such, and as you note, this can potentially be exploited to deliver new genetic material into an organism's genome. I'm not sure what you meant by transduction above, but the term is 'retroviral vector-mediated gene delivery'.
Retroviruses have been trialled for gene therapy for decades. See this sad report on a 2002 trial that apparently succeeded but had unexpected side effects here. However, CRISPR is probably an easier method to use.
You wouldn't attempt to modify a fetus
Some terminology here: a fetus is what an embryo grows into; it's getting bigger and more complex. And as illustrated by Zika-related microcephaly, any messing about with fetal development can have nasty side effects. There are also more cells to modify and you're likely to end up with a 'mosaic' where some cells are genetically different to others within the same organism. If you're attempting to modify the somatic cells of one organ, you might as well do it after the baby is born; if you're attempting to modify every cell in a human (including germ line cells) you'd do it to an egg or embryo.
This study describes a successful attempt to modify embryos using CRISPR. They saw only 1 mosaic in 58 embryos.

First of all, disclaimer: We do not know the effects of every gene in the human genome. The human genome has only 1.2% of its genes that actually seem to be useful. However, the 98.8% of "junk" DNA may have uses that we don't know about. Also, many genes, such as sickle cell anemia, carry unknown benefits, such as offering resistance to malaria. Now, to answer your question...
Viruses
Viruses are probably some of the coolest things on the planet. They infect other organisms, which is a hard task to accomplish. According to Khan Academy they use two cycles.

The lytic cycle: The phage infects a bacterium, hijacks the bacterium to make lots of phages, and then kills the cell by making it explode (lyse).
The lysogenic cycle: The phage infects a bacterium and inserts its DNA into the bacterial chromosome, allowing the phage DNA (now called a prophage) to be copied and passed on along with the cell's own DNA.

Some viruses only use one type of cycle, the lytic cycle. However, you could use a virus with the lysogenic cycle to insert DNA into the target embryo, which could potentially accomplish your goal.


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How do you differenciate between the eukaryotes and prokaryotes?
I wonder how we differentiate between the eukaryotes and prokaryotes.
Eukaryotes:

Eukaryotes (also spelled "eucaryotes") comprise animals, plants, and
   fungi—which are mostly multicellular - as well as various other groups
  that are collectively classified as protists (many of which are
  unicellular).

Prokaryotes:

Prokaryote (also spelled procaryote) comprise any organism that lacks a
  distinct nucleus and other organelles due to the absence of internal membranes. Bacteria are among the best-known prokaryotic organisms.
  The lack of internal membranes in prokaryotes distinguishes them from
  eukaryotes.

Isn't there any other method to know what organisms are eukaryote or prokaryote?

There are lots of ways to distinguish between eukaryotes and prokaryotes, as listed by microbiologynotes.com:
Difference:             Eukaryotes:                Prokaryotes:
-------------------------------------------------------------------------------
Size                    > 5µm                      1-2µm by 1-4µm
Nucleus                 Nucleus with nuclear       No true nucleus; nucleoid
                         membrane
Complexity              Usually multicellular      Unicellular
Chromosome              Multiple linear; histones  Usually single circular;
                                                    no histones
Cell Division           Mitosis, meiosis           Binary fission
Reproduction            Involves meiosis           No meiosis
Zygote                  Diploid                    Merozygotic
Genes                   Expressed individually     Operons
Gas vacuoles            No                         Possible
Mesosome                Yes                        No
Ribosome                Found on membranes         Distributed in cytoplasm
Mitochondria            Usually present            No
Chloroplast             Possible                   No
Cell wall               Simple if present          Freq. present, complex
Endoplasmic Reticulum   Possible                   No
Golgi apparatus         Possible                   No
DNA usage               Transcription in nucleus,  Transcription at the same
                         translation in cytoplasm   time as translation
Duration of cell cycle  Usually long (hours)       Usually short (<1 hour)

N.B.: I have used the list on microbiolgynotes only as an outline, editing as needed.  For instance, Mitochondria is not necessarily present in eukaryotes, neither are chloroplasts.  Also, I have not included everything, since I do not presently have the time to verify everything.

I would like to add several comments. "Mitochondria is not necessarily present in eukaryotes" – this is not entirely true, even those eukaryotes that lack complete mitochondria still posses the remnants. "Ribosomes: Distributed in cytoplasm" – there are several notable exceptions (most notably Gemmata sp. ). "No true nucleus" – again, some members of the PVC group (Gemmata being the most studied of these), enclose the DNA in a membrane-bound compartment. "Genes: Expressed individually/Operons" – some eukaryotes have operons and not all genes are organised in operons in bacteria.

"Cell Division: Binary fission" – a ton of exceptions, including mycelial division and eukaryote-like budding. "Duration of cell cycle: Usually short (<1 hour)" – this is only true for some copiotrophs. "no histones" – some Archaea have true histones.


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ATP stoichiometry of the Na+/K+ pump
The Na+/K+ ATPase pump exports 3 Na+ for every 2 Ka+ imported. This process is ATP dependent, but I have not been able to find how many ATPs are required in each translocation. What is the stoichiometric ATP cost of this reaction?

Sodium/potassium-exchanging ATPase (EC 3.6.3.9):

An enzyme from the plasma membrane of animal cells that catalyzes the efflux of three Na(+) and influx of two K(+) per ATP hydrolyzed.

You can read about the mechanism on Wikipedia:

The pump, after binding ATP, binds 3 intracellular Na+
  ions.
ATP is hydrolyzed, leading to phosphorylation of the pump at a highly conserved aspartate residue and subsequent release of ADP.
A conformational change in the pump exposes the Na+
  ions to the outside. The phosphorylated form of the pump has a low affinity for Na+ ions, so they are released.
The pump binds 2 extracellular K+ ions. This causes the dephosphorylation of the pump, reverting it to its previous conformational state, transporting the K+
  ions into the cell.
The unphosphorylated form of the pump has a higher affinity for Na+
  ions than K+
  ions, so the two bound K+
  ions are released. ATP binds, and the process starts again.

So the stoichiometry is 3 Na+ exported, 2 K+ imported, 1 ATP hydrolyzed. Thanks.


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Can the Na+/K+ pump backwards to generate ATP?
The standard physiological direction of the Na+/K+ pump is to export 3 Na+, import 2 K+, and hydrolyze one ATP to ADP. Can it be driven backwards, importing 3 Na+, exporting 2 K+, and generating ATP? Does this happen in normal cells, and in what conditions?

related: https://biology.stackexchange.com/q/67418/561

All enzymes can theoretically catalyze the reverse reaction.
Researchers have driven the Na+/K+ ATPase to synthesize ATP with artificial ion concentrations:

We have studied the apparent affinity for K at its intracellular discharge sites by measuring the rate of ATP synthesis as a function of the internal K concentration in resealed red blood cell ghosts, where the Na-K pump is driven in reverse by the downhill efflux of K and influx of Na…

But does it happen physiologically, or for cells in culture?

@becko Oh sorry, I didn't see that part of your question. In the paper they drove the reaction with a very high ADP/ATP ratio which I expect wouldn't be found in cells. Technically it is possible for this reverse reaction to occur physiologically, but the ATPase activity will be dominant.

So it seems that the answer is No. I'll wait a bit more before accepting your answer. Thanks again.


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Definition of the different DNA regions
Reading from Oshima et al. (2016):

We identified 3,868 noncoding mutations including 394 located <5 Kb downstream, 1,762 intergenic, 1,621 intronic, 81 <5 Kb upstream, 7 UTR 3′, 2 UTR 5′, and 1 intragenic variants.

