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How would the result of Hershey and Chase experiment been different if protein was the genetic material?
Please answer in simple terms im only in 9th grade.

Hershey and Chase did two experiments to prove that DNA is the carrier of the genetic information.
First, they grew phages (viruses which infect bacteria) in a medium containing radioactive sulphur (35S). This marked all the proteins of the phage (the hull) radioactive. They then used this phage to infect bacteria. To do so, the phage attaches to the surface of the bacteria and injects its genetic material. This looks like in this picture from the Wikipedia page on Bacteriophages:

The bacteria with the attached phages are then blended, so they will loose the attachment to the bacterial surface. The mixture of bacteria and phages is then centrifuged, this makes the heavy bacteria sediment at the bottom of the tube, the lighter phages stay in the supernatant. Hershey and Chase then measured where the radioactivity from the marked phage proteins had gone, since they found it in the supernatant, they knew, that no proteins had entered the bacteria.
If proteins would have been the carrier of the genetic information they would have entered the bacteria and had been found in the sediment inside the bacteria.
In the second experiment (the proof if you want to say so) they marked the DNA of the phages radioactive (with radioactive phosphorus, 32P). They repeated the experiment and found the radioactivity in the sediment with the bacteria, proving, that the DNA had indeed entered the bacteria.
If the DNA wouldn't be the carrier, it wouldn't have entered the bacteria and would have stayed in solution.
The whole experiment is nicely shown in this Wikipedia illustration:


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What kind of detergent should I use in cell culture laboratory for cleaning purposes?
I work on establish a cell culture laboratory in the company where I work. All equipment are new and I want to clean lab before I start to work with cells. Is there any special detergent for cleaning cell culture lab?

No, standard soaps used for washing lab equipment are enough. Our stuff simply goes through the dishwasher and is autoclaved afterwards.

Are you cleaning the equipment, surfaces such as benches or floors, or supplies like glassware?

I agree with Mike, but would like to add that if you are trying to do protein expression for purification, some detergents contain polyethylene glycol (PEG), which will readily bind to many proteins, causing shifts in protein size/weight and potentially effect activity or toxicity. In particular, I have heard that Liquinox can have PEG (depending on the batch?). To avoid this, we'd use DetoJet for low-density cultures and add tergazyme for fermentation-density cultures.

Could you add sources?

I can't tell if you're asking about glassware or work surfaces (hoods, benches etc), but...
We use regular old dawn dish soap in my lab because what's more important than the soap you use to wash you're glassware is the water you use to rinse it.  We teach our undergrads the 3-rinse-rule.  After soaping, every item gets 3 rinses with normal tapwater (or until no more suds forms- whichever comes last) followed by 3 rinses with deionized water.  We have DI water on tap which makes things easier.  I remember rinsing some glassware with acetone or other solvents in organic chem lab, but you shouldn't need to do anything like that for TC.
The same principle holds true for work surfaces.  After cleaning, decontaminate with 70% ethanol, 10% bleach, envirocide or any other BSL2 recommended cleaner.

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Why are the sex chromosomes called X and Y?
Is there a specific reason that the letter Y is used as the symbol for the male chromosome and X is used for the female chromosome?

when Y chromosome being replicated, pair looks like letter Y. When X chromosome being replicated, pair looks like letter X.

Sex Chromosomes and Sex Determination by Ilona Miko

The first inkling that sex chromosomes were unique from all other chromosomes came from experiments conducted by German biologist Hermann Henking in 1891… Henking saw that some wasp sperm cells had 12 chromosomes, while others had only 11. Moreover, while observing the stages of meiosis that formed these sperm cells, Henking noticed that the mysterious twelfth chromosome looked different from all the others. He thus named this chromosome the "X element," to represent its unknown nature.

Wikipedia - Y Chromosome

The Y chromosome was identified as a sex-determining chromosome by Nettie Stevens … during a study of the mealworm Tenebrio molitor … Stevens proposed that chromosomes always existed in pairs and that the Y chromosome was the pair of the X chromosome discovered in 1890 by Hermann Henking … Stevens named the chromosome "Y" simply to follow on from Henking's "X" alphabetically.

I know that this is not the most reputable source, but it does cite a couple of books. Take it as it is. Keep in mind that all human chromosomes, even the Y chromosome, appear as X shaped when replicated and condensed. The Y chromosome is quite acrocentric and so the short arms may appear to be one, but they're not.

During metaphase, all chromosomes look like an X with the exception of the chromosome Y. See below

Why Y then? Well, according to wikipedia, just because the letter Y follows the letter X in the alphabet.
Note that many species don't have sexual chromosomes and note that in many species, the Y-looking chromosome is present in the female but not in the male. In such case we call this Y-looking chromosome W and we call the X-looking chromosome Z. Very likely this post will interest you.

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Can DNA rings, i.e. plasmids, form as Möbius strips?
I know that plasmids can be present in a coiled form, which keeps the DNA strands together when they degenerate, by forming catenases.
I was wondering, however, whether it has been documented to naturally happen or if anybody has ever successfully created a Möbius-strip plasmid. Technically, such a structure could readily form from a single circular strand of DNA, but the literature, as far as I have searched, has remained silent.

Wouldn’t any covalently closer circular DNA with an odd twist be a Mobius strip?

Related to your question, this paper reports Möbius strips created from multiple strands of DNA.

@canadianer you can make this into an answer, since it answers my question.

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Abbreviations for molecules: What are CheW, CheA, CheY?
I've encountered the abbreviations such as "CheW" and "CheA" for certain organic molecules.  For example:

Proteins associating with the Tar complex include the autophosphorylating protein kinase CheA, the transducing protein CheW, the methylating enzyme CheR
  and perhaps the protein phosphatase CheZ.  (Morton-Firth et al. 1999, p. 1060; available here)

What does "Che" stand for?  What do the capital letters at the ends of the abbreviations mean?
Let me know if this would be a better question for chemistry.SE.

Here is the paper that first defined them:
Armstrong JB, Adler J. 1969. Complementation of nonchemotactic mutants of Escherichia coli. Genetics 61:61-66.
Che is an abbreviation of chemotaxis. In this paper, complementation studies revealed three different loci that, when mutated, result in defective chemotaxis. These were termed CheA, CheB and CheC. Originally they were thought to be genes, but the following paper refined the definitions when the CheA locus was found to contain CheA and CheW genes while the CheB locus contains CheB, CheX, CheY and CheZ genes:
Silverman M, Simon M. 1977. Identification of polypeptides necessary for chemotaxis in Escherichia coli. J Bacteriol 130:1317-1325.
I'm not going to search for the discovery of every Che gene, but hopefully you have an idea of where the letters come from.

These are name of proteins.
CheA stands for Chemotaxis protein A


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How often does pre-mRNA processing lead to midstream off-frame errors in eukaryotic mRNAs?
As I understand it, the splicing of introns from pre-mRNAs is not incredibly precise. I've only ever seen nucleotide position ranges given in any description of the involved processes. Since there is quite a bit of looping of pre-mRNAs during processing and given that involved proteins often have effects well downstream from where they bind, this intuitively makes sense.
However, this would be incredibly problematic if true. Most pre-mRNAs are more intron than they are exon. While the precise base offset for the bases padding the start and end of an mRNA are irrelevant due to the start and stop codons, the precise offset for cut locations is very important for any splicing between the start and stop codons. If the splicing of introns regularly lead to cuts that are 1 or 2 bases off (in addition to 0 or more whole codons that have been accidentally removed), then all eukaryotic cells should have lots of (junk) mature mRNAs that have the proper reading frame at their 5' ends but off frame codons at the 3' end or just for stretches in the middle.
Specifically, if pre-mRNA processing has mostly random cut locations in its splicing, I would expect only ${^1/_3}^{rd}$ of mRNAs to retain the reading frame of their parent genes from from start to poly-A. In turn, that would mean only about ${^1/_3}^{rd}$ of synthesized proteins have the proper primary structure. There's no way eukaryotes function with that much kludge running through them.

"the splicing of introns from pre-mRNAs is not incredibly precise.".. Why would you suppose so? Do you have any reference to support this? AFAIK, splicing is decently precise in cases where precision is needed (when there is no alternate splicing involved). However, there can be such frameshifts but since they are not detected with decent coverage in RNAseq experiments, we can assume that such missplicing events are not significantly frequent.

As noted in the comment above, our understanding is that splicing is generally quite precise. Keep in mind also that if you do get a splice error, you have a very high probability of introducing a premature stop codon, which, among other things, will mean that the rest of the mRNA is not translated and is likely to be degraded.


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Why does Edema occur in Kwashiorkor?
Edema in lower leg and face is a symptom of Kwashiorkor. It is the most distinguishing feature of it which distinguishes it from Marasmus. Why would decrease in amount of proteins cause Edema? Why doesn't it occur in Marasmus (which is both protein and energy deficiency)?

I thought I might add that there are many factors that can lead to edema, and the primary cause of edema in different individuals with the same condition may not be the same. On malnutrition such as in Kwashiorkor, many of the bodily systems are compromised. As mpribis said below, abnormal cardiac activity can contribute, as can kidney and liver failure. I suffered from severe edema of the legs due to malnutrition and different doctors attributed different things to the edema; namely, blood tests showed electrolyte imbalance, raised serum albumin and deranged liver enzymes

Why would decrease in amount of proteins cause Edema?

Proteins in the blood (esp. albumin, because it's the most abundant one there) cause fluid to come from the interstitial space into the capillary. This phenomenon is called oncotic pressure. On the other side there is hydrostatic pressure on the vessel wall, which causes fluid to exit the capillaries. This hydrostatic pressure gets lower as the blood passes through the capillary, while the oncotic pressure stays the same, because under normal conditions, proteins don't exit the capillary very much compared to their amount in blood.
In the first part (closer to the arteriole), hydrostatic pressure is bigger, so the fluid exits the capillary site, while as you get closer to the venous site, the hydrostatic pressure gets lower than the oncotic pressure and the fluid flow is reversed. (see picture)
If you lower the amount of proteins in the blood drastically (as in Kwashiorkor) the oncotic pressure is lower and therefore less fluid is reabsorbed from the tissue, which leads to its accumulation there - this results in edema.

