text:
Genetic mapping problem
A prototrophic Hfr strain of E. coli with the genotype trp+ purB- pyrC+ is conjugated with an F- strain with the genotype trp- purB+ pyrC- . The trp gene is known to enter last. The following numbers of recombinants were isolated:
trp+        purB-    pyrC-       [0]
trp+        purB+    pyrC+       [44]
trp+        purB+    pyrC-      [132]
trp+        purB-    pyrC+      [224]
Draw a genetic map that shows the order in which these genes are arranged and the distances between them.

I started off by making these assumptions:
trp+        purB-    pyrC-       0  (the lowest #, must be double recombinant(DC)
trp+        purB+    pyrC+       [44](must be single recombinant(SC)
trp+        purB+    pyrC-      [132](must be single recombinant(SC)
trp+        purB-    pyrC+      [224](the highest #, must be parental(P)
Now since i know which one is DC and which one is P I can find the middle gene:
trp+        purB-    pyrC+  (224)- P
trp+        purB-    pyrC-  (0)-  DC
The only gene that varies is pyrC thus PyrC is the middle gene.
Consequently, the distance from trp-->PyrC=(DC+SC)/400=(0+44)/400= 0.11 or in map units it becomes 11
similarly, the distance from pyrC->pur B=(0+132)/400=0.33 or 33 m.u.
and here's the part im confused about: I only have 1 parental and i cant make the cross to figure out which is  trp-->PyrC and which is  pyrC->pur B. Even though i'm confident i got the right numbers how do i figure which one is 11 and which one is 33???
ps: I know it's a silly question after solving 99% of the problem it just that im used to do mapping with 2 parentals that i get lost when there is only 1 parental.

EDIT:
I actually figured it out, its not a regular genetic mapping problem but the bacterial genetic mapping(in particularly High resolution mapping). Thus, all the steps above are correct and answering my own question the way to figure out which direction it goes is just to compare the parentals given:
trp+ purB- pyrC+

_X_____X____X___
trp- purB+ pyrC-
(NOTE: ignore the trp minus since we solve for it)
doing the crossovers will yield the same results listed above,its just that it's more precise way to know which one is trip --->pyrC and which one is pyrC--->purB
PPS:SMC Bio 22 students doing problem set 1 in the future, you can thank me later.

I actually figured it out, its not a regular genetic mapping problem but the bacterial genetic mapping(in particularly High resolution mapping). Thus, all the steps above are correct and answering my own question the way to figure out which direction it goes is just to compare the parentals given:

I edited the answer and the solution is on the bottom now


text:
Absorbed dose from a CT scan with relation to radiation accidents
I read somewhere that the average CTDIvol in CT scans at hospitals is ~40 mGy. This translates to the 'radiation intensity' at the center of the person, and can also be roughly interpreted as an 'absorbed or equivalent dose', but this is not the organ specific absorbed dose.
From medical literature, particularly the life span studies of RERF,  I read that at 2500 meters the 'absorbed colon dose' was about 5 mGy [1].
Out of curiosity, I tried to figure out at what distance you would have to be from the epicenter of Hiroshima, to get the same level of 'absorbed colon dose' as the average CT Scan.
To convert, the ~40 mGy to 'absorbed colon dose', you use a tissue weighting factor [2]. The tissue weighting factor for the colon is 0.12. So, this means, the average CT Scan results in an 'absorbed colon dose' of ~40 mGy * 0.12 = ~4.8 mGy.
I realize there is a different concept of 'effective dose' that calculates risk of cancer based on organ type and organ weight scanned. That is not of interest for my calculations.
As far as purely 'absorbed dose' of the organs is concerned, is it accurate to say that the the average CT scan has the same effect on a person's organs as it would to someone standing just outside 2500 meters from the epicenter of Hiroshima?
[1] http://www.rerf.jp/general/qa_e/qa2.html
[2] https://www.euronuclear.org/info/encyclopedia/t/tissue-weight-factor.htm

Good question, maybe one for the Physics Stack Exchange site? If I was standing 2.5km from the epicenter of Hiroshima the effect it would have had on my organs (especially my colon) would probably result in them emptying themselves. CT scan doesn't seem to do that... Usually. :)

source: Stack Exchange

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sort: votes


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In the context of heterotrophic theory of abiogenesis, what is an organism that eats other organisms called?
In the heterotrophic theory for the origin of life, we imagine a primordial soup that is rich in organic compounds and the first organisms emerge eating those compounds. Since these organic compounds are external to this early organism, this early organism is a heterotroph. But it is not like any current heterotroph since it doesn't eat other organisms or their byproducts. Is there a special name for this 'type-0' heterotroph?
At some point, some organisms emerge that eat other organisms (i.e. eat those 'type-0' heterotrophs that are already around). These new organisms are more like the standard heterotrophs of today. Is there a special name for this 'type-1' heterotroph?
I am looking for the terminology that distinguishes the heterotroph that eats only organic compounds that are non-organisms in the primordial soup ('type-0')  versus the heterotroph that eats other organisms ('type-1').
Normally, I could call the 'type-0' a primary heterotroph and the 'type-1' a secondary heterotroph. But we usually think of primary heterotrophs as things that eat autotrophs and at the start of the heterotropic theory, there are no autotrophs to eat. The primordial soup of the environment itself is the 'producer'.
If there is no standard name, would it be strange to call the 'type-0' heterotrophs as 'nullary heterotrophs' and the organisms that eat other organisms as 'non-nullary heterotrophs'?

@Artem, it's been a while! Good to see you back on Biology.SE.
I doubt that any rigorous terminology exist to describe these "type-0 heterotrophs" living on "non-organismic" organic compounds.
You might be assuming that early organic matters can naturally be categorized as being fundamentally alive vs fundamentally non-living. It is more a question of philosophy of the definition of life than anything else but, to my experience, most authors who wrote about the definition of life tend to consider early life as a spectrum from "definitely not living" to "definitely a living thing". The existence of this spectrum questions the need for the terminology you are looking for.

Actually it can, but most authors just wants to grant a safe passage for themselves just in case some later experimental evidence shows their hypothesis as being wrong by assuming there is no such thing as a clear distinction between life and non-life. The fact is that such a distinction CAN, in reality, be made if you have a sufficiently advanced understanding of what Life is vs. what it's not, but since we don't have enough evidence for it people just like to assume such a distinction is impossible in both principle and reality.

I just wish to add that the core of the problem is the fact we don't have a complete theory addressing the Life/non-Life border cases and this is why we don't have either proper terminology to address the distinction between a living and non-living entities, nor do we know is the distinction between living and non-living matter a spectrum or clear cut point. The reason too many researchers like to, as I said before, assume it's a spectrum is because that's the risk-aversion scenario for many of them and in such way they can save face if their hypothesis turn out to be incorrect.

If you are a researcher in the field and you know there is a high chance of being incorrect you would prefer to use blurry terms and "a spectrum" vs a clear-cut line because you put less of your reputation in stake if proven wrong, won't you? But that's secondary, to an extent-anthropomorphic feature which doesn't equate with physical reality. And that reality is that the chances of Life being clearly defined and of being a spectrum of characteristics are just about equal. However, that's too much for most people to stick their necks out and claim they can pinpoint it, that's why you will

find most people talking about spectra instead of a number of clearly definable traits to distinguish a living organism from non-living entities. And that's something you will very rarely find mentioned in the papers themselves, this is why I felt like I needed to elucidate the point in the comment section. So you may now appearances can be deceiving and there is the possibility people would just prefer to talk this way in order not to make claims they can't prove, even if said claims can turn out to be reality.