How upstream, downstream and intragenic variants are defined? Shouldn't intragenic variants be classified within intronic variants, and upstream/downstream within intergenic variants?
Edit: By adding the different numbers it seems they are mutual exclusive. While upstream/downstream variants can be defined as intergenic variants that lie close to genes, I haven't found a definition to tell the intragenic variants from the intronic ones.
Edit 2: The only explanation I could think of for intragenic variant is that it is located in a coding region which is not transcribed due to alternative splicing. Can it be possible?

Oshima, Koichi, et al. "Mutational landscape, clonal evolution patterns, and role of RAS mutations in relapsed acute lymphoblastic leukemia." Proceedings of the National Academy of Sciences (2016): 201608420.

You could try sending them a quick email.

We can take a look at the following picture (from wikipedia):

The regions are then:

intergenic: everything outside of the shown gene region
<5 Kb downstream: outside of the transcribed region, but possibly part of the promoter or an enhancer (yellow boxes before coding region).
UTR 5′: in the transcribed region, but not part of the coding region, as shown in the picture (blue box before coding region).
intronic: In the Introns, as shown in the picture (grey boxes)
intragenic: These have to be mutations inside the coding region (red boxes), which is confusing since the authors specifically describe them as 'non-coding' mutations. If you read that as 'mutations that don't change the protein sequence', these could be silent mutations
UTR 3′: in the transcribed region, but not part of the coding region, as shown in the picture (blue box after coding region)
<5 Kb upstream: outside of the transcribed region, but possibly part of an enhancer (yellow boxes after coding region)

Intragenic is not coding (as it's CDS and introns). Intragenic is region from TSS to TTS.

@SEwontLetMeDeleteProfile can you elaborate more on that? Also, what is a TTS?

The Sequence Ontology project defines an intragenic variant as "A variant that occurs within a gene but falls outside of all transcript features. This occurs when alternate transcripts of a gene do not share overlapping sequence." source
Intragenic means the variant is located within the same gene, which only implies that the sequence analysis assigned a certain variant to a gene. So, there is incomplete data regarding the gene product (such as different splice forms).

You can look up the mutation locations here:  http://grch37.ensembl.org/index.html


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Is tunneling of a proton in our DNA a cause of mutations?
Our DNA strands are tight together by hydrogen bonds. Can the proton of Hydrogen tunnel to the other complementary strand, and by this during the replication bind to a different/wrong nucleotide, causing a point mutation?

Perhaps of interest, though not specifically about complementary strand: Florian et al. 1996 (a highly cited paper) http://pubs.acs.org/doi/abs/10.1021/ja951983g

Keto-enol tautomerism involving proton transfer within a single DNA base can lead to mispairing and mutation during replication.  This is touched on in the previous citation provided by tsttst as well as this section from An Introduction to Genetic Analysis. 7th edition: https://www.ncbi.nlm.nih.gov/books/NBK21897/  I have not found a clear statement of whether the proton transfer is over sufficient distance to constitute "tunneling".


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bird identification by its singing
What bird is singing on background in this video?
https://www.youtube.com/watch?v=ckFIDeanJgg

First bird sounds at about 0:18

The bird singing at the beginning sec. 0:18 is a Nightingale (Luscinia megarhynchos). A recording with the same beginning is here http://www.xeno-canto.org/379628


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Why cells have a membrane potential?
What is the function of the membrane potential? Cells invest huge amounts of ATP to drive ion pumps to sustain this potential. Therefore it must have a very important function.
I read somewhere that the membrane potential acts as a battery, which can be used to energize other processes. But probably most of these processes could be energized with ATP just as well, which could be used directly instead of wasting it into building a potential first.
In muscle cells and nerve cells changes in the membrane potential are used to transmit information, so that is one use for it. But what about all the other cells?


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Philosophy of Science question permitted here?
Clarified my question re vernacular - science codependency, shortly after it was put on hold. Also, 'Philosophy of Science' IS a topic in biology stack exchange  Please explain why my post's still on hold?

Questions about what is and is not on-topic are off-topic on Biology.SE! There is meta.Biology.SE for that! I am voting to close.

From wikipedia: Philosophy of science is a sub-field of philosophy concerned with the foundations, methods, and implications of science. There are 150 questions tagged "philosophy of science" on Philosophy.SE. There are only 6 open questions tagged "philosophy of science" on Biology.SE and they really are not about philosophy of science!

Note however, that I doubt Philosophy.SE will accept your question in its current form as it feels quite unclear to me (as I explained on your other post). You should probably try to add links for every concept you refer to and make sure to define the words you're using. Good luck!

I'm voting to close this question as off-topic because this is not a question.

Did you consider posting the original question on Linguistics.SE?


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What kind of snake is this? Seen in Peru along the Inca Trail
I have been searching so much to find out what kind of snake this is. It looked black with white stripes. We found it on the Inca Trail to Machu Picchu in Peru. It was about 2500 m above sea level.

EDIT: Apparently M. medemi only exists in Colombia, not in Peru. Thus, as I'm not sure about the below ID. Instead of deleting the answer (users with <10k cannot see it), I just turned this into a community wiki, so I don't receive any RP.

By the shape of the head and the structure of the rings, it seems to me that this is a Micrurus.
Of course, the lack of yellow/red rings excludes the most common coral species, like Micrurus peruvianus. So, I'd guess this is a Micrurus medemi.
Here is another picture of it, for comparison:

Source: http://www.planetscott.com/speciesdetail/10840/coral-snake-micrurus-medemi
Some M. medemi specimens have white rings (like in your photo) while some have red rings.
They are venomous, but they are not dangerous: all Micrurus species I'm aware of are not aggressive, and bites are not common. As Wikipedia correctly says:

When confronted by humans, coral snakes will almost always attempt to flee, and bite only as a last resort.

The problem with this ID is that there are reports of M. medemi in Colombia and Ecuador, but not in Peru. I'll keep researching this and update this answer when I find a record (or delete it if I don't).

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Where do gut bacteria come from in different organisms
We know that some of the bacteria in our gut come from the food we eat and our environment. I want to know if there is evidence of bacteria being transferred from the mother to her fetus or from the mother to the eggs.
I'm currently working with insects that have plastic-eating bacteria in their gut. They are raised in isolated spaces so those bacteria would have to come from the bran they eat or from their mother. I'm a physics student interested in biophysics so my biology knowledge is still a work in progress. Thank you.

Human babies get coated in birth canal fluids and vaginal microbes as their first encounter with the microbial world, and they absorb 40% of gut microbes from milk.,,, Insects come from eggs and may have no contact with the parents, so you should say which insects you are working on.

For technical information on the subject, perhaps start with "vertical transmission insect symbionts" on google, which will lead to you to a variety of info's. Studies for symbionts of lice, fruit flies, mosquitos, termites, isopods, stinkbugs, butterflies and planthoppers.
Insect Symbiosis Vol 3 page 145 states:
Insects have been shown to use transovarian, egg smearing, and coprophagy, transmission, else entirely from the environment at every generation. There is a list of summaries of different insects that use different methods.
this also has masses of information:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2967712/
Samples for large insects are taken with tweezers, small insects can be dunked in alcohol and then microbes are extracted.
Microbia RNA can be checked for evidence if the symbionts come from the parents. You can probably figure out a variety of methods for transmitting your insects symbionts, simply applying the wanted gut bacteria to the substrate of new cultures. I expect it can work in between species. you can try smearing eggs too.


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Neuroscience of confusion
How does (neuro)science characterize "confusion" that occur to "healthy" persons when engaged on a particular mentally-intensive task?
I would exclude the case where we are rationally and with clear arguments deciding one out of many choices (but remain undecided due to lack of sufficient resource/information). My thinking is more towards the case where, for example, we are trying to understand a mathematical problem and its solution, or an abstract reasoning, but in the process get lost: even have no clear idea of what part is 'not understood', or where to start learning (the parts involved) so that we can understand the original problem.
I am aware that I am unable to make my question very clear, I am actually confused how to formulate my thoughts.