Why doesn't it occur in Marasmus (which is both protein and energy deficiency)?

Sometimes, both features of kwashiorkor and marasmus are present in the patient, which is called marasmic kwashiorkor and the distinction between these two conditions isn't that easy.
However, normally in marasmus, there is also dehydratation present, which balances the effects of decreased oncotic pressure. Cardiac output is usually decreased too, which leads to decrease of hydrostatic pressure, so again, this can counterbalances the decrease of oncotic pressure.

Oedema in malnutrition(kwashiorkor) is due to extra cellular imbalnce of the fluids which is caused by lower albumin level. Where some can see protruded stomach due to enlargement of liver this is caused by imbalance in gastro intestinal system hence causing gut and liver to swell hence diognosed as oedema.


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Why do left and right eyes can require different power of lenses?
Both the eyes almost see the same things throughout our life. It is not like we use one eye more than other that it should become weaker. What causes requirement for different power of lenses for both eyes? Shouldn’t they be same?

Because we have two hands, two feet, two ears, etc., we are tempted to think that we are perfectly symmetrical.  But if you compare the details of your two hands, for example, you will find that the blood vessels are in somewhat different positions, the lines in your palms are different, and the fingerprints of corresponding fingers are different.  The same is true of your eyes: they differ from each other.  These kinds of differences are due to the fact that genetic instructions relating to symmetry during embryo development are not exact; they are approximate.
Probably if you measure the size of the biceps on each arm, or the size of the forearm muscles, you'll find that they are slightly different.  This is partially due to the fact that you use one arm and hand differently from the other: you are right-handed or left-handed.  Similarly, people tend to be left-eyed or right-eyed, using the two eyes differently.  And, people tend to sleep more on one side than the other.  These are differences that emerge due to experiences and habits.
Those factors make it unlikely that the two eyes will ever be identical, and make it likely that eventually they will need different eyeglass prescriptions.


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Difference between Trophic and Tactic movements
What is the difference between Trophic (eg. Chemotrophic) and Tactic (eg. Chemotactic) movements?
In Bryophytes, Anthrezoids are attracted towards Archegonia. This is Chemotactic movement. In Spermatophytes, Pollen tube moves towards Ovule. This is due to Chemotrophic movement.
This is was taught in our school today. But to me, in both cases the male part is attracted to female part using certain chemicles. So what is the difference between them? Broadly speaking, what is the difference between Tactic and Trophic movements?

I think that you got a bit confused about terminology. In fact Chemotrophic is an organism that obtain energy by organic or inorganic molecules.
In your case I think that you want to know the difference between Chemotropism and Chemotaxis.
Chemotropism

Chemo-tropism is the growth of organisms (or parts of an organism, including individual cells) such as bacteria and plants, navigated by chemical stimulus from outside of the organism or organisms part [...]
An example of chemo-tropic movement can be seen during the growth of the pollen tube, where growth is always towards the ovules.

Chemotaxis

Chemotaxis (from chemo- + taxis) is the movement of an organism in response to a chemical stimulus.Somatic cells, bacteria, and other single-cell or multicellular organisms direct their movements according to certain chemicals in their environment. This is important for bacteria to find food (e.g., glucose) by swimming toward the highest concentration of food molecules, or to flee from poisons (e.g., phenol). In multicellular organisms, chemotaxis is critical to early development (e.g., movement of sperm towards the egg during fertilization) and subsequent phases of development (e.g., migration of neurons or lymphocytes) as well as in normal function.

Hence, to sum up (Chemo)taxis is the physical movement of a cell (or an organism) in response to a (chemical) stimulus, as done by the Antherozoids that are attracted towards Archegonia.  However (Chemo)tropism is the growth on organism toward a (chemical) signal, like done by Spermatophytes where pollen tube moves (so it growths) towards the Ovule.
Hope this explanation help you to clarify.


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Which cell organelle is more important in giving colour to petals?
It was a question in our school test and given answer was vacuole. But I think it should be chromoplast as they are the organelles specialised to provide colour. But options were given, so which is more accurate? Is the question controversial (both are correct?)

From what I have seen, a chromoplast is the only correct answer. I cannot find any articles even mentioning a vacuole being used for the storage of pigments in plants. I cannot think of where the test creators would have gotten that information.


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Forest Fires and Horsetails
In our school textbook, it is written that sometime forest fires can occur due to rubbing of two horsetails. In the image that I searched online, the plant itself looks thin and rod like with leaflike structures arising from nodes. But many other plants have similar structure. So it might not be its morphology.
What special thing about horsetail starts the fire? Why don't other plants show same thing?

I didn't believe this was a real thing, and I'm still very skeptical, but it is something that's claimed to happen!

Their stems & leaves have a siliceous epidermis, so if rubbing b/n 2 horsetails occurs, a forest fire may be produced

--The Bottled Ocean of Biology, by Nisarg Desai, 2017
Why don't other plants show same thing? Another plant, bamboo, is supposed to do the same thing:

How these fires originate is uncertain ... it has been suggested that a probable cause is the rubbing together of the silica-coated bamboo stems as they sway in the breeze.

--Burma, by R. Talbot Kelly (2004)
The same claim about bamboo is made in an Indian Government document on forest fire management.
What special thing about horsetail starts the fire? Apparently the claim is that it's the silica in the stems of the plant that is the important factor, and that horsetail and bamboo are both unusual in that regard. This does seem to be true:

... in general, ferns, gymnosperms and angiosperms accumulated less Si in their shoots than non-vascular plant species and horsetails.

--Phylogenetic Variation in the Silicon Composition of Plants
Bamboo isn't mentioned in that article, but the presence of silicon in bamboo is supported elsewhere:

One of the advantages of bamboo over wood is that bamboo contains some silicon in both inner surface (pith-ring) and outer surface (rind) of the bamboo culm.

--Calcium phosphate formation induced on silica in bamboo
As I say I remain very skeptical. There's no evidence shown that this has actually happened. Is it telling that all these claims come from the same general region (India and Burma)? My guess is that this is an old wives' tale that's been written down and uncritically accepted, but if someone has actually seen this happen I'd be happy to be proven wrong, because the idea of plants sparking out flames in the wind is a pretty cool one.
Edit to add a link claiming that bamboo-on-bamboo generates sparks due to the silicates:

The method consists of striking sparks out of  the culm of Schizostachyum bamboo with flint, broken pottery, china or even another piece of bamboo. The sparks that occur by striking the Schizostachyum bamboo are presumably generated by the high silica content in this genus of bamboo.

--Bamboo Strike-A-Light, by Tom Lourens, Ash Kivilaakso and Ed Read (My emphasis)
Edit to add that the overall concept of plants starting their own fires has been seriously looked at; the author is skeptical:

Individual plant traits (such as leaf moisture content, retention of dead branches and foliage, oil rich foliage) are known to affect the flammability of plants but there is no evidence these characters evolved specifically to self-immolate, although some of these traits may have been secondarily modified to increase the propensity to burn. ... It is more parsimonious to conclude plants have evolved mechanisms to tolerate, but not promote, landscape fire.

--Have plants evolved to self-immolate?
Notably, in his list of factors potentially allowing self-immolation, he does not list silica, and horsetail isn't mentioned at all.

What would the underlying chemistry/physics of this be – can silica generate sparks through friction?

Apparently it does! See edit

It's a cool idea and it's visibly a myth. No, Apparently it's never been seriously attempted or proven.
No wood friction ignition techniques that I know of use the sides of stems to obtain the 233 degrees combustion temperature of paper, they use the cross section and atm pressure. Equisetum couldn't achieve that because it's not heavy enough to get that kind of pressure on the stems, and it's not tinder plant. It sounds like they were having 300 kph winds!
There is an Equisetum species known as the scouring rush:
The rough stems have been used to scour or clean pots, and used as sandpaper.
Boiled and dried Equisetum hyemale is used as traditional polishing material, similar to a fine grit sandpaper, in Japan.
The stems are used to make fires:
 The silicated stems were used by Native Americans (and still used by some people today) to start hand-drilled fires.
It's probably the basis of a myth that they can start fires. Many horsetails are marsh plants with very deep roots and water storing rhyzomes. They are well studied for growth after forest fires, but there are no clear references to friction of the plants causing spontaneous combustion of the plant, a dubious theory.
... Ignition temp of various woods  190°-260°

Could be that horsetails, as primitive plants, in certain soils, accumulate and concentrate atoms (hyperaccumulators) and just like certain minerals that spark or certain compounds that flare when dry, are source of ignition ie Flash Powder

this would be better suited as a comment

Is this purely speculation, or is there any evidence for this?

...accumulate atoms?

hyperaccumulation genes (HA genes) are found in over 450 plant species, including Arabidopsis and Brassicaceae.


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Adam's Apple and Voice box
Why is Adam's Apple more prominent in males? Is it due to bigger voice box pushing the cartilage more, or is the cartilage indeed bigger than that in females? I am assuming bigger voice box as males have a "deeper" sound. Is it correct to do so?

Yes, you nailed it!
Adam's apple (aka.  laryngeal prominence) exist in both men and women. It is a piece of bony cartilage called thyroid cartilage that wraps around the larynx (aka. voice box).
The Adam's apple is more prominent in males because males have have a bigger larynx (giving males a deeper voice). In males, the prominent Adam's apple typically appears during adolescence, when the larynx increases in size and the voice becomes deeper.

So the cartilage is prominent because the  voice box pushes it out, right?

It was maybe not clear before. The larynx is what people call voice box (I now clarified this point in my answer). Adam's apple is the cartilage that wraps around the larynx so if the larynx is big, the cartilage will be prominent.