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Is setting high mismatch and gap penalties sufficient to distinguish perfectly mapping reads?
I have a fat pile of 125bp whole genome shotgun reads that have undergone quality control, and I would like to pull out just those reads that do not map perfectly to the genome. When I set extremely high penalties for mismatches and gap opens/extensions (with bwa mem -B 1000 -O [1000,1000] -E [1000,1000]), it looks like the alignments for perfectly mapping reads are shown, and the rest of the reads are reported as unmapped. If this is true, I could then pull out the unmapped reads with samtools -f 4.
Are there any holes in my reasoning here, or will it work to discard all of the reads that map perfectly to the genome?

The short answer: No, setting extremely high penalties (100 or 1000) does not seem to work. I'm not sure why.
The medium answer: Since I posted the question, I did a bit of exploring, and it looks like the reads that perfectly match are the reads that are not soft clipped and that have an edit distance of zero, as indicated by the CIGAR string and NM tag, respectively.
The long answer: See https://standage.github.io/how-to-distinguish-perfectly-mapped-reads-from-a-sambam-file.html.

The preferred way is to map normally and then filter out imperfect matches downstream:
bwa mem ref.fa reads.fq | perl -ane 'print if /^@/ || ($F[5]=~/^\d+M$/ && /\tNM:i:0/)'

Changing the scoring scheme hurts mapping accuracy.

"Changing the scoring scheme hurts mapping accuracy." This is a concern if you want to keep all of the alignments around for other purposes, but is a non-issue if I only want to distinguish perfectly mapped reads vs imperfectly mapped.

I used to consider myself quite the Perl-slinger (I code mostly in Python these days), but I never knew about the -a flag. That's a game changer! +1

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What makes diffculty to make a human bio-tooth compare to a mouse's?
Some time ago I read a news article that said a bio-engineered tooth based on a mouse's would be available around 2015. There was some research about it at King's College in the UK, and many other institutes.
Now, I haven't heard any news that such a thing is available. It seems to be a basic result of stem-cell research, how much difference can there be between a human's tooth and a mouse's?

So what is your question - When will a bionegineered tooth be available? or What is the difference between mouse's tooth and human's? These two questions should be asked seperately in different posts

@TanMath - these two questions are likely very much related, as preclinical animal work typically precedes human stuff. This seems fine.

@AliceD but I find that asking about the difference of two animal's teeth and when bio-teeth are available as two questions that should possibly put in two seperate posts..Plus, this question seems opinion-based as well...

Thanks AliceD, anyway I will write more clearly next time.

I believe you're referring to this 2013 announcement from King's College, Biological tooth replacement -- a step closer. So called "BioTeeth" are sought after because

Current implant-based methods of whole tooth replacement fail to reproduce a natural root structure and as a consequence of the friction from eating and other jaw movement, loss of jaw bone can occur around the implant.

However, Professor Sharpe identified the following obstacle:

What is required is the identification of adult sources of human epithelial and mesenchymal cells that can be obtained in sufficient numbers to make biotooth formation a viable alternative to dental implants.

For some background, consult Biological tooth replacement (2006; Sartaj, Sharpe)
Unfortunately the 2013 article was the last I heard of it - possibly for the aforementioned reason. If you're really interested, you might consider attempting to contact Professor Sharpe yourself.

Thanks for your link and information about obstacle, jzx.

I don't think there is necessary for making "Bio-teeth". It should be more expensive and without any advantage comparing the ceramic teeth or others...
The different between mouse and humans teeth is that mouse' teeth, like toenail, will keep growing, thus they need to shave their teeth all the time. That is the reason they are always eating, and like to bit some stuffs even are not food. But humans teeth stop growing and cannot grow back once broken. There is no point to make a Bio-tooth for mouse. But for human, for the economy point too, there is no reason to make a Bio-tooth..... I can't image any advantage for making Bio-teeth

Thanks for your great explanation about the difference. I wanted to know why the research was difficult even though it was successful on mouse long time ago. Because the bio-tooth has a root structure, I believe that it can be on the ligament instead of directly connecting to jawbone like an implant. At least, wouldn't it reduce the pain when an implant is being installed in gum?


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Learning tensors for evolutionary or developmental biology
I'm looking for book recommendations on tensor algebra for use in biology.
Tensors are being used increasingly in evolutionary biology and developmental biology, it seems.  For example, here is an example of an empirical study that makes use of tensors in its analysis of data: http://rspb.royalsocietypublishing.org/content/282/1819/20151119
There are lots of books on the mathematics of tensors, and many introductions online.  So far, what I have found is that either (a) the presentation is heavily oriented toward physics applications, or (b) the presentation begins from an abstract algebra (or category theory?) point of view.
I'm willing to work through physics-style or abstract algebra presentations of tensor concepts and methods, but I am wondering whether there are any textbooks or other introductions that someone would recommend for biological applications.
(I have read the brief appendix on tensors in Sean Rice's book Evolutionary Theory.  Although I've found his other mathematical appendices and most of the mathematics in the book accessible, the tensor material in the book is too brief for me--I need more.)

The field of tensor decompositons has been discovered in many fields simultaneously, each with their own notation. Many modern notation in fields like CS or STAT have originated from the work of Tamara Kolda
http://www.kolda.net/publication/koba09/
However, this is restricted to the CP and Tucker decomposition, and we have many others now. See
https://arxiv.org/pdf/1609.00893.pdf
and
https://arxiv.org/abs/1708.09165

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Why are mice with a single X chromosome and no Y chromosome males?
I was searching online and I read this article Mice can be male without Y chromosome and this is a part of it:

The experiments demonstrate that there are multiple ways to make males, says Richard Behringer, a developmental geneticist at MD Anderson Cancer Center in Houston. “They’ve done it without any Y chromosome gene information,” he says. “There’s not even a sniff of the Y around.”

I know that mouses are separated to males and females, and they both necessary for reproduction. Can someone please explain to me how could this possibly be? there's a lot of biology specific terms that i did not understand well

Welcome to Biology.SE! You might want to change your title into Why are mice with a single X chromosome and no Y chromosome males?. For the moment the title is really vague.

Definitely, not a duplicate but you might want to read Do males of all sexual species have Y chromosomes? out of curiosity.

might be good to note that in fruit flies the ratio of X to autosomes determines sex, females can carry a Y if they have two X's as well and males can be XO

@Remi.b I change it as you said

@rg255 is that really possible! i didn't know that before

as seen in the methods on this paper for example

This is also true for drosophila. (Though sex determination in it is slightly more complicated.)

Almost all mammals (including mice and humans) have two sexes where the males have a Y chromosome and an X chromosome (whereas females have two X and no Y chromosomes).  This is not the only way organisms can determine sexes, but it's the way mammals evolved to do it.
So how does having a Y cause an individual to be male?  The Y has only a few genes (less than all other chromosomes), but it has genes that occur only on the Y.  One of these in particular, the one called SRY, is the main gene that causes the individual to develop male characteristics.  It mostly does its job indirectly, by making a protein that affects many other genes on other chromosomes that in turn do the work of building and maintaining the male form.
In the experiments reported by the article mentioned in the question, they managed to cause mice without a Y chromosome to develop many male characteristics.  They did this by faking one or two of the actions of SRY.  One of the many actions of SRY is to turn on a gene called Sox9 (which is on a non-Y chromosome), and it turns out Sox9 causes most of the things that make the male mouse form.
So the experimenters found a way to turn on Sox9 without using SRY or anything else from a Y chromosome.  This got them mice that looked male, but didn't produce sperm.  So they did something further that substituted for a Y chromosome, and caused a weak gene on the X to work at many-times strength to do the job that a strong Y gene normally does.  This caused the special "male" mice to produce sperm.  But these sperm were not fully functional (they couldn't swim and enter the egg), so they showed they were essentially sperm by simply using a tiny needle to inject the semi-functional sperm into mouse eggs and have those eggs develop into viable baby mice.
Bottom line, if you use artificial methods to do what the Y chromosome does, you can make male mice which do not have a Y chromosome (and learn some things in the process).

perfect answer for me! @mgkrebbs thank you s much.