Here's an article I found that seems to attempt to address this question, using a kind of machine-learning approach involving "Long Short-Term Memory" (LSTM)-Recurrent Neural Networks (RNN), to classify EEG from participants who were watching either "easy" or "difficult" online lectures - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5620019/ .
It's not a complete account of their process, but the manuscript suggests that gamma-1 frequency bands in the frontal lobe (using a single EEG electrode) were the most valuable feature for distinguishing between trials in which participants were thrown into the middle of a challenging lecture, vs. trials in which participants were viewing the introductory background material at the beginning of the lecture. I'm interested in the same question as the one you proposed, so I hope to see more responses to your post!

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Indirect lineage sorting between human, gorilla and chimpanzee, does it exclude loci reversals (for example on chromosome 12?)
Insights into hominid evolution from the gorilla genome sequence looks at shared genes across human (H), gorilla (G) and chimpanzee (C), and that indirect lineage sorting led to 15% of the gorilla genome being closer to humans, and 15% of the genome being closer to chimpanzees.
In that study or similar studies, is for example the reversed loci in the image below treated as a genetic sequence shared between gorilla and chimpanzee and not with human, or is the specific genes being looked at, so that their position in the genome does not matter?


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Catabolic and Anabolic Reactions
How do we differenciate between catabolic and anabolic reactions?
According to my researches;
Catabolic Reactions

Catabolic reactions (also called “catabolism”) break down larger, more complex molecules into smaller molecules and release energy in the process. The smaller end products of a catabolic reaction may be released as waste or they may be fed into other reactions. The energy that is released by catabolic reactions can be captured and used in many ways. Some of the energy is released as heat and increases the temperature of the cell. Sometimes the energy is stored in the chemical bonds of another molecule. And sometimes it can be used to do work, such as movement of cellular machinery to power the active transport of materials across cell membranes. Catabolic reactions are central to biological processes such as cellular respiration and the digestion of food molecules.

Anabolic Reactions

Anabolic reactions (also referred to as "anabolism") use energy to build more complex molecules from relatively simple raw materials. “Anabolic” and “catabolic” sound similar but are opposites. To remember the difference, it may help to think about how “anabolic steroids” promote the buildup of muscle mass. All of the complex molecules of life — carbohydrates, lipids, proteins, nucleic acids — are generated by anabolic reactions. Anabolic reactions are central to processes like photosynthesis, protein synthesis, and DNA replication.

Here are my questions

Is there water in every chemical reaction?
Do i just need to look at water ($H_{2}O$)?

Regards

Starting of with the basics, reactions are the breaking of bonds in the reactants and the forming of bonds in the products.
To answer your questions about water, there is not always H2O present, although most of the times there is water. You are referring to the hydrolysis and dehydration synthesis reactions, in which water is added or removed, to break down and combine molecules, respectively.
Catabolic reactions are more defined as the net release of energy in the reaction. They break down bigger molecules to smaller molecules. There is a need for energy input to begin the reaction and break the bonds of the reactants, however, the release of energy when the bonds of the products form are far greater, resulting in a net release of energy.
Anabolic reactions are essentially the opposite, where smaller molecules are combined and built up to larger macromolecules, many times with the removal of H2O. This results in a net decrease in free energy, as energy is absorbed/stored in the larger molecule. Energy inputted to break bonds of the reactants are far greater than the small energy released as bonds form.
As you will learn soon, these reactions can be characterized by exergonic/exothermic, and endergonic/endothermic reactions. They can be considered synonymous in many cases.


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Etymology of vimentin
What is the etymology of the intermediate filament , Vimentin?

According to this paper:

From the Latin word vimentum, used to describe arrays of flexible rods,both ordered ones (e.g.,latices,filigres,and wicker-work) and non-ordered ones (e.g.,brushwood).

Vimentin:

Filigree art:


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Full name for stem cells
So during research, my professor mentioned a type of stem cell, a name that was like 5-6 words long, that can be used to treat diabetes by creating an "artificial organ". That hypothetical organ would then be used to create insulin or treat diabetes using other methods.
However I can not remember that name for my life...
This community may not be able to assist me much, as I am aware of the many types of stem cells. This is all the information I have access to, and I cannot contact my professor until the weekend, so it would be great if I could get some prior knowledge about these stem cells; I just need to know the name.....
Thanks in advance.

cool, well I learnt a bit about current stem cell research. insulin is from the pancreas. wikis sais: Pancreatic progenitor cells are multipotent stem cells originating from the developing fore-gut endoderm which have the ability to differentiate into the lineage specific progenitors responsible for the developing pancreas. ............ express a transcription factor called PDX1 (Pancreatic and duodenal homeobox 1). This transcription factor has been shown to give rise to the multipotent stem cell lineages contributing to the endocrine, exocrine and ductal cells of the pancreas

Human Embyronic Stem Cells (hESC) can be programmed to differentiate into a number of different types of tissue depending on the signals you give or withhold.

Source: BioTime
The company Viacyte is actually developing a technology based on hESC that can be used to rescue loss of function in type-1 diabetes, just as an example. Their process takes hESC to pancreatic endoderm after about a month. The pancreatic endoderm has the capacity to differentiate into beta cells, ductal cells and so forth. He could have also been talking about human induced pluripotent stem cells (hiPSC). Like embryonic stem cells, these can differentiate into "anything," but are derived differently.

Thank you so much, he mentioned hIPSC... ill make to read more on it, Thanks again.


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Specific activity vs turnover number of enzymes in BRENDA
From my understanding, the specific activity (A, units: umol/min/mg protein) can be derived from the turnover number (k, units: 1/seg) and the molar mass of an enzyme (MW, units: g/mol):
A = k / MW / 60000
When I try to do this for several entries in the BRENDA database, I don't get an agreement, sometimes the equality is off by an order of magnitude.
However I understand that there can be experimental errors involved, or I might be using the wrong MW (sometimes it is not clear what specific protein the value refers to).
Am I doing something wrong in this calculation?


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How would extraterrestrial organisms be categorized?
Suppose we find bacteria on Mars, we sequence its genome, and find it is genetically similar to $E. Coli$. Would we categorize it in the $Escherichia$ genus? Or would we put it into a seperate system of classification?

This question is indirectly about classification systems of biology. The main points in this question seem to be answered if we ask 2 questions. What happens if we find "life" that is not from the original cells that form our tree of life? Can and do we still base some of our trees of life on aesthetics alone?

@James that's put much more eloquently


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DNA or enzymes — which came first?
Considering that the DNA needs enzymes, to be formed, however enzymes need DNA to be formed too. What biomolecule was created first?

If one is scientifically rigorous, the answer to this question is:

Nobody knows.

If one accepts the most commonly accepted (although not proven) view of the evolution of genomes and catalysis, the answer is:

Enzymes

Explanation
The ‘RNA world’ hypothesis, mentioned by @vkehayas, postulates that the first genome was RNA, not DNA, and the first enzymes were also RNA. DNA genomes arose later (as did protein enzymes, although the timing of that event is irrelevant to the question as originally written).
Alternative Question
If one was not aware that RNA is thought to have preceded DNA as genome, and had not been aware of catalytic RNA, then one might have asked:

Which came first, RNA or protein?

And in fact, this question was originally asked by Francis Crick in the restricted context of  the synthesis of proteins by ribosomes on mRNA and led him to remark.

“It is thus not impossible to imagine that the primitive machinery had
  no protein at all and consisted entirely of RNA.”

The later discovery of catalytic RNA provided a mechanistic basis for an original world in which RNA was a self-replicating genome.
(So the answer to the alternative question is that ‘RNA’ preceded protein.)
Supporting citations
I have kept this answer brief and only provide a single general reference because @vkehayas provides links to other questions about this topic on this list.