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Why do I see an inverted image of an object when I close my eyes?
If I stare at an object for a long time and close my eyes, at first I can still see the object with my eyes closed. But the image I see with my eyes closed is inverted: dark colors appear as light and light colors appear as dark. Why is that?

I think it is because of light adaptation. The rods that are perceiving strong light, downregulate their response. But when the light is suddenly withdrawn then the rods that are adapted to perceive bright light cannot immediately sense dim light.
There are two forms of adaptation- fast and slow. The fast one is Ca²⁺ dependent- decrease in Ca causes cGMP to increase which in turn depolarizes the cell. Calcium modulates this process by other means also. This article suggests that slow adpatation is  because of an allosteric binding of cGMP on transducin-phosphodiesterase complex, which stabilizes this transition state and delays the signaling.
Adaptation can also happen because of photobleaching of rhodopsin.
I don't know how an image "remains" in the eye for a while. I believe it is because of asymmetric slow light adaptation between different spatially distributed rods(some rods take a while to readapt to dim conditions).
Similar effect you can feel with colour vision also. You keep staring at green for a while, then when you see something else it appears reddish.


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How is mRNA directed out of the nucleus to its ultimate cytoplasmic location?
In the process of translation, I learnt that following formation the mRNA must exit the nucleus through a nuclear pore and attach to a ribosome.
My question is how does mRNA navigate itself out of this pore, and find itself a ribosome to bind to?
Is this a process of diffusion or is there any other mechanism involved?

Maybe this thread helps? https://biology.stackexchange.com/questions/1736/rna-or-ribosome-which-one-moves-during-translation

Hello Dwarz! That was helpful but I think the motion being discussed there is that as the mRNA moves through the ribosome, while I am puzzled by how it arrives there. Thanks though, it was interesting to know

There is a complex progress involving many proteins that directs RNAs to the nuclear pore complex and ensures that they are moved into the cytoplasm. Below is part of a diagram (edited) from a Nature review article on this topic, showing the transport of mRNA. It is available from the authors online.

Another general review with an illustrative poster is by SR Carmody and SR Wente, and can be found in the Journal of Cell Science.
As far as I am aware, interaction of mRNA with cytoplasmic ribosomes occurs by diffusion. Direction of the ribosomes to specific locations, such as the endoplasmic reticulum, can occur, but is generally through recognition of features of the nascent peptide after tranlation has started. The Wikipedia article on protein targeting provides an introduction to this area.


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An efficient and free method of assembling a large number of Sanger sequencing reads?
I have a rather large number of Sanger Sequencing reads.
Is there a automated method in either Ugene or a similiar freeware that allows you to quickly assemble forward and reverse reads. Ideally something where the suffix of the filename will allow the software to automatically know which is the forward and reverse read.
Any help would be much appreciated as I'm not keen to do each sequence by hand in Bioedit.

Have you considered SPAdes? It's a popular, state of the art assembler that should work with Sanger sequencing reads.
http://cab.spbu.ru/software/spades/

What about the old Phred, Phrad and Consed suite of programs?

Thank you for answering, but it would be appreciated if you could at least provide a link to these programs. As it is anyone would have to search.


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Can viruses survive super-saturated salt solution?
There is little evidence of biological activity in the Dead Sea (a salt-water lake). In addition, human blood cells do not survive in too much salt water as they shrink and die.
So I wondered whether viruses survive in super-saturated salt water. If they survive what allows them to survive and tolerate the high salt concentration? If they do not survive, what is the mechanism of their destruction?

since viruses may contain no water and are not undergoing metabolic process why do you think salt would affect them?

This issue was studied in Virus inactivation by salt (NaCl) and phosphate supplemented salt in a 3D collagen matrix model for natural sausage casings International Journal of Food Microbiology Volume 148, Pages 128–134.
Saturated NaCl was tested on 4 types of virus, foot-and-mouth-disease virus (FMDV), classical swine fever virus (CSFV), swine vesicular disease virus (SVDV) and African swine fever virus (ASFV) at four different temperatures:4, 12, 20 and 25 °C for a period of 30 days.
For ASFV, but not the other 3 viruses, saturated NaCl had a significant effect of inactivating the virus, on a days timescale.

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Why is thymine not incorporated into mRNA?
I am aware that in transcription uracil bonds to adenine and not thymine. But what is it that actually prevents thymine from bonding to adenine in transcription, that is not present in replication?

Nice question! But sadly, it comes under the category of questions about which we don't know everything yet. We don't yet know how RNA Polymerase differentiates between uracil and thymine while adding nucleotides to growing mRNA chain (at least, I was unable to find research papers online), most probably because it has proved difficult to know the exact mechanism of RNA synthesis which RNA polymerase undergoes. But we do know what factors it could use to do so. For general introduction, these factors are:

mRNA chains contain NTPs instead of dNTPs. Now, TTP is very (very) rarely found in cells. So, RNA Polymerase can look for 2'-OH in nucleotide for adding base (pay attention that RNA polymerase is not known to have proofreading mechanisms, but there is growing evidence that RNA polymerase can correct a faulty base pair matching, see Thomas et al). RNA polymerases are known to be able to distinguish between NTPs and dNTPs (Svetlov et al), although the precise mechanisms in multi-subunit RNA polymerase remain elusive. Yet, this property certainly plays a role (refer to EDIT 1 for details about this).
UTP and dTTP have another basic structural difference: of a methyl group. This difference is crucial for differentiating the two, especially for DNA repair machinery. It is so because cytosine can spontaneously convert to uracil (by deamination). So, there has to be something for repair enzymes to look for while repairing mutated cytosine, and a methyl group saves thymine from repair. See the following image for comparison:
source

Just for information, we know the flip side i.e. how DNA polymerases prevent dUTP from adding in DNA chains, because dUTP is much more common than TTP. Simply saying, they don't. Mutations can (and do) occur, leading to faulty addition of dUTP in DNA. But, this is where repair machinery helps. Cells contain an enzyme, uracil DNA glycosylase, which replaces uracil by thymine in DNA (Longo et al). So, until we find the exact mechanism for RNA polymerase, you can assume that it uses much similar mechanism for proofreading (along with the first one of course).
EDIT 1: I will add some details about the mechanism of base pair matching by RNA polymerase as just leaving the point at yet, this property certainly plays a role makes the answer misleading to some people. But, because putting the whole mechanism here would make the answer too long and also out-of-scope (keeping in mind you asked 'why', not 'how'), I'll try to keep this part as small as possible. Giving a diagram for better understanding:

Pay attention at the Tyr639 and His784 (sugar discriminators), this is how the RNA polymerase distinguishes NTP from dNTP. It has also been shown that removing Tyr639 will convert the RNA polymerase to DNA polymerase(!), though removing His784 would just decrease its activity, suggesting its role to be minor w.r.t. Tyr639. For more information, have a look at this page from Brooklyn college website.
EDIT 2: In another answer, the answerer says RNA synthesis requires rNTPs instead of dNTPS as precursors, but does not explain why it is so (which is indeed an important part). So I'll add that part in my answer. It can be explained by following points:

The sugar discriminators of RNA polymerase (describe above) do not allow dNTPs to add to the growing chain. Thus dNTPs cannot act as substrates for RNA synthesis.
The enzyme for synthesis of thymine (dTTP) is thymidylate synthase, which requires dUMP as substrate. Thus, it is not possible to create rTTP instead of dTTP.
Conversion of uracil to thymine requires energy, meaning uracil is energetically less expensive than thymine. This also directly explains (partly) why mRNA doesn't incorporate thymine into the chain.
Degradation of mRNA requires an enzyme ribonuclease which cannot degrade dNTPs. Also, in the mechanism of degradation of mRNA, 2' -OH plays a role. This can be explained by diagram below:

As is visible, 2' -OH is an important part for RNA degradation. Thus, it wouldn't be possible to degrade mRNA in this way if it contained dNTPs.

References:

Matthew J Thomas, Angelina A Platas, Diane K Hawley, Transcriptional Fidelity and Proofreading by RNA Polymerase II, Cell, Volume 93, Issue 4, 15 May 1998, Pages 627-637, ISSN 0092-8674, http://dx.doi.org/10.1016/S0092-8674(00)81191-5.
Svetlov V. Vassylyev D.G. Artsimovitch I. Discrimination against deoxyribonucleotide substrates by bacterial RNA polymerase J. Biol. Chem.  2004 279 3808738090
Mary C. Longo, Mark S. Berninger, James L. Hartley, Use of uracil DNA glycosylase to control carry-over contamination in polymerase chain reactions, Gene, Volume 93, Issue 1, 1 September 1990, Pages 125-128, ISSN 0378-1119, http://dx.doi.org/10.1016/0378-1119(90)90145-H.
Dziuda, D.M. (2010). Data Mining for Genomics and Proteomics: Analysis of Gene and Protein Expression Data. Wiley
Roberts, Gordon C. K. et al. “THE MECHANISM OF ACTION OF RIBONUCLEASE.” Proceedings of the National Academy of Sciences of the United States of America 62.4 (1969): 1151–1158.

Not trying to be too critical, but I think that's a bad assumption to make. Also, the structural difference between thymine and uracil doesn't seem particularly relevant since RNAP could not possibly use it to distinguish them. The mechanism of sugar selection by nucleotide polymerases seems to be pretty well understood. See this article, for example. Combine that with your assertion that TTP is rare in cells and a plausible answer seems apparent.

@canadianer dude thats jackpot! Where did you find that paper? Also, the point with base selection is that its precise mechanism in RNAPs is not known (thats why you also said possibly). And as long as something is quite not known, I don't think any assumption could be bad. Yet, its about opinions, who knows even the assumption might get true? :)

One main feature of polymerases is that they have multiple substrates and don't disntiguish them by the nucleobase. Given that they have to accommodate larger purine moieties, I don't see how the methyl group of thymine could be used to distinguish it from uracil.