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Is there a free alternative to Gelcompar for comparing banding patterns across multiple gels?
In order to run my microbial community samples from my experiments through DGGE, I was required to use multiple gels.
Thus it is necessary to compare banding patterns across more than one gel.  This means that I need some way of assessing whether the 4th band on gel #1 is the same OTU as the 4th band on gel #2.
The industry standard for this procedure seems to be the Gelcompar software.  Unfortunately this software is greater than $10,000 and is proprietary (thus, not open science friendly).
Does there exist a free (ideally as in speech and beer) alternative to Gelcompar?

Do you have any programming skills? Because ImageJ immediately comes to mind. You'd just have to modify a little the already existing gel tools...

I second the ImageJ recommendation. It's already well setup for gel analysis, and people do use it for DGGE (e.g http://www.springerimages.com/Images/LifeSciences/1-10.1007_s10482-007-9143-9-0)

Here's an ImageJ mailing list entry about DGGE... http://imagej.1557.n6.nabble.com/gel-analysis-td3703740.html

Try this one
Pavel, A. B. & Vasile, C. I. PyElph - a software tool for gel images analysis and phylogenetics. BMC Bioinformatics 13, 9+ (2012).
You can download here
http://sourceforge.net/projects/pyelph/


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Is there a good field methods book that covers terrestrial ecology?
In the past I have used Limnological Analysis by Wetzel and Likens and Methods in Stream Ecology edited by Hauer and Lamberti to develop labs and research methods for courses and projects with an aquatic focus.
These books detail the standard methods of lotic and lentic ecology with some emphasis on utilizing the methods in undergraduate or graduate level courses.
I am now developing a biogeochemistry course that is not limited to aquatic systems and I am looking for a summary of field methods for terrestrial systems.
Is there a book that summarizes terrestrial field ecology methods similar to Wetzel and Likens and Hauer and Lamberti?

I'd be curious to know if the book I suggested (Methods in Ecosystem Science) meets your needs, or if you find an alternative.

Methods in Ecosystem Science edited by Oswaldo Sala, Rob Jackson, Hal Mooney, and Robert Howarth is a classic standard reference used by many (most?) ecosystem ecologists.

Take a look at Field and Laboratory Methods for General Ecology by James E. Brower, Jerrold H. Zar, and Carl N. von Ende.
If you are only interested in plant sampling techniques, an great resource published by U.S. Bureau of Land Management is Measuring & Monitoring Plant Populations by Caryl L. Elzinga, Daniel W. Salzer, and John W. Willoughby.
Another great resource that covers wildlife research and management techniques (2 volume set) is The Wildlife Techniques Manual published by The Wildlife Society and edited by Nova J. Silvy.


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How does cerebrospinal fluid circulate in the central nervous system?
Cerebrospinal fluid (CSF) is produced in the choroid plexus of the lateral ventricles and in the 4th ventricle of the brain.  CSF then circulates through the ventricles of the brain and the subarachnoid space of the meninges.  CSF is returned to the venous system via the arachnoid granulations connecting the subrachnoid space with the superior sagittal sinus at the superior portion of the neurocranium.

What circulates the CSF such that it can return to the venous system against gravity?
In other words, why does CSF not all just pool in the caudal cistern?

There are several points here.
Arachnoid granulations are not the only "sinks" for CSF.
Even though it is true that most of the CSF is eliminated from ventricular system and subarachnoid space through these granulations, there are also suggestions that there are also other potential mechanism of shunting CSF into the venous system:

Cranial nerves leaving CNS go through dura mater and these holes are not sealed, so it is suggested that some CSF can just go along the nerves and then accumulate in the lymphatic nodes in submucus.
Dura mater is mostly perforated at the area of lamina cribrosa, that basically separates the nasal holes and our brain. Leaking through multiple small holes here CSF is accumulated into the lymphatic submucusal nodes, found in abundance here. This way is considered to be primary CSF drainage way in newborns who don't have a well developed granularities in (sub)arachnoid space.
Spinal nerves, especially in the upper part of the spinal cord, also leave unsealed holes and the presence of lymphatic nodes adjacent to the places where these nerves leave the verterbral column also make them a potential place for CSF drainage.

Arachnoid granularitis do not only drain, they are capable of active CSF uptake.
CFS is not just "circulating" here going from the place of its origin in lateral ventricles to venous system. The granularities are here to actively resorb this fluid, meaning that they effectively take it up forming vacuoles and then excrete it to the venous system. Constant uptake leads to the pressure gradient (see also below!) that acts as a driving force for CSF.
Venous system has generally low pressure, thus sucking the CSF up to drainage points.
Speaking about drainage we also should consider the fact that the venous system has a pressure lower than the atmospheric pressure and much lower than pressure in any middle-sized arterial vessels. This is reached by having elastic walls and by transmitting the negative pressure from the mediastinum during the inhale, when the diaphragm and the thorax expand. This negative pressure propagates mostly to the connected vessels, including sinus system. Due to the elastic wall other parts of venous system can accommodate this negative pressure constrict their lumen, but not the sinus system which has a hard external framework formed by dura mater and bones. That is here we can measure the lowest pressure and this is the pressure that sucks CSF in into the venous system.
I hope that answers your question.

Does this mean that a purpose of yawning is to get the CSF flowing?

Perhaps you should add some references.

It is something of a misnomer to speak of CSF “circulation,” particularly in the spinal canal, as there is no continuous loop circulation of CSF as there is in the cardiovascular system.

For quite some time, it has been known that CSF movement results from the formation of new CSF and motion of cilia on the surface of the choroid plexus and ependyma lining the ventricles. - Fluids and Barriers of the CNS

The "circulation" of the CSF, as already mentioned, is something of a misnomer. CSF is not known to "circulate" in the manner of blood. It does get agitated by pressure differentials, and it is 'circulated' in terms of being reabsorbed and replaced every 6-7 hours. Other than that, no circulation occurs.
Blood circulation is not generated only by the heart. Pressure differentials throughout the body affect the circulation of blood as well. One that is easily demonstrated (first documented in 1733) is the effect of intrathoracic (chest) pressure on circulation. The blood pressure of healthy people falls during spontaneous inspiration. When someone takes a deep breath, the blood return to the heart via the vena cava decreases, and pressure is exerted on the right atrium. Both cause decreased filling, which will drop blood pressure. Although this is best demonstrated with a blood pressure cuff, it can be demonstrated without. An unrecommended method is exemplified in a childhood game of passing out. A Valsalva maneuver (deep breath and glottal closure) decreases blood flow to the heart. Squeezing the chest further decreases return, resulting in fainting.
The same pressure differentials agitate the CSF. Additionally, smaller movements were seen with pressure differentials caused by the beating of the heart.

By employing this respiration-induced spin labeling bSSFP cine method, we were able to visualize CSF movement induced by respiratory excursions. CSF moved cephalad (16.4 ± 7.7 mm) during deep inhalation and caudad (11.6 ± 3.0 mm) during deep exhalation in the prepontine cisternal area. Small but rapid cephalad (3.0 ± 0.4 mm) and caudad (3.0 ± 0.5 mm) movement was observed in the same region during breath holding and is thought to reflect cardiac pulsations.