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is Xanthosine Xanthine plus ribose?
I'm so confused. I used to think Xanthosine is Xanthine with a ribose instead of H but it appears to me as if it isn't. If you look at the picture in top-right of its wikipedia page you will see that the Imidazole is reversed from the picture in here also the picture in the bottom of this page in additional images section is like the second one. I'm sorry if didn't use the right chemical terms! I'm no chemist. Also I while I was searching I saw different images for Adenine and Guanine where the Imidazole loop was reversed in some by reversed I mean like the position of NH and N was reversed with respect to the Benzene loop!
P.S. It would be great if you could also teach me the correct way to ask this question by means of the chemical terms I should use.
P.S.S I hope it is not a wikipedia problem!

All they’ve done is flip the picture…

Have you ever heard of PubChem? It's a great resource for chemical structures as well as other information.

@canadianer no it is not. pay attention to the relative position of NH in Imidazole to the Os in the Benzene Ring.

@anongoodnurse according to PubChem the image at https://en.wikipedia.org/wiki/Xanthine is wrong. but is PubChem completely reliable?

They are the same. The purine imidazole can exist in two tautomeric forms.

@canadianer I understand that they are tautomers but I don't understand how they are the same! I think they are not the same bc altho the imidazole  is symmetric, the other ring is not. and since there are two bonds between them they can't turn so it matters so much don't you agree that they will look differently under an electron microscope?

9H-xanthine (https://www.ebi.ac.uk/chebi/searchId.do?chebiId=17712) is a tautomer of 7H-xanthine (https://www.ebi.ac.uk/chebi/searchId.do?chebiId=CHEBI:48517)

I guess it depends on your definition of "same". Tautomers are often considered to be the same compound even though they are constitutional isomers.

On the question "Is PubChem/Wikipedia/etc completely reliable?" the answer is "not completely!". It is very hard to get all chemical data 100% correct, but there are efforts to cross-check and validate such data with experts...

@canadianer I was just imagining there were long carbon chains instead of hydrogen in imidazole and another chain in the other ring and then I thought the structure would vary so much because the angle between the carbon chains would be so different and thus different properties. But if you say tautomers are considered to be the same compounds then I suppose such things just don't happen often and the properties of tautomers are almost just the same. Thanks for your explanation.

The two structures are tautomers of one another:

Tautomers are often considered the same compound even though they are really constitutional isomers. Technically they are called 7H-xanthine and 9H-xanthine, respectively (thanks to gilleain for the links).


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Vaccines against bacterial endotoxins
Today in class, there was a discussion going on about what part of pathogens(which can act as an antigen) can be used to make vaccines.
There was this point where our teacher said that bacterial exotoxins can be used for making vaccines.
My questions are-

Can bacterial endotoxins be used in making of vaccines?
If not,  then why is it so? What are the problems we face ?

There are several papers that use alkaline hydrolysis to delipidate or "detoxify" the endotoxin for use as a vaccine (1, 2, 3). The point of many of these papers is to develop a detoxified LPS (dLPS) vaccine to protect against sepsis in the pathogenesis and treatment of gram-negative infections. The detoxification is important, as the lipid-A portion of the LPS contributes significantly to sepsis. In this case you would be targeting the O-antigen or core oligosaccharide.
So one of the problems that I can see is that there are many bacterial serotypes, comprised of many different O- and core groups. I'm not aware of any vaccines with that sort of breadth. Issue two is you get an infection and you need to administer these vaccines quite fast, if not prophylactically, as adaptive immunity takes a number of days to come to speed.
It's also not clear to me whether a prophylactic vaccine to E. coli is useful to the populace at large, epidemiologically (just as an example).
The field also seems to lack clinical data on tolerability and efficacy, which is what I'd be more interested in, e.g. is it safe for humans and does it work?

So they are just under trial and aren't used as prophylaxis because 1) of the differences in core groups of the LPS of the same bacterial species. So,  speaking prophylactically , the vaccine will be effective against only one strain of that bacterial species and not as whole. 2) we still don't have any idea on the efficiency and safety of these vaccines.Am i getting that correct? Furthur, can you provide a link to the structure of endotoxin(LPS) . I really don't have much idea about the A-portion and O- part you talked about but I'm interested in finding out.

@anamikaSingh You have this idea of multivalent vaccines. For example, the conventional flu vaccine is trivalent, consisting of live attenuated bacteria from the three groups predicted to cause the most sickness that year. The strains the following year may differ due to mutation (aka antigenic drift). So it's not to say that you can't have multivalent vaccines, for example, but it's costly and laborious to produce a product against so many different serotypes. And yes, the other issue is that they don't seem to be well-tested clinically.

This is a fair structural representation: http://html.scirp.org/file/5-2270721x6.png.


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Why isn't photosynthesis catabolic reaction?
Here is the chemical equation of photosynthesis
$$CO_2 + H_{2}O \longrightarrow C_{6}H_{12}O_{6} + O_2 $$
We see that the water is in reactant side of the equation. By the way, It ought to be catabolic reaction. However, It seems anabolic reaction on my textbook.

What should we think for this reaction?
How do we get If energy turned out in product side of the equation?
Why isn't photosynthesis catabolic reaction?

How do you define catabolic reactions in the first place? From what I see, the only thing I could say is "water on the reactant side != hydrolysis"

@another'Homosapien' That's my bad.

Possible duplicate of Catabolic and Anabolic Reactions

Catabolic reactions are those that make larger/more complex molecules into those that are smaller/less complex, releasing energy.
Anabolic reactions are those that makes smaller/less complex molecules into those that are larger/more complex, costing energy.
Photosynthesis takes two of the least complex molecules from the perspective of biology, carbon dioxide and water, and forms glucose which is high-energy and complex - this is clearly an anabolic reaction.
The only way I can interpret your question is that you were misunderstanding the definitions of catabolic and anabolic.


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I'm trying to unserstand Yamanaka's iPS cells paper
Can someone please explain to me what is the beta-geo cassette and why is it used? I understand that it was inserted in the Fbx15 gene, and this gene is present in ES cells, and I believe this cassette is used as a marker of the Fbx15 locus, but why does it have resistance genes (beta-galactosidase and neomycin), what are they resistant for? What is their role? Thanks!

Same paper?
https://biology.stackexchange.com/questions/8063/role-of-fbx15-in-es-cells-and-its-use-in-assaying-for-ips-cells-yamanaka-paper

This question is incomprehensible as it stands. If you ask a question relating to a specific paper, not only should you give a citation but describe the system the system you do not understand. Please take the guided tour and read how to write a good question for SE Biology.

Suppose you want to insert a cassette in a gene.  How will you know it is there?  What if only a small percentage of cells are successfully transfected?  What if your reagents were bad.  You do not want to waste time on cels that did not take up your cassette.
Those resistance genes are for detection of the presence of the cassette in a cell (or colony derived from a single cell).  You can have other things ride along with your cassette that will let you detect its presence.  Neomycin resistance: if you grow the cells that you have engineered in the presence of neomycin, only the ones that successfully got your cassette will live because the cassette gave them resistance.  All the ones that did not take up the cassette, or took it up wrong will die.
An active beta-galactosidase gene can work on a substrate to make a blue color.

An active enzyme may be detected using X-gal, which forms an intense
  blue product after cleavage by β-galactosidase, and is easy to
  identify and quantify.

Again this lets you detect cells (or colonies of cells) which have successfully taken up your cassette.