@david any doubt that arises from my answer is a demand for me clear it out. Anyways, your opinion has only made my answer better, and thanks for that :)

The answer to this question is quite straightforward:

Thymine is not incorporated into mRNA because the precursors of RNA
  synthesis are ribonucleoside triphosphates (not the free bases) and
  there is no pathway for the synthesis ribothymidine triphosphate
  (rTTP) in cells — only for the synthesis of deoxthymidine triphosphate
  (dTTP).

I suspect that this rather naïve question arises from the misconception, common among those exposed only to brief popular accounts of the topic, that free bases are the precursors of nucleic acids. In fact it is the nucleoside triphosphates, that are the precursors, and the key difference between RNA and DNA is between the sugars ribose and 2-dexoyribose. It is obvious that RNA polymerases are specific for ribonucleoside triphosphates, otherwise deoxyribose would be found in RNA.
Rider: Why is there dTTP but not rTTP?
Although not strictly part of the answer, I think that it may provide a perspective on the topic to explain why there is no rTTP in cells, even though there is dTTP. This is because of the way dTTP is synthesized — not the trendiest of topics — but one involving enzymes that are so crucial to DNA synthesis that certain large DNA viruses encode their own copies.* The diagrams below are my own. A more extensive account can be found in Chapter 25 of Berg et al. online — Nucleotide Biosynthesis.
There are synthesis pathways for rAMP, rGMP, rUTP and rCTP. (The first three of these need to be converted to the triphosphates for RNA synthesis.) For DNA synthesis the ribose ring of the rNDPs is reduced to deoxyribose. Note that this produces dUDP which is subsequently converted to dUTP:

To produce dTTP, dUTP is converted to dUMP, which is methylated to dTMP by the enzyme thymidylate synthase. (dTMP is then converted to dTTP.)

The free bases do not occur in cells as a result of synthetic reactions, but as nucleoside monophosphates. However free thymine is generated during the degradation of DNA. This can be ‘salvaged’ by the pathway including thymidine kinase:

*These are the herpes viruses. Although not found in every case, the following enzymes occur in various herpes virus genomes: ribonucleotide reductase, thymidylate synthase, dUTPase, dihydrofolate reductase and thymidine kinase.

Although an answer has already been accepted, I have posted this because I think the accepted answer confuses the issue. It may seem strange that I have added a long rider regarding DNA metabolism when the question is about RNA, but I think it important to understand the metabolism of thymine in cells in order to appreciate why there is no rTTP. It also helps to illustrate the metabolic interconversions (and their energetic costs) that were required to allow DNA genomes to supplant the presumed earlier RNA genomes.

I only found first two paragraphs of your answer relevant to the question. Also, just writing "RNA contains uracil because uracil is precursor of RNA synthesis" doesn't really answer the question. The question just changes to "why is uracil a precursor of RNA synthesis?" in this case. See my answer, I've that part in it too.

@another'Homosapien' — I have edited my answer slightly to make it clear that the section on lack of rTTP is a rider rather than an essential part of the answer. By presenting the answer as a single sentence in highlighted quotes, I allow the reader to see my point immediately. He may chose whether or not he wishes to read further about the metabolism of thymine, which the heading makes clear is a rider to the answer. I think it is illuminating, you do not. We are each entitled to our opinons.

@GerardoFurtado — Thank you. Your answer to the question of why T not U is used in DNA is already on SE Biology at: http://biology.stackexchange.com/questions/171/why-is-thymine-rather-than-uracil-used-in-dna/24785#24785.

@gerardofurtado actually both yes and no. When I read the question, I still get it as "why does mRNA not contain thymine in place of uracil?" because thats what (IMO) OP wants to know (as they selected my answer when I answered that part). So, from my side, this answer does seem insufficient, but it would be sufficient for the ones who take the question in its literal meaning.

The question is clearly mechanistic/practical with its focus on the hydrogen bonding of the bases. There is no way the poster is concerned with the philosophical/evolutionary question of why if thymine is "good" didn't it replace uracil in RNA. I have posted that as a quite separate question: http://biology.stackexchange.com/questions/57990/why-is-uracil-rather-than-thymine-used-in-rna


text:
Validation of houskeeping genes in a mixture of cDNAs of two species
I have a parasite sample (mixed with host blood) and I need to check gene expressions of parasite using relative quantification (RT_qPCR). For this, I need a good housekeeping gene. I chose 10 genes (suggested as housekeeping) that I need to validate and after choose the most stable one(s). My problem is that my parasite cDNA is mixed with host cDNA and it is impossible to separate them or count the parasite. I do not know how I could choose the best housekeeping gene in this case? I do not have the real amount of parasite cDNA used for qPCR, and I do not have any good internal control. Basically, it is circular problem: In order to validate my target gene I need a good housekeeping gene for internal control, but I do not have an internal control to make relative quantification of my housekeeping genes and to chose the best one. Could you please suggest any study or method that deals with such a case?

Is the parasite genome sequenced?  If so, you may be able to identify a gene that is different enough from host to parasite to design parasite specific primers?

Your qRT-PCR primers should be specific to one species or another in at least one of the housekeeping genes you choose, it's unlikely all 10 primer pairs work on both species.

Two possibilities:

Design primers based on differences in the sequences of the gene for the same protein between the two organisms. (Suggested by @Artem)
Identify an aspect of the metabolism of your parasite that is not present in the host, then use enzymes from that pathway. If the parasite is a worm and the host a mammal, for example, you should surely be able to find something.

We have primers that distinguish mouse and human Beta-Actin and GAPDH for engraftment experiments. It's not difficult to simply design primers to target one species and not another.

@Artem — Don't tell me, tell the poster in an answer. Only comment on my answer if you think there is a flaw in it, not to point out an alternative.

Because comments are not answers, and SE Biology has a specific question and answer model I have incorporated Artem's comment into my answer. This way it will be useful for anyone else with the same question. (I do not need the points that will accrue when it is marked up or accepted, which should now be done, I think.)


text:
What is the effect of the wavelength on the spectrophotometric measurements of protein?
Does the wavelength setting affect the absorbance reading of a spectrophotometer? For example, if I am using a spectrophotometer at 550 nm to determine the protein concentration of my samples, would my results be different if I analyze them at 500 nm?

I don't understand your question, can you clarify it?

The change in absorption due to concentration (Beer's Law) is the most at the wavelength of maximum absorption. But using another wavelength should give you similar results, but they would be so accurate.

correct me if I'm wrong. The change of the wavelength would result in a lower absorption, but it will be similar to the one with the bigger wavelength.

Molecules will have a certain range of absorbance with a peak at a certain point. A wavelength longer than the peak absorbance and shorter than the peak absorbance will result in more light being recorded by the detector. You can determine peak absorbance by taking several readings of the same sample  and varying the wavelength of the spectrophotometer. you will need to make very small changes around the peak to find the exact peak wavelength, but you should be able to find it this way. On the opposite sides of the peak, absorbance will fall off to near 0 if you have calibrated for solvent.

@AMR perfectly described what I mean by wavelength of maximum absorption. You should do your analysis at this wavelength. But if you do it at another wavelength, then it will give you similar results but the result would be less accurate.

In addendum, keeping the wavelength around the absorption maximum for the light-attenuating species avoids introducing error into Beer's Law. There are limitations to the law, outlined here where we can see that around the lambda max, there's little change in absorption per unit wavelength:

In case B, this would end up returning a bad extinction coefficient! You can experimentally determine this point either by testing the solution at different wavelengths or more accurately, running a program where the machine goes through it's entire wavelength range and measures absorption for you. You'll get a parabola where the maximum is your lambda max, so it's solvable by calculating the maxima if necessary (take the first derivative, set y'= 0, solve for y when x = (y'=0) for the associated ordered pair). You also want to be careful when you're using something like the Bradford assay where the bound form of the dye shifts the lambda max!

Nice information +1. However, in an experiment I would not expect the wavelength of the incident light to change (if the light is monochromatic). Also, I do not understand Figure B. Why would absorbance vs concentration become non-linear for non-λmax wavelengths?

I think this is the explanation here. As far as the math goes I'll admit I'm not actually 100%!

Light absorption happens because of interaction of light with electrons (in a way) such that the energy of the light is transferred to some electrons that moves them to a higher energy state.
As per quantum chemistry (Bohr's model of hydrogen can be referred for a basic understanding), there are distinct energy states (solutions of the Schrödinger equation) and there are no intermediate levels. Therefore, to excite an electron to a higher energy level the energy of the incident light should match the energy gap between the ground state and the excited state.
In a molecule, there are different electrons, that reside in different orbitals and environments; only a few electrons can be exited by the energy that UV-Visible range of the electromagnetic spectrum can provide. These electrons are typically referred to as chromophores. You should refer to a book on spectroscopy for more details. A molecule can have multiple chromophores and each may absorb a different wavelength.
Having said that, there are energy bands (multiple closely spaced energy levels) in the molecule instead of fixed energy state which allows absorption in a range of wavelengths around a value at which the absorption is maximum. The wavelength vs absorption graph will give a peak at the maximum (which usually looks symmetrical but not always necessarily be so).

 From ChemWiki

The width of this absorption band would differ between different chromophores; so in your hypothetical case, some chromophore which has an absorption maximum at 580nm may absorb 530nm while another chromophore with same maximum, may not.
The Beer-Lambert's law will hold for all wavelengths that can be absorbed i.e. the absorbance would be proportional to the concentration of the molecule (unless there are complex phenomena like energy transfers that may be dependent on concentration; this is unlikely in dilute solutions).
As a practical suggestion, I would say that if your spectrophotometer has fixed options then choose the wavelength that is closest to the absorption maximum.
If you see the above example graph and let's say your aim is to quantify nitrophenolate in a mixture of nitrophenol and nitophenolate. Then a measurement at 350nm instead of 400nm would give you erroneous result. In other cases a 50nm difference may not matter (for e.g. measuring at 450 for the nitrophenolate). It all depends on what you are analysing. You should know the molecule that you are analysing.