This image from Wikipedia shows "circulation" that normally occurs with heartbeat.

There are other factors that cause movement of CSF, but they are intermittent and variable.
Influence of respiration on cerebrospinal fluid movement using magnetic resonance spin labeling, Yamada et. al., Fluids and Barriers of the CNS 2013, 10:36
MRI showing pulsation of CSF

CSF is actively pumped in an ebb and flow manner by the pressure with our respiratory mechanism transmitted through the pelvic diaphram onto the sacral bone that pulls on the spinal dural membranes attached at S2. Think about it: the pelvic and thoracic diaphragm are linked in a respiratory phasic contraction (confirmed with MRI). The pulling on the sacral end of the dural membranes via the pelvic floor muscle will squeeze the CSF up the spinal canal into the brain with inspiration. This is a much stronger force than any ciliary or cardic induced influence of CSF flow. Recent MRI studies have confirmed this as well.

Circulation of cerebrospinal fluid (CSF) through the ventricular system is driven by motile cilia on ependymal cells of the brain.
Hagenlocher C1, Walentek P, M Ller C, Thumberger T, Feistel K.Ciliogenesis and cerebrospinal fluid flow in the developing Xenopus brain are regulated by foxj1.Cilia. 2013 Sep 24;2(1):12. doi: 10.1186/2046-2530-2-12.

We were talking about humans and not frogs.


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Calvin cycle:synthesis of glucose
For synthesis of one molecule of glucose,six turns of calvin cycle are required.
One molecule of carbon dioxide combines with ribulose bisphosphate (RuBP) to form a stable product of two molecules of phosphoglycerate (PGA). This is called carboxylation. Then 2 molecules of PGA undergoes reduction to form 2 molecules of phosphoglyceraldehyde (PGAL).
My question is whether there 2 molecules of PGAL goes in the regeneration of RuBP or in the synthesis of glucose.

Your question is not clear. "is the reaction stopped at PGAL ... till 12 moleules of it are not produced" --- what do you mean? Which reaction, there are several reactions in the cycle?  Where does your number 12 molecules of PGAL come from?  What do you mean by "are not produced"? Please elaborate and explain.

I have edited the question.

@AliceD@canadianer@James@another'Homo sapien'@Chris. I have edited the question.Please can u specify which part u all have not understood.And a good answer is also given by Roland which answered my question.So I don't get it what u all have not understood

Moderators, I also think this question was closed too quickly. Initially it was unclear, but I think it is now perfectly valid. I'm voting to reopen.

The quick answer is "both", but the stoichiometry is not 1-to-1. The stoichiometry of the calvin cycle doesn't add up when thinking about a single molecules making one "turn" of the cycle. There is only one carbon (CO2) added, but three carbons (in PGAL) leave, which obviously cannot work.
What's happening is that multiple molecules are processed at the same time. The cycle is of course just a set of enzymes that continually catalyze their reactions, so there are always lots of molecules available for enzymes act on, and the cycle doesn't "get stuck" just because things don't add up in a single turn. The "regenerating" steps between PGAL and RuBP produce 3 molecules of RuBP from 5 molecules of PGAL (15 carbons total). Carboxylating these 3 RuBP molecules adds 3 carbons, so that one PGAL molecule can leave the cycle.
The reason for this odd stoichiometry is that the cycle needs to turn 3-carbon sugars (PGAL) into 5-carbon sugars (RuBP), which is rather complicated. Several enzymes work together in a complicated series of reactions to achieve this. A good resource for learning about the details is the MetaCyc database, where you can explore all the molecular details of the pathway.


text:
Synthesis of adenosine diphosphate?
Where does the ADP come from? As in before ADP was made from ATP and visa-versa how is it conceived that they appeared in nature?

You can't synthesize ADP from just hydrogen; it also requires carbon, oxygen, nitrogen and phosphorous.

Cool so step 1, carbon oxygen nitrogen and phosphorous are all created through fusion from products up from hydrogen. That star eventually yields iron and explodes, what happens next?

Adenosine diphosphate is a nucleotide, specifically a purine nucleotide, since it contains a double ring. These nucleotides are synthesized by cells from amino acids and other nutrients in a rather long and complicated biochemical pathway. You can find information about this pathway in any biochemical textbook, or see this page in Wikipedia.

Your answer is inadequate because it assumes the preexistence of the product.

@kpie  No, it doesn't.  The purines are synthesized from simpler building blocks, like amino acids.  I suggest you read up on the biosynthesis pathway.

ATP -> ADP provides energy at several junctures of the pathways you referenced. like you can't synthesize IMP without ATP, and you can't get credit for answering this question without actually answering it. I'm pretty much looking for someone to layout their theories on life and here you are diminishing the question with your ego.


text:
How does the adaptive immune system store information?
I am quite curious about this:

Where and how is knowledge that the adaptive immune system accumulates stored?
What is the "memory size limit" of this storage method if there is any?
Why cant this knowledge be transferred between individuals like we transfer computer antivirus definitions?

Are you thinking of the adaptive immune system? There is also "knowledge" in the innate immune system, in the form of generically coded receptors, but that part is fixed for each individual.

Yes, this question is about knowledge acquired during the life of a person, not present since birth

Welcome to Biology.SE! Although the question is nice, biologists generally don't recommend using such an analogy since both these pictures (of immune system and computer storage) don't superimpose clearly. I'd recommend you first study more about immune system, especially adaptive immune system and HLA.

@another'Homosapien'  I agree the computer analogy is not great, but it could still be interesting to consider information content of adaptive immunity (like the number of possible hypervariable region sequences etc).

@roland that would be interesting, but it would also be problematic to scale this up (which would eventually become necessary). Also, I wanted to first make this sure that the OP knows what stuff we'd talking about while using this analogy.

There is probably no precise answer to this question since, as others pointed out, the adaptive immune system is not really comparable to a computer. That said, here are a some items you might want to look into.
Question 1: the main site of information storage for the adaptive immune system is a special region of DNA in T and B lymphocytes that encodes immunoglobulins, the proteins that these cells use to recognize foreign organisms. The sequence stored in this special DNA region can be rearranged by hypermutation and recombination mechanisms. This occurs early in the life of T and B lymphocytes, so that each cell gets a unique DNA sequence. Those cells that later on happen to recognize invaders will multiply as part of the immune response, and they will later survive as memory cells, so that their specific DNA sequences are retained. If the same infection happen again later in life, these memory cells will help the immune system respond more quickly.
Question 2: the region of DNA used is on the order of 1 million bases long, and it has been estimated that the human immune system can generate around $10^{11}$ different immunoglobulins. How to interpret these numbers in terms of "memory size" is not clear to me though. On one hand, 1 million bases is equivalent to 250 kbytes (each nucleotide base storing 2 bits); but on the other hand, $10^{11}$ as an integer can be stored in 37 bits. I guess it depends on what level of information you consider.
Question 3: there is no mechanism for directly transfering information between lymphocytes. Lymphocytes cannot read and write their DNA at will, and they are not able to simply copy sequences from each other. Rather, their diversity comes from first randomly re-shuffling their immunoglobulin-coding DNA, followed by selection of the successful cells --- this is a brute-force, random-search method, like evolution itself. Also, lymphocytes from unrelated individuals will generally interpret each other as invaders, causing an immune response. However, it is possible to experimentally "edit" the "memory" of lymphocytes extracted from blood using genetic techniques. This has for example recently been explored to "train" cancer patients own lymphocytes to attack cancer cells, in some cases with remarkably good results.