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How to correctly preserve organic matter with ethylene and polyethylene glycol?
I am trying to preserve and dye flowers, especially roses. Let me walk you through the process I am trying to optimize:
1) Soaking flowers in 96%-ethanol for a day to dehydrate them. This step removes a lot of the color from the petals - red roses for example become faint pink. The flower itself becomes brittle to the touch, since almost all water is removed.
2) Putting the dehydrated flower into a mix of 96%-ethanol, polyethylene glycol 400 and reactive dye which is used in textile industry. I am still experimenting with the ration of ethanol:PEG. Soaking duration is a couple of days. In theory, the PEG gets into the cells of the petals - this preserves the petals and gives them most of their flexibility back.
3) Removing the flower from the mix and rinsing it for a minute in 96%-ethanol. This should remove the excessive PEG on the surface of the petals. Otherwise it looks glossy and stays sticky.
My problem begins at step 1): If I remove a flower from the dehydrating ethanol-bath, the petals turn opaque in a weird way. Some connected areas of a petal start to change their appearance abruptly (some sort of bursting, cracking, rupturing)! This starts some seconds after removing the petal from the ethanol and after a couple of minutes, almost all of the petal has turned opaque. Usually the outer edges of the petals don't turn opaque. I am not sure about this, but could it be, that the ethanol somehow destroys the cells of the petals? Is this a behaviour that is to be expected or am I doing something wrong? I think I would benefit a lot if I could understand where this abrupt change of quality comes from.
it doesn't matter, if I remove the flower after step 1, 2 or 3, the result is always this abruptly turning opaque behaviour.
Since my goal is to dye them to look nice and pretty, I need to find the mistake I am making. I was hoping you experts could help me.
You find two pics of already dyed petals attached.
(I wouldn't mind if they stay all transparent. In that case the petals should not turn opaque. But I also wouldn't mind if they become opaque - but on 100% of their surface. Also at the outer edges. This actually may be better - I think it looks nice this way.)

I find that using mixture of PEG 400 and Ethanol 2:1 reduce the transparency. You also need to bake the pental in microwave 360w for 15 seconds. Still some small transparency but acceptable.

Hello, nice answer! This question was deemed worth of an answer, so why not upvote it? Vote early, vote often to encourage new users and keep the community alive!


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Are vertebrate wings and fins considered vertebrate limbs?
I have come across many articles which seem to suggest (but do not explicitly state) that limbs refer to arms and legs. My confusion stems from the fact that does the term vertebrate limb also include vertebrate wings and vertebrate fins or only refer to arms and legs of vertebrates. I would be grateful for clarification.
A simple google definition states that it does include the wings of birds however I would like to know if this is also the case in evolutionary biology or not.
I also refer you to this article
Yano, T., & Tamura, K. (2013). The making of differences between fins and limbs. Journal of Anatomy, 222(1), 100–113.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3552418/
Are vertebrate wings and fins considered vertebrate limbs?
Based on other articles I have read wings are included in the definition of limbs but I am not sure whether fins are included.

There is no alternative definition of "limb" in evolutionary biology. Legs, arms, wings and fins are all limbs. Note that a prehensile tail can also be called a limb. From wikipedia > limb

A limb (from the Old English lim), or extremity, is a jointed, or prehensile (as octopus arms or new world monkey tails), appendage of the human or other animal body.

You can have a look at Cohn et al. (1997), where the term limb is used to refer to legs, arms, wings and fins.
Apparently some authors (as OP has shown examples in the comments) use the term differently. I think it is always made clear so as to not yield to any possible confusion. If you've ever been confused, you might want to let us know which article got you confused.

This article seems to suggest otherwise: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2408990/ . The title clearly implies that fins and limbs are different

It is a book review, not a peer reviewed article. This book review indeed uses the term differently. I think it should not yield to confusion about the meaning of what is said or does it? If anyone use the term differently (as it si the case in this book review), hopefully it should be clear enough as to not yield to any possible confusion. If you've ever been confused, you might want to let us know which article got you confused.

https://www.nature.com/nature/journal/v466/n7303/pdf/nature09137.pdf This article again implies that there's a difference between fins and limbs. Zhang et al. (2010) Loss of fish actinotrichia proteins and the fin-to-limb
transition. doi:10.1038/nature09137

Remi is right, authors are free to use limb how they please. Note nature articles are prone to imprecise language becasue they are written with a wider audience in mind. In the last case the author is using limb as short hand becasue writing "non-fin limb" each time starts to get grammatically messy.

In the article you link, they are clearly using the term 'limb' as excluding fins. It looks like the expression limb-to-fins is quite leading many authors to exclude fins from the term of limbs. I don't think this yield to any confusion though, does it? You will just have to accept that different authors may use different definitions

Thank you for your clarification. So basically the term limb in an article is that as defined by the article but in a broader view of the term in biology outside a specific article it includes fins?


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Can chromosomal crossover undo itself?
If I have alleles AB on one chromosome and ab on another, and if A and B are far from each other (and also a and b), then there is a lot of chromosomal crossovers happening. If I crossover 7 times, will I end up with the same chromosomes as if I cross over once?

Are you asking if the chromosomes can remain entirely identical or just with respect to AB/ab?

Good thinking. Yes, it is theoretically possible. It is often modelled like this. Have a look at this answer for the maths.
Note however, that to my understanding (and I might be wrong) there is typically either 0 or 1 crossover per pair of chromosomes as cross-over is directly related to the way homologous chromosomes bind together during prophase I of the meiosis by the synapsis. My confusion lies in the fact that, I think, there are sometimes (often?) several synapsis per chromosome pair. Hopefully, someone else will be able to clarify this for us.
As a consequence, the genome-wide recombination rate in humans is almost exactly 23 in humans (Wang et al., 2012). So in practice, such mulitple crossover would very rarely (if ever) happen.

See also.

My experience trying to recombine transgenic constructs in Drosophila is in line with 1 crossover per chromosome being common and >1 extremely rare.

That's quite an interesting question. Crossing over occur during meiosis, there can be more than one in a chromosome indeed. Let's say two crossing over occurs in the same chromosome (the one with your markers A and B), if they both occured in between your markers, you will see no difference. As you said your markers are far from each other you have a good probability to observe that. If your markers were close, your chance to observe a double crossing over is really low.
Also, there is some mechanisms preventing two crossing over to occur too close from each other. I can't tell you exactly what it is about. There is a type of Crossing over not subject to this rule though...
Double crossing over can be an issue when working on genetic maps (using crossing over to determine the order of marker on map). As if this occur we have no way to choose between 0 crossing over or 2 crossing over (meaning markers are actually far from each other.
If you want more explanation about this wide topic, I would suggest you to read this scientific work. They are working on removing inhibition for crossing over and achieve to multiply the number of crossing over by 9 in Arabiodpsis!

Synapsis is the pairing of homologous chromosomes, one from each parent. Crossover occurs following synapsis. The points at which crossover occurs are called chiasmata, and appear to be genetically determined.  However, it seems that they are not always at the same locations on homologous chromosomes from different individuals.
That said, the likelihood of crossover being reversed on one chromosome would depend on a series of lucky coincidences and some serious inbreeding, but could conceivably happen.  For crossover to be reversed on all chromosomes would be staggeringly unlikely.


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Can any organism possibly have the capability to create a new species every time it reproduces?
There are lots of different kinds of living organism in our planet. So i was wondering if such an organism could possibly exist?
Can any organism possibly exist, that would have the capability to acquire some genetic information of the organism it consumes, and pass that along with its own genetic information, forming a new species every single time it reproduces.

You should look up the definition of a 'species' - just taking up additional genetic information doesn't make a new species (and wouldn't be viable over multiple generations). Species are usually defined based on their ability to reproduce with each other - and having an organism that cant reproduce with the direct F1 should be possible at least in theory (you can look into yeast mating types for possible mechanisms).

Concept of species
First have a look at How could humans have interbred with Neanderthals if we're a different species? to better understand the concept of species.
I will assume that you are using the "biological species definition" which is based on reproductive isolation.

Can any organism possibly have the capability to create a new species every time it reproduces?