The Bohr model is only valid for hydrogen. However the Schrödinger Equation takes into account all the rest... so I would probably edit, to just mention Schrödinger.

From Chemistry 8th Ed - Zumdahl & Zumdahl "At first Bohr's model appeared very promising. The energy levels calculated by Bohr closely agreed with the values obtained from the hydrogen emission spectrum. However, when Bohr's model was applied to atoms other than hydrogen, it did not work at all. Although some attempts were made to adapt the model using elliptical orbits, it was concluded that Bohr's model was fundamentally incorrect."

@AMR We are not even arguing which is the best atomic model. I had mentioned Bohr's model because it is easy to understand for a beginner in spectroscopy. Though it is obsolete, the fundamentals that describe energy levels are not incorrect even though they are applicable only for hydrogen atom. I cannot take the OP through a course on quantum mechanics. Nothing that I had said is misleading I guess; however, for your satisfaction I made the edit :)

I would probably have mentioned something about conjugated systems reducing the energy of the photon needed to get the electrons to change energies, resulting in "absorbing" longer wavelengths and probably not worried about mentioning Bohr and the Man with the Cat, as the OPs lab exam is more likely to have a question about why PNP can absorb light in the visible spectrum that about quantum theory,... but then that is just me.

@AMR Conjugation is just one case but there can be several ways including splitting of orbitals, interaction with solvent or other dipoles in the molecule, etc. That will go in a different direction altogether. Best to avoid that IMO.


text:
How can I fit the A595 of my unknown samples to the data?
While I was conducting the Bradford Assay experiment to determine the concentration of my unknowns, I ended up by having an A595 for my unknown samples that is higher than the A595 of the standards. How can I resolve this issue?
wishes.. Micheal.

Just find out slop of your standard curve and then calculate unknown concentration from that. this might be helpful to you.

When you run a bradford assay the bound form of the dye shifts the absorption max to 595nm. This is what your spectrometer should be set to when you're running the assay. You make a standard graph because you can calculate an extinction coefficient ε from the slope of the graph. Beer's law says that A = εcl where your path length is determined by the cuvette you used, and c is your concentration. So you take your absorption that you obtained and solve for c! Canadianer makes an excellent point below, however, so make sure your methods make sense!

You could, depending on what you are doing, extrapolate your standard curve to include the absorbance of your samples. This, however, is not recommended since absorbance is linear only within a certain range. It's best to dilute your samples so that they fall within the range of the standard curve while also ensuring that your standard curve is, in fact, linear.


text:
Do any non-human species have packed abs?
The classic "six-pack abs" in humans is due to tendons stretched across the abdominal muscles and low body fat. Do any other animals have a similar arrangement of tendons that could result in visible "n-pack abs" for a sufficiently low body fat individual?

Most animals are quadripedal and therefore their abdomens are generally not exposed. Perhaps the tendinous intersections required for the abdominal flexibility required for a bipedal posture. See here.


text:
Do mutagens ever increase the "rate of evolution"?
There are a lot of sci-fi plots where mutagens, especially radiation, cause some organism to evolve at an accelerated rate. Obviously evolution does not occur within a single organism and most of the authors behind these works are more concerned with finding a justification for a desired plot rather than adhering to known science. Nonetheless, I'm curious to know if there is any well-known case where such a scenario is true. (To get one obvious reply out of the way, all evolution that we've observed on Earth occurs in the presence of the background radiation experienced on Earth. Also, although mutagens by definition increase the rate of mutation, those mutations can of course be harmful, so the question is whether the effective "rate of evolution" can be increased rather than the rate of mutation.)
Is there any well-known case where introducing mutagens can increase the "rate of evolution" in an experimental evolution study?
By "rate of evolution", I'm informally referring to either the amount of time or the number of generations that pass before some beneficial mutation occurs and is selected for. For example, in the E. Coli strains from Lenski's E. coli evolution experiments, are there any known cases where a mutagen reduces the amount of time or the number of generations required for a non-citrate-metabolizing E. coli strain to acquire the ability to metabolize citrate?

The Ames test comes to mind, though it’s specifically designed to detect beneficial mutations in response to a mutagen.

Yes, although what you mean by increasing the rate of evolution is a little vague. Plant breeders regularly use mutagens of various types to increase the mutation rate. The mutants are then screened for useful traits, and useful mutants are cross-bred with existing lines.

Chemical mutagens like EMS and DMS, radiation and transposons are used
  to generate mutants with desirable traits to be bred with other
  cultivars – a process known as Mutation Breeding. Classical plant
  breeders also generate genetic diversity within a species by
  exploiting a process called somaclonal variation, which occurs in
  plants produced from tissue culture, particularly plants derived from
  callus. Induced polyploidy, and the addition or removal of chromosomes
  using a technique called chromosome engineering may also be used.

Wikipedia: Plant breeding

Do mutagens ever increase the “rate of evolution”? [..] By "rate of evolution", I'm informally referring to either the amount of time or the number of generations that pass before some beneficial mutation occurs and is selected for

This is a very unusual definition of "rate of evolution" but I'm happy to consider it if you want.
If more mutations happen per generation, then it takes less time for a beneficial mutation to happen. So yes!
By rate of evolution, some people may like to refer to the rate at which neutral mutations fix (fixation=reaching a frequency of 1 in the population). If $\mu$ is the mutation rate, then $2N\mu$ mutations are produced each generation (assuming diploidy), and a fraction $\frac{1}{2N}$ of them fix (as they are neutral), this means that the rate of fixation is $\frac{2N\mu}{2N} = \mu$. So, again increasing the mutation rate increases the rate of fixation of neutral mutations. It is actually true also for deleterious and beneficial mutations but the computation is a little more complicated.
Note however, that there is a point after which the mutation rate is so high, that your population might be drawn to exctinction. This is called a mutational meltdown. Mutational meltdown is unlikely to happen unless the population size is already small to start with and/or the mutation rate is really really high.

But OP seems to be looking for a documented case where the rate of fixation of advantageous mutations (a combination of mutation rate, strength of selection, and population size) has been shown to increase in an environment with a higher overall mutation rate ...

Perhaps you can also comment about mutation-selection balance. I guess that would be a relevant factor here.


text:
Are mitochondria dead?
In the video "What is Life? Is Death Real?", the subject of mitochondria is raised at 2:58. At 3:12, the narrator says "[mitochondria] are not alive any more: they are dead."
What currents of thought lead to this affirmation?
When I search for mitochondria are dead on Google, I get many links about the role of mitochondria in cell death, but I don't see anywhere that the assertion in this video is discussed.

idea probably is that mitochondria can't survive outside the host cell.

@aaaaaa: That seems a strange qualification, since most (probably all) organisms can't survive outside the environment they're adapted to.  Humans, for instance, die pretty quick if you don't provide them with oxygen and keep them between roughly -50°-50°C.

See this related post

@jamesqf SolarLunix made a great point, please consider accepting it

also, i find all question like "what is life"useless in our fight against death and disease.

Does it really matter why some Youtuber decided they are alive or not? Clearly an argument can be made for them being alive (have DNA, replicate, process chemicals) and not being alive (cannot survive very long outside cells, not very complex) and it comes down to an arbitrary distinction. It's an irrelevant concern, nothing about your (or anyone's) life would change if the Czar of Science decreed one way or another.

http://arxiv.org/abs/1207.4803 "...determining which phase (non-life or life) a given system is in requires dynamical information and therefore can only be inferred by identifying causal architecture."

related: Can you consider a human as alive, or is it the cells on the body that are alive?

You should restate the argument given in the video in your question (to make it more self-contained), and highlight what parts you find unclear. At the moment, I think the question is unclear, and answers will mostly depend on how you define the terms alive, dead, and life (you haven't included working definitions of these concepts in your question).

SolarLunix posted an excellent answer detailing the criteria for being classified as "alive", and showed that by those criteria, mitochondria could be considered as "dead".
However, I would argue that the narrator's statement in your video does not make any sense. The currently-accepted theory of the evolution of mitochondria (and possibly other organelles) from free-living prokaryotes is called symbiogenesis and postulates that the mitochondrial progenitors began living symbiotically with the precursors to eukaryotes some 1.5 billion years ago. Life originated on Earth about 3.5 billion years ago, so eukaryotic cells (carrying mitochondria) have been around for a little less than half of that time.
In that incredibly large span of time (if you counted 1 number per second, you'd reach 1.5 billion in about 47.5 years), what used to be an independent organism (we assume) has become an organelle - an integral part of the eukaryotic cell. It absolutely could not survive outside the cell on its own, and relies on signals from the cell (mainly, the cell's energy needs as detected by "sensor" proteins to key molecules like glucose and ATP) to reproduce.
Therefore, it is most appropriate to think of mitochondria simply as another organelle, just like the endoplasmic reticulum, lysosomes, or the nucleus. It doesn't make sense to think of those other structures as "alive" or "dead", just as it doesn't make sense to think of mitochondria in the same way. Yes, they used to be independent, but are no longer; instead they are a well-integrated part of the whole cell.

My thoughts exactly. Though here's an interesting observation: individual human cells are alive, but individual human organs are not. Both are constituent parts of the human organism, and individual cells are even strongly dependent on the rest of the body. Our individual cells have evolved from their ancient independent forms into the super-symbiotic system of the modern body. They form structures (organs) which are not alive, but those structures combine to form something that is alive. The longer I stare at this strange system, the less inclined I am to care about the definition of life.

So, long story short, they are no more "dead" as a part of a cell, than, let's say, liver as a part of human body? Do I get your meaning right?

@Mołot correct. We don't think of the liver, or spleen, or lungs as "alive" or "dead", and it doesn't make sense to think of organelles in that regard as well.