Thanks, this is the information I was looking for! Sorry if I didn't formulate my question properly, as I come from computer science background.


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How many cell membranes are oxygen and carbon dioxide diffuse through in the lungs?
In the lungs, oxygen and carbon dioxide pass through cell membranes by diffusion.
Which row is correct?

The correct answer is D, but I think it should be B. I can only think about three layers as maximum which are; epithelium of alveolus, endothelium of capillaries and the membrane of red blood cell. I don't know what are remainings.
Any help would be much appreciated!

Assuming that user24284 /Jam's answer is the correct way to think about it (I think it is), the question is a bit ambiguous. We don't know where to stop: should we track O2 until it reaches blood? or the final destination cells (where O2 is actually consumed)? In the latter case, the correct answer is not actually more than 5, since the oxygen also has to exit the erythrocyte (+1), enter the destination cell (+1), cross mitochondrial membranes...

This looks like a homework question.


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In cell division, are daughter cells identical?
I understand that after a cell replicates, there will be two daughter cells instead of one. But wouldn't one of them be the old cell that created the second one?
The old cell having gone through G0, interphase, and mitosis and after dividing wouldn't it be somewhat different from the new cell (the old cell's telomeres having shortened, having already undergone the cell cycle and so on)?

There is one large cell with the duplicated chromosomes that then is split down the middle to make the two daughter cells. Its like taking a slice of bread and ripping it in two, to a degree.

Here is a picture to expand on my comment better. From wikipedia:

In the above diagram, the red chromosome represents one homolog while the blue chromosome represents the other homolog in the pair. After replication in Interphase, you have two homologs, each consisting of duplicated sister chromatids. You can see how we have the one enlarged cell in Mitosis be cleaved into two daughter(diploid) cells.

Actually, the answer is not obvious. @RoSiv gives the textbook case of symmetric cell division, where the two new cells can indeed be considered identical, and this is valid in many cases. But there are also cases of asymmetric cell division, where the "mother" and "daughter" cell are clearly different.
In asymmetric cell division, the parent cell is polarized already before division by gathering certain proteins at one end of the plasma membrane. Therefore, during replication one of the the two new cells obtains certain proteins while the other does not, which makes them distinct. See this article for details.
Asymmetric cell division occurs among other things during embryo development, where it is important to establish body plan asymmetry. It is also the basis for the stem cell concept: stem cells are thought to divide asymmetrically so that the "mother cell" remains a stem cell (stays immortal) while the "daughter cell" becomes mortal and differentiates.

I see. Thank you for further explanations and detailing.


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How should "the human genome" be interpreted?
What does sequencing "the human genome" mean? Don't individuals have unique genomes?

Certainly individuals have unique genomes. The human genome sequencing project used DNA from a handful of volunteers, and the reference human genome that resulted from this project can be thought of as an "average" genome for those individuals. Where sequences differed between the individuals, a representative consensus sequence was chosen. Hence, the sequence of a gene from a given individual may not perfectly match the reference genome, although mostly the differences are small: genetic difference between humans is estimated to be around 0.1 --- 0.4%, which means a few million base pairs in total.
As DNA sequencing is nowadays orders of magnitude cheaper, genomes for larger number of individuals are being sequenced; see for example the 1000 genomes project.

A good start to an answer - might you want to talk about SNPs and gene variants (various blood groups, for instance) to get into a little more detail?

What percent of genome same for each individuals and What is the maximum number of genetically unique individuals that human genome allows?

@Abusayed  added a point about % differences. Theoretically I guess there are 4^(3*10^9) possible genomes with 3 billion base pairs, but of course it doesn't work like that  :)  But still there is enough variation that there is virtually no chance of encountering two completely identical genomes by chance.

@MattDMo, feel free to edit if you want.  It was a short, focused question though and I didn't want to respond with a population genetics lecture ;)

@Abu sayed: You might also be interested in these two facts: 1. The human reference genome's current release is version 20 (hg38). 2. Every newborn carries about 60-100 (which is not much at all) new private SNV due to mutations in the parents germline.

I think there are two concepts that you need to understand to understand what "sequence the human genome" mean; within vs between species variation and genome consensus
Within vs between species variation
There is indeed variation in the human population. We are not clones of each other. One can for example consider the average number of pairwise differences as a statistics of variation. Consider the two following sequences

ATCAATTCAGAA
AGCAATTAAGAA

Here, there are 2 pairwise differences. One can average the number of pairwise differences among any pair of individuals to get the average number of pairwise differences. The average number of pairwise differences within species is much lower than the average number of pairwise differences among species. It therefore makes sense to consider a standard genome of a species as variation within the species is negligible compared to variation among species.
Genome consensus
In order to obtain the "human genome", we samples DNA from a number of people, sequence them and then try to form a consensus among al these slightly different genomes. You can think of this consensus as some kind of average genome. Consider for example the following sequences:

AATGCA
AATGCA
AATGTA
AATGCA
AATGCG
AATGCA
AATGCA
ATTGCA
AATGCA

Sure, there is some variation but a priori AATGCA seems to be a good consensus.
Interestingly, it is very likely nobody on earth has the exact same genome as the consensus genome just. One simple reason is that there are sequencing errors occuring at a known rate but the other reason is that as sequences becomes long enough (the whole genome), every single individual carries at least one rare mutation that will not end up in the consensus.


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Does the energy from ATP hydrolysis vary among different cells?
I know that when ATP is hydrolyzed into ADP it gives 7.3 kcal/mol. The question is, does this value vary among different types of cells?

NADH and FADH are not hydrolyzed, but they can be oxidized, and the resulting energy used to drive ATP synthesis in mitochondria.  Can you give a source for your numbers?  3.7 calories (kcal / mol) for ATP hydrolysis sounds way too low.

thanks for your comment. yes, you are right it oxidized and it gives 7.3, I wrote it by mistake. I will edit the question. thanks again.

I see, you are simply asking about the energy of ATP hydrolysis.  The way you question was worded, it sounds like you were asking about the total energy from NADH and FADH2 oxidation. And you got an answer on that. I will edit to clarify.

Yes, the energy from ATP hydrolysis can vary between different cell types and condition, because it depends on several factors. Hence, you will find different values in various textbooks.
First, like any chemical reaction, the free energy $\Delta G$ of ATP hydrolysis depends on the concentrations of the reactants. You can explore different values of $\Delta G$ with this calculation tool. Typical values are [ATP] = 10 mM, [ADP] = 1 mM and [P$_i$] = 20 mM, which gives $\Delta G$ = 42 kJ/mol (10 kcal/mol). But all these concentrations can vary between cells, and there is not much data available on intracellular concentrations in specific cell types. Many textbooks give free energy values denoted $\Delta G^{\circ}{'}$ which are calculated at concentrations of 1M, which is of course completely unphysiological.
In addition, the $\Delta G$ is strongly affected by the concentration of Mg$^{2+}$, because this ion associates with phosphate groups and alters their free energy. It also depends on pH, since the phosphate groups can take up/release protons. If you are interested, an in depth analysis is found here.

The point you make is valid, that the actual free energy of hydrolysis of ATP can differ from the standard free energy. However the OP asks about variation in “different types of cells”, by which I presume he means e.g. muscle v. liver. Surely the answer to this is either “no” or “we don‘t know”.

I don't think it's just a matter of getting the textbook values right. Because the free energy depends quite a bit on concentrations of reactants, it can differ between cell types or conditions. For example, the reaction quotient ATP/(ADP * Pi) can drop as much as 50-fold in exercising muscle  (http://jap.physiology.org/content/73/2/728)  You're right though that we don't know much about these parameters between various cell types, as intracellular concentrations are hard to measure accurately.