The question is mainly non-sense. In short, if it is true that all offspring are a new species, it means that by definition the lineage is asexual and then the concept of species is typically considered to be of little interest. Let's consider both asexual and sexual lineages separately to maybe clarify what I mean.
Asexual lineages
For exclusively asexually reproducing lineages, either we decide the question makes no sense because the concept of species does not apply to them. Or we decide the concept of species applies and then every individual is necessarily a new species. So, yes, by definition there is no exclusively asexually reproducing lineages where a new species isn't created at every reproductive event.
Sexual lineages
For sexual lineages, the question would make no sense either as if it was the case that every individual was it's own species, then the lineage would be asexual!

Absolutely impossible.  There are several basic reasons:
1. Genetic modification isn't that simple
Not going to go into the mechanics of it, but suffice it to say that you can't perform genetic modification simply by having the cells of one species close to the cells of another.  It requires complex techniques, such as shooting the new code at the host genome along with metal particles, shock or heat treating the receptor cell, etc.
2. This "feature" would not make a species more viable
If the species were around, just say for the past 1,000 years (+++), imagine the quantity of information that would have been gathered.  Besides being unable to reproduce with others of its kind due to genetic incompatibility, the extra information being added every generation would make the species so laden with "features" that they would very quickly start to use their utility.
Furthermore, the gained "features" would tend to make the predator more like its prey.  This would not help it and its progeny to survive; rather it would hinder them from catching additional prey.  If a fox, for instance, begins to shrink because it has been eating mice, the time will quickly come when it will no longer be able to catch the mice.
3. Somatic cells are not reproductive cells
I'm aware this isn't necessarily in your question, and quite possibly you did not mean to imply it, but as long as I'm here, it's worth the effort to point out that in a lot of predatory organisms, reproduction takes place via meiosis, fertilization, etc.  That is to say, even if the new DNA were to be absorbed by the cells and by some unbelievable chance, the code were to be copied into the genome of the host's cells, that trait would not be passed on to offspring unless the code were also implanted in the carrier's reproductive cells.
Even if that happened, you would once again have the issue that the additional codon sequences would very likely make it impossible for the reproductive cell to bind with another "equivalent" gamete.

Sorry, but no.  Just - no.

Sources:

How to Make a GMO: Chelsea Powell, Harvard University, Aug 2015

Perhaps you should be less dogmatic about point 1: Bacterial natural transformation by highly fragmented and damaged DNA and Wikipedia:Natural Transformation

@vkehayas Hmm, interesting, never seen that before.  Thanks for the share.


text:
What is a DNA clamp exactly?
I used to think that a DNA clamp is a protein. But today I noticed it doesn't appear in this picture. Then I went to it's Wikipedia page, where it was written:

A DNA clamp, also known as a sliding clamp, is a protein fold that
  serves as a processivity-promoting factor in DNA replication. As a
  critical component of the DNA polymerase III holoenzyme, the clamp
  protein binds DNA polymerase and prevents this enzyme from
  dissociating from the template DNA strand. The clamp-polymerase
  protein–protein interactions are stronger and more specific than the
  direct interactions between the polymerase and the template DNA strand

Which I find a little confusing. For now it seems to me like DNA clamp is a subunit of DNA Polymerase and it doesn't have any function by itself and it is not an actual protein but it binds to Polymerase and becomes functional. Can somebody please clarify this matter to me?!

The reason it doesn't appear in some diagrams is because every diagram needs to achieve a balance between including all known details, and leaving out details to not overload the reader. The clamp isn't essential to understanding the basics of DNA replication, so it gets left out a lot.

Your partly right both ways.  In a sense, the DNA clamp is a protein, in another sense, it's only part of a protein.  What it actually is is what we call a protein sub-unit, which is a protein, but which binds with other protein sub-units to form complex proteins.
In order to understand this, you have to remember what a protein is.  A protein is, in essence, a chain of amino acids.  Those can be short chains, long chains, medium chains: but they're all proteins.  Sometimes, a few short proteins (sub-units) will bind together to form one long protein (protein complex).  This is what happens in the case of a DNA clamp.
Basically, the DNA clamp is (an) independent protein unit(s) which has (have) the ability to encircle the DNA strand and travel along it.  They bind to the polymerase, which is why you don't see them on your diagram.  Their function is, very simply, to make it possible for the polymerase to stay closely attached to the DNA stand.

Sources:

DNA Repair (Amst). 2009 May 1; 8(5): 570–578


text:
Is natural selection a tautology, and therefore not truly falsifiable?
I've heard the argument from a lot of creationists that all the evidence for natural selection (and by extension, evolution) in general is worthless because natural selection is so flexible that it could cover all the data, no matter what we discovered. In essence, that natural selection is a tautology:

Survival of the fittest. What is 'fit'? What survives.

There are other creationists, however, that admit that natural selection could be falsified. These are split into two groups:

The ones that say, if you rephrase natural selection as a non-tautology, it becomes obvious that it doesn't work:

Natural selection has been criticized as a tautology. This would be a major problem for evolutionary biology, if true, because tautological statements can't be falsified and, therefore, can't be scientific. There is merit to this critique insofar as the theory of natural selection is indeed generally described in a tautological manner. However, natural selection can be described non-tautologically if we’re careful. Natural selection should be defined as the theory that attempts to predict and retrodict evolutionary change through environmental forces acting upon organisms. However, this re-framing comes at a cost: it reveals, based on our current knowledge of evolutionary forces, the lack of ability to make accurate predictions about expected changes except in the most simple of circumstances.

And those that say that the falsifying options provided by natural science are impossible to actually use. Here are some of those falsifying options:

Charles Darwin himself proposed a rather strong test of evolution: "If it could be demonstrated that any complex organ existed, which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down." [Darwin1859, pg. 175]. This is the basis of claims by various intelligent design writers that various biological structures, such as the vertebrate immune system or the bacterial flagellum, are "irreducibly complex" -- they consist of multiple components that could not develop in the absence of the others. However, these structures have been exhaustively studied in the scientific literature, and scientists have demonstrated entirely plausible evolutionary pathways. See Complexity.

Famed biologist J. B. S. Haldane, when asked what evidence could disprove evolution, mentioned "fossil rabbits in the Precambrian era" [Ridley2004, pg. 66]. This is because mammals, according to current scientific analysis, did not emerge until approximately 40 million years ago, whereas the Precambrian era is prior to approximately 570 million years, when only the most primitive organisms existed on earth.
Biologists had long conjectured that human chromosome number two was the result of a fusion of two corresponding chromosomes in most other primates. If DNA analysis of these chromosomes had shown that this was not the case, then modern evolutionary theory would indeed be drawn into question. This "fusion hypothesis" was indeed confirmed, rather dramatically, in 1993 (and further in 2005), by the identification of the exact point of fusion. For additional details see DNA.
Modern DNA sequencing technology has provided a rigorous test of evolution, far beyond the wildest dreams of Charles Darwin. In particular, comparison of DNA sequences between organisms can be used as a measure of relatedness, and can further be used to actually construct the most likely "family tree" hierarchical relationship between a set of organisms. Such analyses have been done, and the results so far dramatically confirm the family tree that had been earlier constructed solely based on comparisons of body structure and biochemistry. For additional details see DNA.

Is there any way to save natural selection? To do so, we need to:

Prove it can be explained non-tautologically
Prove that it does make useful predictions
Give falsifying experiments that are reproducable and actually possible.

I'm voting to close this question as off-topic because it is not a question about biology in the terms of SE Biology, but an attempt to initiate discussion about the provability of the theory of evolution by natural selection, a topic that must have been discussed ad nauseam.

Welcome to Biology SE! Please have a look at these closely related questions: https://biology.stackexchange.com/questions/64688/the-falsifiability-of-natural-selection and https://biology.stackexchange.com/questions/40579/is-evolution-a-fact. You will find many more by using the search bar at the top of the page. If there's still something that you need to ask, please edit your question to specify exactly what is still unclear to you.