Short answer: According to the definition of life, yes, Mitochondria are "dead".

To be considered alive an organism must meet the following criteria:

organized structure performing a specific function
an ability to sustain existence, e.g. by nourishment
an ability to respond to stimuli or to its environment
capable of adapting
an ability to germinate or reproduce

Are Mitochondria organised?
Yes, they have a structure that allows them to metabolise energy brought to it by the cell.
Can Mitochondria sustain their own existence?
No, many of the genes that mitochondria need to function are no longer in the mitochondria. They need the host cell to provide much of what they need for them.
Note that I am pointing to the Mitochondria's genetics. They used to be included in the Mitochondria itself and have been moved into the cell host DNA. This is why I consider them to be "dead" because they are no longer their own organism, they are an organelle that helps the cell stay alive.
We can stop here since this disqualifies Mitochondria from being considered alive. However, for completion, I will continue.
Can Mitochondria respond to stimuli?
Yes, in order for it to divide it receives signalling from the cell. I would consider this a response to its environment.
Can Mitochondria reproduce?
Yes, their reproduction is much like a bacteria reproduces - through a process called fission.

Conclusion: Since Mitochondria cannot sustain existence, alone (thanks to no longer holding their full genome) they are dead.

This question seems like a (meaningless) exercise in semantics. By this logic, then my skin and heart are "dead", since they can't sustain their own existence.

The issue I am having is that it seems like you have gone from "Not alive" to "Is dead". Are all things that are not alive dead?  Eg the sun is not alive, but I would not call it dead. A spoon is not alive, but also not dead  (Also Cthulu :-P).
I feel like to be dead you means be "not alive" and also "previously was alive."
(whether previously alive refers to individuals or not I am not so sure.)

-1. By your logic, parasites such as tapeworms (which can't survive outside their hosts) are dead.

@Oxinabox Btw.. I can argue that sun is alive :P.. It is self sustaining and perhaps will some day die.. It is organized and can adapt to stimuli (at the celestial level of course). Earth is alive too that way.. SolarLunix: Actually every living organism is living only with respect to its environment. Heterotrophs are dependent on autotrophs (but we cannot call them dead, can we)

I do think that "sustain their own existence" is a remarkably high bar, of which I am unaware of any member of any species attaining.  Humans, for instance, do not survive long in the cold vacuum of space without anything sustaining them.  Most every biology text I am aware of recognizes that we live in a network, not in isolation.

Just move one comma in your conclusion: "since mitochondria cannot sustain existence, alone they are dead". Inside cells, on the other hand, party on. Anyway, I think you're using a definition of "a living organism" or "a form of life" (and even then one has to be generous as regards independence, as others have noted). It doesn't imply a definition of "dead" that is or sensibly can be applied to parts of living organisms.

@Sparhawk but unlike Mitochondria, your skin and heart have the genetics to survive on their own.

@MarchHo but unlike Mitochondria, tapeworms have their full genetics and their offspring can move into a different host. Mitochondria are stuck in the same host lineage from generation 1 to generation infinity.

@SolarLunix That argument is not consistent with the points in your answer.

@Sparhawk I specifically pointed out the genetics as to why they are not able to survive on their own. I made it clearer since the point wasn't obvious. I can edit again if you still think I wasn't clear enough on that point.

@CortAmmon it does seem like a remarkably high bar, but I was t looking at putting them in another place so much as I was looking at them in relation to what they used to be. Because all of their genetics are no longer located within them anymore I don't consider them an organism, just an organelle.

@SteveJessop done, thanks. You made a good point.

@Oxinabox
I think that when talking about biology, you're either dead or alive. anything in between if caused by our lack of understanding. The sun cannot be analysed in the same manner as a plant (if you pick the sun then i would pick any random rock. Is it alive?)
Why isn't the sun alive if it fits all the given criteria except reproduction  - which, if we wanna be picky about it, then mules are dead.
So, the way i see it, the first distinction to be made is whether we are talking inanimate or not.

@SolarLunix If one wishes to look at "what they were" to develop a subjective position on whether they are alive, that is fine.  I just find it important to note that any argument which claims to have declare the livingness or deadness of something to be "case closed" runs into trouble with definitions.  The line between them is not as crisp as we may wish.  For example, instead of "sustains existence," Wikipedia has "metabolism," which a mitochondria clearly has.

The sustain its own existance part is too vague to make sense. Everything requires an ecosystem to sustain it: we can't sustain ourselves without food! Many vitamins, amino acids,  etc. Cannot be made by the human body because we lack genes for that; so are we not-alive like the mitochondrea?

@Sparhawk skin and heart cannot survive on their own. The component cells need things that are made by others. And it's not just a matter of being switched off, as no cell in the human body can make vitamin C, as the gene for that has been moved out to the "host" ecosystem at large.  Out genetics are no longer located within our cells, in exactly the same manner  as SolarLinux points out for mitochondrea.

@JDługosz : "Our genetics are no longer located within our cells..." that is subtle and frightening!

I would like to expand a bit on SolarLunix's post, because the logic used in the conclusion would also mean that endosymbionts, such as https://en.wikipedia.org/wiki/Buchnera_(bacterium), who cannot survive outside their host are also "dead".
I think many of us disagree with that notion, so instead I would say that it's the fact that so many of their genes have been relocated to the nucleus that makes them organelles and thus substructures of the eukaryotic cell and thus "dead".
Ultimately though, I think it's more a matter of semantics, since you could argue that they represent an advanced stage of endosymbiosis.

Agreed. And if we're moved just a few miles (straight up or down) from our environment, we survive just as poorly as various endosymbionts.

That's what I was saying that everyone seems to have missed....

@user2338816 or a few thousand north or south

What a brilliant question for promoting a discussion.  Mitochondria definitely reproduce, they maintain a better energy flow than any other part of the cell, and they maintain a very low entropy state by exploiting that energy flow.  It may not be a textbook answer but being alive really is about decreasing your local entropy by exploiting a flow of energy.  I suspect that mitochondria have ceased to change under the pressures of natural selection, but so what - they have been practically perfect for a billion years.

Jeremy England's hypothesis that life arises naturally as a way to capture energy and dissipate it as heat: https://www.quantamagazine.org/20140122-a-new-physics-theory-of-life/


text:
Is there a schema for how human behavior is genetically determined?
It seem one can distinguish three different kinds of genetic determinism of common patterns of human behavior:

behavior that is directly wired into our nervous system, e.g. face-related mirror neurons and chewing,
behavior that is within reach of operand conditioning, i.e. that is predisposed by certain features of our bodies (and environment) and relatively easily discoverable by exploration, e.g. how to throw something,
behavior that is passed on culturally, e.g. tool use.

Does there exist something like this in the literature?

The standard is to group any phenotypic variance such as variance in behaviour in a population as being caused by environmental or genetic variance. I don't have a good understanding about the difference between your two first points. Brain is a predisposed feature of our bodies causing a behaviour.

I think the nature-nurture issue of human behavior is one on which libraries can be filled. Moreover, this question, if 'schema' refers to "organized pattern of thought or behavior that organizes categories of information and the relationships among them" https://en.wikipedia.org/wiki/Schema_(psychology) this Q is better suited for CogSci.SE. However, even there it will likely be closed given the vastness of the topic. I vote to close here. You may, or may have more luck at CogSci.

We can only observe correlations
Let's just talk about statistics. You can see a correlation between two things only if there is variation for these two things. It therefore, make no sense to look at a single trait that has no variance and ask "is it genetically coded?". The only thing that makes sense is to understand what variables explain the observed variance for the trait of interest. Here, in your question, you are interested in behavioural traits. This answer stands for behavioural traits as it stands for any other phenotypic traits.
What variables could explain variance in a given trait?
To make it easy, let's consider only two variables, genetics and environment. In reality, one should consider other variables such as epigenetic for example. The total variance in phenotype that you observe is the result of the addition of the variance of this phenotype that is due to genetics variance ($V_G$) and the variance of this phenotype that is due to environmental variance ($V_E$) and their covariance ($COV_{GE}$). In other words:
$$V_P≈V_E+V_G+COV_{GE}$$
It is very common to express the phenotypic variance as being the sum of the genetic and environmental variances (and some others such as epigenetic variance). However, you are free to make this partitioning as you feel it useful for you.
Let's investigate those variables a bit further
Of course, $V_E$ and $V_G$ can be further decoupled into a sum of variances (and covariances). And you are free to do the decoupling exactly as you want to. For example $V_E$ could be defined as the sum of the phenotypic variance that is due to variance in temperature ($V_T$), the phenotypic variance that is due to variance in water availability ($V_W$) and the phenotypic variance that is due to variance in the culture of the parents ($V_P$) (and all the covariance). $V_E = V_T + V_W + V_P + ... $
Similarly, the genetic variance $V_G$ can be further decoupled. It is standard to decouple this variance in dominance vs additive effects (relating to the genetic architecture underlying the trait) but this won't be of great help to you. How about talking about variance in the genes affecting brain morphology $V_B$ and variance in the genes affecting hormones concentration $V_H$ and their covariance (epistasis and pleiotropy) $V_G = V_B + V_H + ...$.
Common schema
To my knowledge there is no common schema in how to partition those variances for the specific study of the mechanistic of behaviour. I don't really understand what is the partitioning that you're suggesting in your post but I am hoping that this answer can help you to think further and eventually come up with a satisfying schema.

Thank you for this beautiful answer; it helped me to grasp some key concepts. It's quite difficult to understand my schema in terms of generic variance. It seems that it successively plays a less immediate role: Behaviors in (1) are presumably highly correlated with certain genes, in (2) there is more a dependence on the environment and in (3) the behavior depends on embodiment and situatedness.