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Can a cell survive temporarily without oxygen?
Can temporary denial of oxygen to a cell damage the cell? Will the cell continue to live in partially damaged condition if the supply of oxygen and nutrients are restored?

Can you provide more information as to what kind of cell? I am assuming you are talking about a human cell but please remember that there are many other cell types out there. Especially when we extend the conversation to bacterial cells that are able to grow/thrive in anaerobic conditions.

I was talking about human cell, thanks for responding.

This is really interesting because the answer largely depends on the severity of the damage, the length of the damaging condition, the type of damage incurred, and the type of cell incurring the damage.
For a real life example, irreparable DNA damage as by irradiation or drugs tends to be lethal to a cell. The severity of the damage may affect how long a cell has to live, however. For example, PBMC we irradiated with X gy tend to stay alive for 10-15 days (they actually don't divide though, due to the damage). Why did we pick that number? Too low a dose the cells persist, and too high you obliterate them. For reference, my experiements require my PBMC to be alive for a few days but disappear from the culture over time, so X gy is just an optimized value. Gy (gray) is an SI value for dose of ionizing radiation.
What you call a temporary denial of oxygen is actually referred to as intermittent hypoxia, or in a prolonged case just hypoxia. Human cells regularly survive in hypoxia by altering their metabolic pathways when OxPhos can't be utilized anymore. These changes are assisted by oxygen-sensing molecules that change the transcriptional profile of the cell. HIF1a comes to mind, a hypoxia inducible factor, which is regularly induced by PI3K and MAPK (typical cellular signals). It's typically kept in check by other oxygen sensitive proteins like VHL, but in hypoxia the effects of HIF1a action are entirely beneficial. So when the cell returns to "normoxia" it can typically reprogram into OxPhos (caveats exist, tumors for example).
So to answer your question yes, the cells will survive (in nutrient deprivation, too, but with a different mechanism), but they have to make a lot of changes first.


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Protein in fruits
Why do fruits have such a low protein content (with a few exceptions) ? Don't seeds need protein while growing up? In comparison, the egg of a hen contains lots of protein, used to make a chick.

Do plants need proteins in high quantity like animals?

I think this premise of this question may be wrong.  As @jamesq points out in his answer, the sugar in fruits are generally not used by the seed, but consumed by animals.  The relevant comparison is between seeds and animal eggs, and I don't think it's true that eggs generally contain more protein than seeds.  A sesame seed for example has more protein (per weight) than a chicken egg (see https://ndb.nal.usda.gov/ndb/search/list ).

@Roland, You should make this an answer, the question is based on a misunderstanding so correcting is a good answer.

It is don't have time to document this enough to make it a good answer but it's too long for a comment so I'll post it anyway.
A big difference between plants and animals is how they get their food, that implies they have different elements to work with. Proteins are made of amino acids, which contain nitrogen, meaning to make proteins you need lots of nitrogen. Plants get their energy from converting CO2 to carbohydrates; this is a plentiful source of carbon, but they can't get nitrogen that way. There are two ways of getting nitrogen: from the ground, and from converting atmospheric nitrogen to organic nitrogen, a process so energy-intensive that only bacteria evolved the ability to do it and only some plants use those bacteria (basically feeding them some of their hard-won carbohydrates "in exchange for" the organic nitrogen compounds).
Animals on the other hand get their food from plants, which contain all the carbon they might need and contain much higher concentrations of nitrogen than you find in the ground (the plant basically went to a lot of trouble to get all that nitrogen from a large volume of ground into its comparatively small body, or to convert atmospheric nitrogen into organic, useable nitrogen), or from animals which contain even higher concentrations of nitrogen. Note by the way that some herbivorous animals are limited by lack of nitrogen as well; I'm thinking of pollinating insects which can struggle to live off of sugary nectar alone and also need to eat some of the protein-rich pollen even though that's much less advantageous from the point of view of the plant (sugar being very easy to make for the plant but proteins much less so).
Obviously animals who eat other animals don't need to worry about nitrogen intake much at all, other than making sure they get food in general, because the animals they're eating will contain pretty much the same carbon:nitrogen ratio they themselves contain.
tl;dr: the egg contains more proteins than the seed because the chicken that made the egg ate a whole lot of seeds, and all the protein in those seeds ended up concentrated in that one egg.
EDIT: running into this much later I realized I missed a pretty vital half of the question, because there is a difference between fruits and seeds. The difference is the following: nitrogen is precious for plants so they'll try and use it for very important things. Seeds are very important to the plant, so while a seed has less protein than an egg it will still have lots of protein by plant standards. Fruits now, that's another story. Like the sugary nectar, fruits are a bribe for animals, a bit of food offered to them so that they'll spread the plant's seeds. And like with the sugary nectar, the plant has every incentive to pack that bribe full of cheap carbohydrates and as few precious proteins as it can manage.

many seeds contain more protein by weight than an egg, eggs are just bigger than most seeds.

Oh dear. I might need to actually document this answer, at this point I can't exactly pretend "I don't have time" do I

If we look at just the fruits people generally eat, the fruit part is seldom (if ever) needed for the seed(s) contained within the fruit to sprout.  Rather than the fruit being nutrition for the seed, it seems to be more of a lure.  Fruit-eating creatures  eat the tasty fruit and so disperse the seeds, perhaps contributing a packet of nitrogen-rich fertilizer.  The plant thus has an evolutionary incentive to make the fruits inexpensive to produce yet tasty, so lots of sugars, few proteins.
You can compare this with flowers that produce nectar to attract pollinators.

In brief the lower protein content of a seed compared to an egg is caused by two reasons.
(1) The structural components of a plant versus that of an animal.
The structural components of plant is made by cellulose which is made of glucose subunits. Animal in contrast are have large amount of muscle tissue to allow movement and much of animal is held together by collagen and keritine. All these components are different types of protein which are build from amino acid sub-units.
Hence to build a seedling you need glucose. To build a chick you need amino acids.
(2) Metabolism. A plant can build all amino acids that it needs from glucose and fixed nitrogen source. Animals in contrast are not as self sufficient. Some amino acids cannot be synthesized and must be obtained from an external source.
Hence a seed need not carry much or as varied quantity of amino acids. In fact this metabolic completeness has been used as an anti herbivore defense mechanism. Many seeds are severally deficient in one or more amino acids. Any animal that feeds solely on just one type of a seed would experience malnutrition.
An egg however has to carry more amino acids, especially the essential amino acids that it cannot synthesis from other amino acids.


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What (if anything) about tuberculosis makes producing a highly effective vaccine difficult?
What about tuberculosis makes it difficult to produce a safe vaccine that is effective at producing an immunogenic response in >99% of individuals against all strains of the bacteria?
I am aware of the BCG vaccine which has a variable efficacy depending on how it is measured and am aware of the 4 current vaccine candidates (MVA85A, rBCG30, 72F fusion protein, and ESAT6-Ag85b fusion protein). I am curious about the very specific question of aspects of the bacteria that make the TB vaccine difficult.
Many, many thanks.

The fact that it stays dormant for a while and resides in lungs, which makes it difficult for drugs to access it and diagnose its presence until its late!