Ah, thank you. The first one I've already looked at, and while helpful was not exactly what I needed and the second I will look at. In any case, I know how to use a search bar, thanks. @David, if this topic has been discussed ad nauseam (which I'm sure it has!), could you please point me to some resources on it? Aside from one article, I'm having a hard time using Google to find anything useful.

There is a helpful discussion along these lines in Dawkins' The Extended Phenotype, chapter 10.

Fossil rabbits in the Precambrian are hardly a disproof of the theory.  It could be some rare collapse of more modern rock into an older layer ... time travel ... convergent evolution ... a spacefaring species of alien bunnies! :)  Really, as we glumly watch COVID evolving before our eyes to come back and perhaps evade our vaccines, it is hard to imagine any single piece of fossil data strong enough to disprove the whole theory.

I think @Remi.b's answer is great and really the only way to answer your questions is with a comprehensive introduction to evolution. However, I wanted to address the tautology issue more directly.
First, the "survival of the fittest" seems like a tautology with "natural selection" because it is not a description of how natural selection works, rather, it is a phrase meant as a synonym for natural selection, to help describe the result to someone unfamiliar with the phrase.
Let me use an analogy: it would be like if you were a very new learner of English, and I told you "Joe's truck has more mass than an elephant!"
If you aren't really familiar with the term "mass" in English, this phrase could be confusing. So I explain instead that "Joe's truck is heavier than an elephant." If you know the word "heavy" this is easier to understand.
However, there is a tautology there! the car is actually heavier because it has more mass, but that does not make either phrase untrue or untestable: it's just another way of saying the same thing within a context (i.e., those statements are the same if they are exposed to the same gravity).
The testable hypothesis that natural selection makes is that, given 2 things: 1) a population where individuals have traits that give them different chances of survival, and 2) some way for offspring to inherit traits from their parent(s), then the population over time will consist of individuals who are more likely to possess the traits that gave a high chance of survival.
Following this, should the environment change in some way such that a different trait is now beneficial, that trait will increase in prevalence.
There are way too many experiments to summarize here that show 1), 2), and a combination of 1) and 2), as well as experiments that show that indeed, when you have 1) and 2) you get natural selection.

Since this post just got bumped to the top of the active question list, I've got to poke. I know it'll be a pain, but I think your answer would be made even stronger for those coming across it if you can actually cite one or two or three papers that you allude to in your final paragraph. Not a must, as the rest of your answer makes your point well. But, if you have time, link/cite something here...+1 btw for simple explanation

The tautology argument is an attack on a rare phrasing and not on the nature of the theory of evolution.
First, the theory of evolution is way more than just natural selection but let's ignore that for the moment.
The phrasing 'Survival of the Fittest' was first suggested by Herbert Spencer and was later used by Darwin when he changed the title of the fourth chapter from "NATURAL SELECTION" to "NATURAL SELECTION; OR THE SURVIVAL OF THE FITTEST" (Thanks @BryanKrause for his comment).
It is before all a labelling. A catchy sentence to refer to the process of Natural Selection. In no way does it mean that Natural Selection is a non-sensical explanation.
Natural Selection is easy enough to understand for a layman that you can make you own opinion
Luckily, the concept of Natural Selection is really easy to understand. It does not take any a priori knowledge in Science to understand it and if you have a look at any intro course to evolutionary biology you will understand it yourself.
There are thousands of good sources of information on the subject online. If you want to learn about it, do not look at straw man and other fake explanations from creationist (and other religious extremist) websites! Consider for example Understanding Evolution or many of our posts on Biology.SE such as this one for example. You can also get any intro text book (see here for recommendations).
How does natural selection work?
Here is a copy paste of my answer here. It explains the very basic concept of natural selection through the so-called Lewontin recipe and gives a somewhat silly, but easy, example with a population of pens!
The Lewontin recipe says that natural selection occurs whenever:

Individuals in a population varies in terms of a given trait
This trait has some (additive) heritability. Here is one of the several posts that explain the concept of heritability. It might be slightly a post that is a bit advanced for you though but shortly speaking it means that offspring are more similar to their parents more than they are to other non-kin individuals in the population.
The fitness varies (not necessarily linearly) as the trait varies.

Simple example:

In a population, there are blue pens and red pens
Reproduction is asexual and blue pens create other blue pens while red pens create other red pens.
blue pens make more offspring than red pens.

Of course, there exist strict mathematical formulations of this process that you can learn in any introduction to evolutionary genetics.
Your questions
Note that your questions are all way too broad for a single post (and your question could be closed as too broad) but I wanted to try to give you a hand anyway.

Prove it can be explained non-tautologically

There is no "proof" in science, only evidence. But let's ignore that for the moment.
Please have a look at any intro course to evolutionary biology (see above).

Prove that it does make useful predictions

Please have a look at any intro course to evolutionary biology (see above). Afterward, you can eventually have a look at Is evolution a predictive theory?.

Give falsifying experiments that are reproducable and actually possible.

Please have a look at Demonstrable and repeatable examples of evolution which lists thousands of evidences explained in layman terms.
There are thousands (tens of thousands maybe?) of papers published every year extending our understanding of evolutionary processes! It is hard to know which one you would be interested in!
Related post
You should have a look at Is evolution a fact?

"Survival of the fittest" was Herbert Spencer's term, not Darwin's, though Darwin later referred to and used that phrasing.

@BryanKrause Thank you for correcting me. I knew it but somehow managed to got it wrong when writing! I've corrected this mistake.

I'm really interested in the history of science and it's really interesting when a rhetorical choice like "survival of the fittest" comes back to haunt a bit. It was really taken as a nice, simple way to convey what selection meant but it has been so contorted since. There are a lots of other examples of where this has happened in science (our insistence on using the word 'theory' in english, is one other example, to mean 'stuff we have figured out' instead of the colloquial 'random idea I just came up with').

@BryanKrause regarding "theory", it's even worse: in Greek, θεωρία is the act of observing, the sight, the act of looking at. It has the same root of "theatre".  So, it has more to do with "empiric evidence" or "collected data" than with "rational explanation for this phenomenon". It is, indeed, a very bad choice for what it is supposed to mean in sciences.

@Remi.b regarding the "survival of the fittest" phrase, not only Darwin never said that in the first edition, but he also never used the word "evolution" (actually, there is the verb "evolved", in the last page of the book). On the 6th edition he uses "evolution" no less than 15 times. As I always say, the 1st edition is the edition anyone should choose to read. It is by far the best one: all the changes he did in the subsequent editions were for the worse.

Natural selection is an observation, not a tautology.  We can certainly imagine worlds - call them Disney ecologies (or for the religiously inclined, Gardens of Eden) - in which natural selection simply doesn't happen.  E.g. each species is independently created, and each pair of a species has exactly two offspring before dying of old age.
This is easy enough to imagine, just as it's easy to imagine a flat Earth enclosed in a dome of "firmament" but it simply doesn't match what we observe happening in the world we live in.

Surprisingly, there seems to not have been any mention of Karl Popper, who famously argued that Darwinism is tautological and not testable/falsifiable. This answer will just give some quotes from Popper:
1963:

There is a difficulty with Darwinism. While Lamarckism appears to be not only refutable but actually refuted (because the kind of acquired adaptations which Lamarck envisaged do not appear to be hereditary), it is far from clear what we should consider a possible refutation of the theory of natural selection. If, more especially, we accept the statistical definition of fitness which defines fitness by actual survival, then the theory of the survival of the fittest becomes tautological, and irrefutable

1965:

the trouble about evolutionary theory is its tautological, or almost tautological, character: the difficulty is that Darwinism and natural selection, though extremely important, explain evolution by 'the survival of the fittest' (a term due to Herbert Spencer). Yet there does not seem to be much difference, if any, between the assertion 'those that survive are the fittest' and the tautology 'those that survive are those that survive'. For we have, I am afraid, no other criterion of fitness than actual survival, so that we conclude from the fact that some organisms have survived that they were the fittest, or those best adapted to the conditions of life.
This shows that Darwinism, with all its great virtues, is by no means a perfect theory. It is in need of a restatement which makes it less vague.