The code for a fit phenotype is successively outsourced from genetics to memetics. The genetic code still facilitates the common behavioral patterns, but doesn't fully specify those in the latter groups since they require both an environmental and even a sociocultural context in the case of (3). Behaviors in this category are rather developed over generations, while those in (2) are discoverable within a lifetime (mostly before adulthood).


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Are there any mammals whose males can feed with milk?
Are there any mammals whose males can feed the offsprings with milk from the breasts?

@GriffinEvo: Birds are not mammals, meaning the question may still be valid.

See the answer to the question, it covers mammals too. @ChrisStronks

I edited the title of the linked Q so that it is clear that it also covers mammals.


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Why do teeth decay of sugar?
Sugars is a common component in diet of mammals. Why then their teeth did not develop resistence to sugar decay?

The reason for the decay are ever evolving bacteria, which happen to be very hard to overcome, even nowdays. There is a lot of research centered towards protein interactions, even mapping whole interactomes, which would help us get rid of decay, yet naturally our system wasn't able to evolve as fast as technological advances, but bacteria did.


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A Hadeeth on the fly
I think most biologists here on this site will not  consider my question below to be unfit for posting on Biology SE.
I came across this article about the hadeeth (a hadeeth is a saying of the Prophet Muhammad (peace be upon him)) on a fly:

"If a housefly falls in the drink of anyone of you, he should dip it (in the
  drink), for the one of its wings has a disease and the other has the cure of
  the disease." [Bukhari, vol. 4: 537].

where an attempt is made to show the truthfulness of the hadeeth with an experiment: they dip a fly into water in a petri dish wholly and partially in another petri dish and different kinds of bacteria appear in each petri dish. This experiment is carried out 3 times and results are different in each round. (Please, read that article thoroughly before answering) I want to know biologists' point of view on that experiment, i.e.
Do you believe this hadeeth based on the experiment? (i. e. do you consider it to be pseudoscience or not? If yes, please provide your proofs.)
Can pathogenic bacteria arise in such an impressive quantity in water just by dipping fly into water? If yes, could you explain how?
Do you agree with the notion in the hadeeth 'he should dip it (in the drink)?
Thanks very much for your answers in advance!

Can you explain what hadeeth is, for those who do not know?

@kmm I have added the explanation.

It would be a good idea to summarize the experiment here in the text of your question, rather than just linking to a report of the experiment.

@DeNovo I edited it a bit.

Please read the guidlines about asking questions on this site. When your question involves asking whether people "believe" in assertions in religious texts (whether or not based on published peer-reviewed work) or agree with notions in religious texts, you are clearly asking a subjective question. Such questions are, I am afraid, most definitely off-topic here.

I think most English speakers would be more likely to understand the spelling "Hadith".  That said, it would improve the question if you just explained what the claim in the Hadith is, rather than expecting people to follow links or do research.  Even then, I'd expect it to be unsuitable for this site.  Perhaps the Skeptics site would accept it?

@Martin Klvana: Who says it's a metaphor, and not a statement meant to be taken literally?  Other than people trying to defend the claims of their particular religion, of course :-)

'The text no doubt has many interpretations. For a start, petri dishes were a different technology 1300 years ago, so it depends on what kind of petri dish. Agar for example is a kind of sugary jel which has been raised above 100'C, I dunno who in the arabic world knew that kind of biotechnology. perhaps add to the wiki page on petri dish history.

@Martin Klvana: The Hadith aren't really philosophical texts.  They are simply people's recollections of the words and actions of Muhammed, collected after his death.  See the Wikipedia article as a start: https://en.wikipedia.org/wiki/Hadith

@Martin Klvana: That is simply not true.  There are many, perhaps most, myths which simply aren't true, from the myths about various gods (what we normally think of as myths) to the stories about George Washington and the cherry tree.  The Hadith are not myths: the closest modern-day equivalent would be oral history projects.

What about Articles #1 to #4 on http://www.answering-christianity.com/hadiths_of_the_fly.htm concerning the hadeeth.  Maybe those can serve as evidences?

Rephrasing your question
Allow me to start by saying that I barely know the term Hadeeth / Hadith mean. Of course I have checked on wikipedia but its definition is vastly unrelated to any concept in science. I think it won't be necessary for me to use this term, I will use a more classical, scientific terminology. As I barely understand the term, I do not really understand your question phrased as

Do you believe this hadeeth based on the experiment?

I can however answer to the questions

Is this document a fair description of a natural phenomenon?
Is this document contribute to our understanding of a scientific phenomenon?

The answer to both of these questions are "absolutely not"!
Lack of methodology and definition of the expectation
The document is extremely unclear, provides a very poor description of the methods and does not provide any suggested interpretation of the results. After reading it several times, I have little idea what the treatments are.
Note that this document is not peer reviewed and does not follow an appropriate format (no introduction, no method section, just a religious quotes, a citation from the Quran and images with a vague legend). It is just a document that someone wrote and uploaded online.
As @BryanKrause perfeclty said in the comment below

[I]n science the burden is on the person making a claim to defend it and provide appropriate support - there is no point in proving a claim true or false if it lacks documentation of the methodology. Being poorly written in terms of lacking adequate description is hardly better than lacking any experiment at all

In short, this document does not make any contribution to our understanding of a natural phenomenon.
The claim is very unlikely to be true
The expectation implicitly suggested to be tested is something like (my own phrasing)

If a fly barely touch (with one wing only) the media, then the media will be full bacteria but if the whole fly (with both wings) touch the media then the media will remain clean.

This expectation is highly unlikely to be true. If it were to be true, it would probably lead to a major revision of our understanding of microbiology or of the biology of flies (whichever species is considered)! Also, there is no reason to expect that in some petri dish only one bacterial species would have invaded, while in another only another bacterial species. Also, the pictures don't really match what the species described IMO. Hence, if the authors claim that this document report the results of a scientific experiment (I am not saying they make this claim), then I very much think this is a case of scientific dishonesty or at least a case of very poor understanding of how to perform a scientific experiment.

I used the term 'Hadeeth' meaning a 'saying'. I agree that the document is poorly written (lacks description).

@Tug'Tegin It is not only an issue of the phrasing however. Please consider reading my edited answer.

@Tug'Tegin An important part of this answer that isn't made completely explicit is that in science the burden is on the person making a claim to defend it and provide appropriate support - there is no point in proving a claim true or false if it lacks documentation of the methodology. Being poorly written in terms of lacking adequate description is hardly better than lacking any experiment at all.

While I sometimes wish I could down vote some comments, I would wish I can double upvote @BryanKrause comment!

I wish there were more people like Abdus Salam among Muslims.

Some may (rightfully) disagree with my phrasing of the expectation (but I had to write out an expectation as the document does not offer any). That being said whether or not the expectation is met in an experimental set up and what it means for the islamic faith is of course not to be discussed on a science website.

You can read Articles #1 to #4 on http://www.answering-christianity.com/hadiths_of_the_fly.htm concerning the hadeeth. Maybe those can serve as evidences?

Diseases and infections carried by house flies include, but are not limited to:

typhoid
cholera
dysentery
salmonella
anthrax
transmission of the eggs of parasitic worms

Of these, exactly zero have been shown to be cured or in any way influenced by flies in a positive sense.
And, of these, exactly zero have proposed mechanisms (however outlandish the claim) of treating or curing any one of the above-mentioned diseases.
To paraphrase, there does not exist a hypothesis, nor an experiment, nor evidence for the claim. It is entirely and scientifically unsubstantiated.

On a less scientific note: it's clearly and demonstrably unwise to assume that there is any prescient scientific validity in this claim. It reads and sounds like a metaphor, perhaps somewhat along the lines of what doesn't kill you only makes you stronger. Taking metaphors literally is a very erroneous mistake to make, and unfortunately this error is a dead giveaway of exactly how shallow and uninspired one's interpretation of a religious text is. I don't think it's unreasonable to say that such an interpretation today would be a bastardization of the text. My two cents!


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Phytomass and photosynthesis
I have been introduced to the term "phytomass" and I was wondering if phytomass can be both photosynthetic and non-photosynthetic?

"Biomass is defined as live material, necromass as dead, attached material.
Biomass + necromass form the "standing crop" or phytomass." (from https://link.springer.com/chapter/10.1007%2F978-3-642-68786-0_22)

But even if we were only talking about biomass, there is only a loose correlation between that and photosynthetic activity -  think about single-celled algae, where 'every' cell is photosynthesizing, versus trees, where most cells are non-photosynthesizing, and there may even be times where none are (in trees that loose their foliage in winter).

Oh I see. Is true though that phytomass has both photosynthesising and non-photosynthesising components (with the majority being non-photosynthesising)?

That depends on what those 'components' are - if you are counting cells, the answer is a clear yes, if you are counting organisms the answer would be no, and if talk about mass, i don't know.  - 'Phytomass' and 'biomass' are both in need of a qualification if you are going to use those terms - 'biomass' might also be the sum of all living organisms, and is also sometimes used for some types of harvest (plant matter for instance), where the 'bio' only refers to the formerly living state of the matter...

.. also note that in my answer - citation the phytomass only comprises 'attached' dead material, whereas sometimes it can also comprise all dead former plant material.


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Light/Heavy Isotopes in Living Organisms
I was wondering, why are lighter isotopes (e.g. carbon-12 as opposed to carbon-13) preferentially used by life on Earth? Is their increased stability the only factor?
Thanks in advance!

99% of carbon is carbon-12, so it makes sense that it would incorporated by life in higher abundance. Perhaps I don't understand your question.

I appreciate your response, but I think my question is poorly phrased. I am trying to understand why a negative carbon isotopic signature is suggestive of life. For example, if the carbon isotopic ratio of the methane detected on mars was showed to be more abundant in carbon-12 than carbon-13 (negative value), why is this suggestive of life? Do living systems prefer lighter isotopes? We only have Earth as a suitable analog, but is the a biologically reason why this is (and not merely a question of abundance)? Thanks a lot :)

Hi Julian, interesting question. I look forward to reading a response.