Thats an interesting and complex question. First, Mycobacteria tuberculosis is present for a long time in the human population and evolved to evade our immune system. One of the keys are glycolipids and sugars which are part of the bacterial cell wall. These either help suppressing an immune response or help the bacteria to enter host cells in which they can stay without being identified by the immune system. See references 1-3 for details on this topic.
Then most tuberculosis infections are hold of by the immune system, mostly they come up, when the carriers immune system is compromised. M. tuberculosis can successfully hide inside macrophages and multiply there and start an infection from this hiding place. See references 4 and 5 for more details here.
One of the main problems with the development of new vaccines is that this takes quite a long time from successful experiments in the lab to the availability of a usable vaccine. Tuberculosis has been neglected here for decades. Then the market for such a vaccine wasn't deemed lucrative enough from the pharma companies, as this is mostly important for poor and developing countries. For use there, the vaccine needs to be cheap and easy to administer. Additionally humans are the main host for M.tuberculosis which makes chossing appropriate animal models for research and testing not an easy task.
The development of novel vaccine candidates follow different routes. First, there are live vaccinations, which mainly consist of modified strains of the BCG vaccine strain. Then there are vaccines in the development which are supposed to support the immune answer by BCG and finally, there are vaccines which are independent of BCG and are mostly composed from proteins of the outer bacterial cell wall. For an overview about this field, I can recommend the review articles 6 and 7, if you want to go deeper in the field, also the references 8-10.

References

Mycobacterium tuberculosis Cell Wall Glycolipids Directly Inhibit
CD4+ T-Cell Activation by Interfering with Proximal T-Cell-Receptor
Signaling
Divergent Effects of Mycobacterial Cell Wall Glycolipids on
Maturation and Function of Human Monocyte-Derived Dendritic Cells
Interactions between Mycobacterium tuberculosis and host cells: are
mycobacterial sugars the key?
Annulling a dangerous liaison: vaccination strategies against AIDS
and tuberculosis
Macrophages Play a Dual Role during Pulmonary Tuberculosis in Mice
Vaccines against Tuberculosis: Where Are We and Where Do We Need to
Go?
Vaccine against tuberculosis: what’s new
Tuberculosis vaccines: past, present and future.
Childhood tuberculosis: old and new vaccines.
Exploiting the mycobacterial cell wall to design improved vaccines
against tuberculosis


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Theoretically, is domestication of (virtually) any animal possible?
Looking at ones that manage well alongside us human animals, such as dogs and cats, we see that this is possible for evolved, distant animals to have heritable, preferable traits around people. However, when especially looking at lions and the like, it doesn't seem to work out as well.
Some people have tigers as pets, but in general it is believed that they are more "wild" and not as tame and domesticated as other animals (such as dogs and cats).
Is it possible to selectively breed and enable any animal to be more like dogs and cats? Even sharks? Tigers? Alligators?
If domestication worked so well with dogs and cats, such as them living (for the most part) peacefully and well with people, wouldn't the process be beneficial for other animals so we could all live better side-by-side?
In short, can you theoretically get any animal to have heritable traits?

I understand your overall question, but your last question doesn't really fit in: all animals have heritable traits.

Domestication of animals was not performed so that we live better side by side but because they were beneficial for human needs so we domesticated them. Best example is dogs that were used as protection for live stocks. I'm no zoologist to respond to your question but so long as they have a nervous system that can learn, I don't see what not. even snails and drosophila can learn tasks such as maze solving but that doesn't necessarily domesticate them so i guess it depends on how developed their NS is and what you define as domestication.

have you heard of the 40 year long Russian experiment to tame foxes? Quite interesting. Have a look at it.

Maybe the first question is. Are dogs and cats domesticated because they are predisposed to domestication?

It depends somewhat how we define domesticated - I keep flies in a lab, just as a farmer keeps cows in a field, but is this the same as training a pet?

@Bez: But a lot of work had to be done on the ancestral wolf before it could become a reliable livestock guardian - and indeed, many dog breeds don't work as guards.  So what was the initial impetus?  One idea is that dogs basically domesticated themselves, having discovered that there were advantages to living with humans.  Some would go so far as to suggest that dogs domesticated humans...

As the previous answers clarify, all organisms have heritable traits that may be manipulated through selective breeding. It is the pragmatics that can be prohibitively challenging. From an (zoo)archaeological point of view, few animals have actually been domesticated, and only recently in our species' history. The dog is an unusual case, perhaps domesticated 14,000 years ago; most domesticated animals only show skeletal changes within the last 10,000 years. Cats, compared to livestock's total dependence on humans, are 'barely' domesticated--they got used to humans while camping out in Egyptian storehouses where all the mice were, perhaps around 4,000 years ago, but even today a fluffy house cat will revert to a feral state if abandoned.
Many animals are behaviourally unsuitable for domestication. If an animal is dangerously aggressive, for example, they cannot be penned and isolated--so the many controlled generations it takes to reduce their baseline aggression cannot occur. Humans also tend to co-opt pre-existing social structures in a species, such as becoming the 'alpha' in a dog pack or the head 'ram' of a sheep herd. Species without a hierarchy or herd mentality are difficult to control and keep track of, and so do not lend themselves to human care.
You mentioned tigers in your question. Tigers have little to offer people (other than pelts), they're massive/aggressive, and they're jungle loners. You can't raise a herd of tigers; they'll kill each other and the survivor will kill you. That they're carnivores is also challenging, since a carnivore is much more expensive to feed than a bunch of grass-munching sheep. Altogether, there was never a situation in prehistory that would have turned tigers into giant house cats. House cats eat unwanted mice; tigers eat your cattle (and children). The occasional tiger 'pet' won't change that.
Domestication, outside of recent experiments (like the Russian foxes mentioned above), has always been a protracted, indirect process. People started interfering with animals that were already useful in some way(s). Dogs offer warmth, hunting aid, defence, transport, and (in a pinch) food. Alligators, tigers, and sharks are not useful enough to make the danger and cost of raising them worthwhile. Even if you did eventually produce a 'human-friendly' shark, there would still be a 'wild' population ready to eat you--and your complacent pet sharks, too!
For a very readable explanation, try the chapter on domestication in Jared Diamond's (1997) Guns, Germs, and Steel.

I understand the question as "can you get any animal to have heritable traits selected by humans?"
This definition of domestication implies that a population of animals can be bred for a sufficiently long period of time, so that humans can select hereditary traits that fit their needs. Humans could provide selective pressure that creates a new variety with different traits. So according to the laws of evolution, I would say it could theoretically be done for any living being.
But there may be species that could be reluctant to such a control, e.g. animals that we have difficulties to reproduce in captivity for whatever reasons (polar bears?), or isolate from their wild congeners (genetic isolation is a generally a pre-requisite to domestication). For them, domestication could take too much effort or a longer time than humans would be willing to spend.

So, are you supporting his theory that all animals could be domesticated? Just that some take more time than others.

It really depends on the definition of domestication. I'll edit my answer to clarify.

I understand the question as "can you get any animal to have heritable traits selected by humans?" : replace "heritable traits" with "the specific set of heritable traits that we call domestication" & you'll be there.

As everybody, I don't fully understand your question. Can you please add your definition of domestication?
Would you consider domestication as soon as human can select for heritable traits? If yes, then the question may be split in two:
Do all animal populations have heritable traits?
Yes! But Depending on what kind of traits you want to consider no variance (yielding to no heritability) may exist in the population. For example, you'll have a hard time to select crocodiles to have fluffy hair as there is no variance in "hair fluffiness" in the population. Crocodiles have no hair.
However, some practical issues exist. For example, it might be hard to select for a given behavior if the animal is so small that we can hardly observe them during a sufficient amount of time to know whether or not the individual display this behavior. Typically, it might be hard to select for specific traits in a population of a species that live inside another species (endosymbionte, endoparasite).
Are humans able to breed any animal species?
No, we're not! Many species do not breed in captivity or do not even survive in captivity. This is due to our lack of knowledge of the ecology and social behavior of the species in question.