1969:

Biologists (especially Fisher) felt compelled to define as “more fit” those which more often survive. Thus, what once looked like a promising explanatory theory becomes quite empty. The statement “Evolution tends to produce higher forms because only the fittest survive” may sound like an explanation. But if we substitute here for “the fittest” its defining phrase, we get: “Evolution tends to produce higher forms because those forms which more often survive more often survive.” So our “because” phrase has degenerated into a tautology. But tautology cannot explain anything. All tautologies are equivalent to “All tables are tables” or “Those who live long are those who live long.”

1972:

A central problem of evolutionary theory is the following: according to this theory, animals which are not well adapted to their changing environment perish; consequently those which survive (up to a certain moment) must be well adapted. This formula is little short of tautological, because ‘for the moment well adapted’ means much the same as ‘has those qualities which made it survive so far.’ In other words, a considerable part of Darwinism is not of the nature of an empirical theory, but it is a logical truism

1974:

the theory of natural selection is not a testable scientific theory, but a metaphysical research programme

1974:

Adaptation or fitness is defined by modern evolutionists as survival value, and can be measured by actual success in survival: there is hardly any possibility of testing a theory as feeble as this

For more details & discussion, see "Popper’s Shifting Appraisal of Evolutionary Theory" (2017).

+1 for exploring the more philosophical aspect of the question, but I'd say the answer is still incomplete. Can you add some of the theories proposed/experiments performed in response to Popper's arguments, just to make the answer more 'balanced'? :)

I think both my own and Remi's answer (also jamesqf's) already argue for why Popper is completely missing the point in these quotes by using a straw man. Darwin's theory is not that the fit survive, it is that because the fit survive, populations change composition according to relative fitness. If that appears tautological it's only because it's totally true. Indeed the principle (apart from mechanistic details) is pretty boring scientifically these days, but it certainly wasn't when it was first raised.

The "survival of the fittest" statement which Darwin recommended as the best formulation of his idea of "natural selection" is definitely a tautology because there is no other operational definition of fitness besides survival (or reproduction). So, survive (reproduce) are those who survive(reproduce).
Darwin naively attempted to imitate the process of selection of domesticated species assuming that new species are produced by "natural selection" in the same way as dogs are produced from wolves. The poor guy was probably not familiar with the facts: the species produced by selection are inferior to the original ones. Dogs are inferior to wolves since they lost a lot of vital features. Moreover, this loss of information is irreversible: you cannot produce a wolf from a spaniel by selection.
In an abstract form, it is quite simple. There is a law: the complexity of a result of a selection algorithm cannot exceed the complexity of the algorithm. Therefore, any selection results in the information loss, and no new information can be produced by selection.

I'm not clear what you are trying to explain here. It is true that selection itself would lead to loss of diversity (information, in other words) but you are forgetting that mutation (and other processes that cause genetic alteration) keep adding more information. Although, the phrase "survival of the fittest" may seem tautological, it is not really so. Fitness is the ability to survive a condition. Although it depends on the condition, it is a property that existed in a population prior to the selection. After the selection, these fit individuals are the ones that survive.

So, it would be great if you can clarify what you are really saying. BTW, it is not impossible to make a wolf from a spaniel considering the fact that humans (or any complex multicellular organism) evolved from a unicellular ancestor.

If  "Fitness is the ability to survive a condition" then the fittest are those who survive. Survival of those who survive. Anything else?

And it is not a fact that humans (or any complex organisms) evolved as a result of (whatever) selection. It is an opinion, and it is logically faulty.


text:
Difference between cytospin and metaphase spread protocol
I would like to know what exactly is the difference between cytospin and metaphase protocol. I'm a data scientist helping a medical lab and I receive images of cells with particular types of DNA. The DNA comes stained with DAPI. However, other times, if the scientists can pinpoint a particular gene in the DNA, they stain it with FISH. I asked the following: When I separate the image into the separate color signals (RGB),  will I see the DNA in both the green gray scale images and the blue gray scale images, I was told that you can but it won't be that clear since cytospin spread protocol has worse quality than metaphase spread protocol.
What exactly is the scientist referring to? I looked at some articles but the methodologies are a bit beyond me and it would be helpful if it can be answered in broader terms.


text:
Question about different gametes that can be produced
I have a question from a past exam that asks the following:
"For the organism of genotype AABbCcDDEe (homozygous for 2 genes, heterozygous for 3 genes), how many different types of gametes will be made if the C gene and the E gene are linked on the same chromosome while the remaining genes are all on different chromosomes?"
However, I have no answer key, and these answers are the choices:
A. 2
B. 3
C. 4
D. 8
E. 9
Here's my approach to the question:
We have 5 traits, and each trait consists of 2 alleles. To make functional gametes, each gamete must receive one of each allele so that it can survive. Clearly, for AA and DD, there's only one choice: A, and D.
However, for Bb, Cc, and Ee, things are a little different.
C and E are linked on the same chromosome. c and e are on different chromosomes. Therefore, a gamete can have either CE, or c and e. Similarly, a gamete can have either B or b.
Therefore, shouldn't we be able to create 4 different types of gametes?:
ABCDE, ABcDe, AbCDE, AbcDe
So wouldn't the answer be C. 4?
Please show me any mistakes I might be making, or any gaps in my understanding. This would be very much appreciated.
Thank you!

You are correct
Assuming that by linked, the question assumes perfect linkage (no cross-over ever happen), then your answer is correct! Good job!
Comments
Here are a few comments though...

We have 5 traits, and each trait consists of 2 alleles.

There are 5 loci. A locus does not necessarily match to a single trait and a single trait does not necessarily match to a single locus. Actually, it is very very rarely (if ever) the case.

To make functional gametes, each gamete must receive one of each allele so that it can survive.

This is not necessarily true. A "normal meiosis" (not leading to variation in copy number) may create a non-viable genotype and a "abnormal meiosis" (leading to variation in copy number) may create a viable genotype. But, it is true that we will only assume "normal meiosis" for this answer.

Hi there, thank you very much for answering my question and giving additional advice. Sorry that I couldn't get around to accepting your answer and giving feedback straight away. Your answer helped put these concepts I learned into greater context since it seemed like I had a kind of naive understanding of meiosis.


text:
How do racing pigeons know the way back to their roost?
I have read that a standard way to do pigeon racing is that the male and female are separated and the pigeon races to its mate.
My understanding that in these cases the roost is several miles away from the release point. How does the pigeon know how to find the roost?
I have heard that sometimes they will hold up the mate in the air, but at several miles away, how would that help.

They find their way back even if they have been moved in complete darkness by using, indeed, magnetoreception. They can sense the direction of where they come from using the earth magnetic field. I believe there is still some debate about how magnetic fields are sensed by pigeons, the latest fashionable idea being that this is through a "warm" quantum process. I don't know if that's correct, but there is clear evidence that there are magnetic-sensitive cells in the pigeons nervous system (Wu & Dickman, 2007). This will only lead pigeons to the approximate location of their home, but once they are close enough they can recognize where they live visually. Pigeons are released everyday so they know the local environment of their home.
I'm quite sure this has nothing to do with the pigeons mates. This is probably some ridiculous idea people had in the middle-age and people kept repeating it because that sort of intuitively makes sense, but when you think carefully about it, it really doesn't.
Wu, L. Q., & Dickman, J. D. (2012). Neural correlates of a magnetic sense. science, 336(6084), 1054-1057.