I had never heard of this before, but after a bit of searching I think I found what you are referring to. I believe this Wikipedia article should answer your question. This is definitely out of my field, but I may try and formulate answer if someone more knowledgeable doesn’t come along. Interesting question!

Thanks for you help! I look forward to reading an answer.


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What are different firing rates in different regions in the human brain?
Could it for example be that neurons that are concerned with high-order thought and medium-term planning fire more slowly, or is it expected that all neurons rather fire more or less at the same rate?
Here is an article on the average firing rate: http://aiimpacts.org/rate-of-neuron-firing/
Is the assumption that the measurements tend to be biased by accounting only for visually responsive cells warranted?

The article, has a classical engineering approach (might be wrong I just skimmed it), not that it's a bad thing. The general criticism of bias against sparsely coding neurons is correct, don't know how they can say its a factor of 10 or anything else though.
Average firing rate of one neuron only makes sense in relation to a different condition. For example in sensory neuroscience studies, we say a neuron likes a stimulus if the average firing rate of this neuron while the stimulus is presented is higher than in an equal period in the absence of the that stimulus. Conversely a neuron dislikes a stimulus when the average firing rate goes down.
Average firing rate across all neurons also is a weird measure as neurons have different baseline firing, different morphologies, are part of different circuits and have different functions in these circuits. It would be like saying that the average of a normal distribution is enough to describe it ignoring its variance.
Regarding the question itself a couple of things should be better defined: what is higher order thought? and medium time planning of what?
Neurons certainly do not all fire at the same rate, however rate implies a time constant and most importantly when one averages across multiple neurons one must have a criterion of selecting them which begs the question: Which neurons? How does one defines an area of the brain? Morphologically? Functionally? Genetically? Furthermore, what is its relevant time constant? These seem like basic obvious questions however they don't seem to have a clear and defined answer yet.
You seem to have a particular architecture in mind with multiple areas that have different functions, I assume you are modeling it. All models are wrong (yeah yeah I know its a cliche) which is to say that every model has a particular set of more or less valid assumptions. You just have to know what these assumptions are and what you can conclude given these assumptions. So basically there isn't really an answer to your question from the biology side we're still blind scientists in a dark room looking for the brain dead cat that is hiding the light switch.
Once I figure out the function of an arbitrarily defined brain area I'll let you know its time constant, then again it is arbitrarily defined and I cannot possibly figure out its function in all possible conditions without having assumptions of my own of how things should work...


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Understanding Illumina Adapters
I am currently working on a project where I need to trim the adapters off of some single end read RNA-Seq data, and I want to know which sequences to cleave.  Illumina TruSeq adapters were used.  I have tried following Tuft's explanation and make sense of Illumina's video, but I am left with several unresolved questions.
The TruSeq Universal adapter, seems to be what binds to the flow cell and is
AATGATACGGCGACCACCGAGATCTACACTCTTTCCCTACACGACGCTCTTCCGATCT

The TruSeq Adapter Index N is
 GATCGGAAGAGCACACGTCTGAACTCCAGTCAC-NNNNNN-ATCTCGTATGCCGTCTTCTGCTTG

My impression of how the cDNA fragment attached to the adapters is :
(flow cell)
||
||
||                                             (Index Adapter)                                               (Universal Adapter)
||    3'                                                                5'                          3'                                                        5'
||    GTTCGTCTTCTGCCGTATGCTCTA-NNNNNN-CACTGACCTCAAGTCTGCACACGAGAAGGCTAGA                           TCTAGCCTTCTCGCAGCACATCCCTTTCTCACATCTAGAGCCACCAGCGGCATAGTAA
||                                                         ||||||||||||||                           ||||||||||||||                                                              <----- Must get denatured!
||        5'   AATGATCGGCGACCACCGAGATCTACACTCTTTCCCTACACGACGCTCTTCCGATCT--(5' MY DNA FRAGMENT 3')--AGATCGGAAGAGCACACGTCTGAACTCCAGTCAC‐NNNNNN‐ATCTCGTATGCCGTCTTCTGCTTG
||-------------TTACTAGCCGCTGGTGGCT                                     3'                           5'                                                                3'
||
||             ^(Flow cell oligo)              ^(Universal Adapter)                                            ^(Index Adapter)
||
||                                     TGTGAGAAAGGGATGTGCTGCGAGAAGGCTAGA                           TCTAGCCTTCTCGTGTGCAGACTTGAGGTCAGTGTG
||
||                                             ^(Read 1 Primer)                                                ^(Read 2 Primer)
||
||
||                                                                                TAGAGCATACGGCAGAAGACGAAC----------||
||
||                                                                                ^(Flow cell oligo)
||

Here are my questions :

Is this image correct in the single stranded case?
Do I have the correct primer binding site (used for the actual sequencing)?
Do I have the correct oligo for paired end reads, i.e. TAGAGCATACGGCAGAAGACGAAC---------?
Do I have the correct primer (and it's site) for the index read?

 Per Illumina, I guess I need to include this :
"Oligonucleotide sequences © 2007-2013 Illumina, Inc. All rights reserved. Derivative
works created by Illumina customers are authorized for use with Illumina instruments
and products only. All other uses are strictly prohibited."


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Why do soap molecules not break down your skin cells when you wash your hands?
Soap molecules are similar in structure to phospholipids and interact with the cell membrane.  They can clearly cause damage to the cell membrane.
If this is the case, why then, does soap not break down your skin every time you use it?  The skin cells, keratinocytes still have a membrane, so wouldn't soap attack our skin in the same way it does to plant cells and cause deterioration?

You know skin has really complicated structure. It really depents on what do you mean by break down skin. Did you mean by this something like tear it a part ??

@L.Diago I think this is an interesting question. Soap destroys lipid bilayers. What structures/mechanisms exist in the skin that prevents the destruction of our own cells?

@James i just want to know what did he mean by break down your skin. If he want to know why does his skin is not damaged after he used soap i rather recommened to study some basic anorganic and organic chemistry.

Still it is not biological problem rather chemistry problem. By chemical point of view its just a combination on neutralization of pH from NaOH, and saturation of fatty acid by NaOH.

@James wouldn't that just be the top layer of your skin, the epidermis, which has keratinocytes that cover your skin with keratin protein so that things like soap don't reach the cell's membrane.

@LDiago it's exactly a biological problem (how does soap interact with mammalian skin). If you want to be reductive, you could say any biological problem is either a physics problem, a math problem, or both.

The outer most layer of the mammalian epidermis (cornified layer or stratum corneum) is composed of 15-20 layers of dead cells called corneocytes, which are basically dead keratinocytes filled with keratin intermediate filament cross-linked other proteins as well as some lipids. As keratinocytes differentiate into corneocytes (a process called cornification), the plasma membrane is replaced by what is called a conified envelope which is composed of cross-linked structural proteins and some lipids (more details in here).
Surfactants in soap do interact with components of the cornfield layer such as keratin but not in the same way they would with the lipid bilayer of a typical plasma membrane. Outcome of such interaction depends on the kind of soap as well as amount and duration of application among other factors, but even a normal soap, upon normal use on a normal skin, may cause some keratin denaturation. But the cornified layer is actually continually shed (process called desquamation) and replaced by keratinocytes that proliferate in the inner most layer of the epidermis.
You can find more details on effect of detergents on skin here and here. You can also find useful info on skin structure here and here.

So is the answer that soap does break down your skin, but just a little bit and it gets replaced quickly?

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2674689/
"The SC [stratum corneum] consists of corneocytes, keratinocytes that have undergone terminal differentiation, surrounded by a neutral lipid-enriched, extracellular matrix composed primarily of ceramides, cholesterol, and free fatty acids. The hydrophobic extracellular lipid matrix provides the principal barrier to the transcutaneous movement of water and electrolytes."
The keratinocytes have an extracellular ground substance that basically bar things like soap and water from diffusing/otherwise entering the body; this is even a part of our innate immune system.
The answer then is the keratinized stratified squamous epithelial extracellular matrix.


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Is CRISPR being utilized when scientists use the CRISPR/Cas9 system to edit genes?
"CRISPR" and "Cas9" are different things. When a virus attacks a bacteria, the bacteria stores the viral code of the virus in CRISPR. And when the virus attacks again the Cas9 protein uses the RNA in the CRISPR to find the viral DNA and then destroy it.
So, what is the use of CRISPR when scientists use the CRISPR/Cas9 system to edit genes, as we have already given the Cas9 protein a guide RNA?
Sorry if this is a stupid question, I am new to genetic engineering and couldn't find the answer on google.

I might be wrong here. But, when a virus attacks a bacteria, the bacteria stores the viral code of the virus in SPACERS and not CRISPR. 'Spacers' refer to the segments of DNA between the CRISPR.

Figure 1. Process of bacterial immunity mediated by CRISPR/Cas9. Scissors are Cas9 enzyme, black diamonds are CRISPR elements in DNA.
As suggested in the comment, there are some subtle differences here. Cas9 knows where to cut based on the spacer (the colored squares). That serves as a guide to the enzyme through sequence complementarity of the transcribed spacer RNA in the crisprRNA (crRNA, shown as the squiggled black line with a green piece).
The crRNA itself is composed of the spacer and also a transcribed CRISPR repeat (black diamonds), which form the structural hairpin of the RNA molecule (the squiggly black piece) that allows Cas9 to recognize it as a crRNA. Otherwise the spacer would just be a random little piece of RNA floating around the cell; with a full mature crRNA Cas9 knows how to bind to both the crRNA and the spacer-defined target to do its cutting.
To directly answer your question then, the crRNA is the guide RNA. You have a CRISPR (or CRISPR-like) sequence already in there. It doesn't exist in the array named as CRISPR in bacteria, but the functional component allowing the enzyme to bind and then recognize the target exists in there.
It's a little more complex than that in the actual organisms, if you have more questions I recommend reading more on wikipedia.