Not all animals are equally predisposed for domestication. To be easily domesticated, animal should have:

Flexible diet - and not compete with humans for food
Reasonably fast growth rate
Ability to be bred in captivity
Pleasant disposition
Temperament which makes it unlikely to panic
Modifiable social hierarchy

Wikipedia link above has plenty of details.
So sharks, tigers and alligators are (according to above) are NOT good candidates, because of 4 and 6 at least. Alligators are bred in captivity in farms but are not really domesticated.
See also dates and places of domestication.

There are also two very different kinds of domestication.  Most domesticated species we keep around as a source of food, so their domestication equates to being able to conveniently keep & raise them.  A few we form working partnerships with: notably dogs & horses, but to some degree camels, draft cattle, llamas, and a few others.

No and yes.
What you perceive as domestication has a lot to do with intelligence or even social intelligence of animals.
Common fish is too stupid (from our point of view), to have any social bond with humans. Mammals are usually much closer and have similar structure of intelligence and patterns of behaviour.
That only if you consider domestication as something more and not just human utilization as with breeding fish for food, spiders and snakes for fun (or even snakes for rat-catching, as some African tribes did according to wiki).
So not all animals could be domesticated, they need certain qualities, mostly connected (or we are connecting them) with intelligence.
However, once you look at mammals, which usually have enough social intelligence, you could breed them into domestic animals. It would be hard, there would usually be no other purpose than "We can, so we do", but you could. There were various experiments. One is famous Russian experiment with foxes, another is infamous Hitler's experiment with cows (experiment with bringing back Aurochs, Heck cattle, cows were "undomesticated"). There, in controlled environment, true genetic plasticity of behaviour were showed.
Note that as other posters wrote, this is theoretical. In nature and by natural means, domestication was always hindered by immediate usefulness (not even potential future usefulness). Most of domesticated animals are highly social in their natural form and not very aggressive. Even big cats are quite close. Tigers not as much as cheetahs, which were traditionally bred (or kept as pet) from ancient times.

In short, can you theoretically get any animal to have heritable traits?

All animals have heritable traits. That's genetics.


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sex limited genome transmission
In general, for dioecious species, a large portion of the genome passed from parents to offspring of both sexes - in mammals the X-chromosomes and autosomes are passed from a mother to both daughters and sons, and autosomes from the father to both sons and daughters. Only the small amount of genes present in the Y-chromosome and mitochondria are inherited solely within one sex.
Is there any species (not just mammals) where most, or even all, of the genome is inherited in a sex-specific trajectory? What is the most sex-limited genome known to researchers?

In birds and reptiles females are the heterogametic sex with allosome configuration ZW. However it has been reported that a homogametic WW female boa was born by parthenogenesis. So it means that although W is shorter than Z, it can still support life. So I guess that ZW system in general exchanges more sex-limited genetic material than XY system.
Platypus has 5 pairs of sex chromosomes. See here. This can qualify as the top case of sex-limited transmission.

Platypus just HAS to be utterly weird on every level ...

Is there any species (not just mammals) where most, or even all, of the genome is inherited in a sex-specific trajectory?

Here are a bunch of cases and specific examples that may interest you

There is a species of ants where both genders evolve to be able to reproduce by parthenogenesis (which means that males might be call females as well). In this species, the two genders mate together to create workers that do not reproduce! Therefore, when you look at the phylogenetic tree you can see that males and females are on two totally separate branches as there is reproductive isolation between the sexes in terms of fertile offspring. There is an article by L. Keller on the subject.
In the amazon molly, there are no males. But it is interesting because females need sperm to start the development of their ovules although they don't even use the genetic material of the sperm. Therefore, the amazon mollies need to find mates in sister species. In consequence, they imitate the females of the other species. There is a recent article from Hanna Kokko that investigate with a mathematical model how such system may be able (not cause the extinction of the amazon molly or of the sister species).
Sex-specific segregation distorter. Nasonia sp. may be an interesting case study
Haplo-diploidy. In ants for example, sons receive genetic material from their mother only. They are haploid.
if the rate of sexual reproduction is different from 1 then, females are responsible for more than half of the inherited genes in the next generation.

I apologize for the lack of references $\ddot \smile$

The new mexico whiptail reproduces purely through parthenogenesis. The species itself originates as a hybrid of two other species of whiptail, but the hybridization can't make fertile males. The females can reproduce through parthenogenesis so that's how the species continues to exist. So 100% of the genome is passed mother to daughter for many generations, very few new mexico whiptails are made through a fresh hybridization of the parental species.
http://en.wikipedia.org/wiki/Cnemidophorus_neomexicanus


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How was Crisper Cas9 function discovered?
What paper outlines the discovery of how the CRIPER DNA, CrRNA, and Cas9 interact?

The two "classic" papers cited in terms of Crispr/Cas9 discovery include the Doudna/Charpentier initial discovery, and the Feng Zhang application to gene editing.  There is an ongoing, famous patent dispute as to whom really discovered the Crispr/Cas9 gene editing technology.
As a quick timeline that better answers your question, a good publication is Cell Paper and there is actually a great podcast, but I will summarize:

Yoshizumi Ishino et al. in 1987 Discovers Crispr mechanism - the authors simply noticed the odd regular repeats of DNA in bacteria and noted: “no sequence homologous to these has been found elsewhere in procaryotes, and the biological significance of these sequences is not known.”
Francisco Mojica in 1993-2005 - Furthers research into CRISPR, at this time the terms has been coined by Jansen, however it is Mojica who really notices the Crispr pattern in several bacterium and suggests that it is involved with an immune response.
Alexander Bolotin in 2005 - Looking into the bacteria Streptococcus thermophilus, Bolotin discovers that the genetic material in between the spacers is viral DNA, providing definitive evidence of the Crispr hypothesis.
Marakova in 2006 - First proposal that the protein Cas9 can be used in a bacterial adaptive immune response, although Bolotin is also credited around this time from noticing the use of Cas9.
Koonin in 2006 - The first one to piece the Crispr storage of viral DNA and the Cas9 reports of an immune response together as a related system that might be able to use the Crispr DNA with Cas9 in an immune system.
Marraffini in 2007 - Studying the Crispr-Cas9 system further, he provides the first definitive microbiological evidence that Cas9 is a programmable restriction enzyme, and that it targets DNA not RNA. At the same time Philippe Horvath, Danisco France also provided the best evidence yet of the adaptive immunity system.
Doudna and Carpentier in 2010 - Through sequencing, definitively put the Crispr and Cas9 system together as complete unit that is able to cut DNA, they also described tracRNA as the RNA piece that join with Cas9 to program DNA cutting.
Feng Zhang in 2013 - While Doudna previously suggested that the Cas9 system could be used to target mammalian DNA, Zhang was the first one to actually that it was possible and therefore open to the door as the Crispr/Casa9 system as a tool that easily edit genomes.

While I definitley missed several key steps, and did not fully explain the actual mechanism of Crispr/Cas9, I think this provides a decent timeline.  For more information about the actual mechanism see: Harvard, Wired, Science News.

This paper will tell you about it.https://www.ncbi.nlm.nih.gov/pubmed/?term=A+Programable+Dual-RNA-Guided+Endonuclease+In+Adaptive+Bacterial+Immunity
I am not allowed to seee the full text,but there it is.
Here is a full text link of that paper
http://science.sciencemag.org/content/337/6096/816.full


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Frequency modulation of parasympathicus and sympathicus
According to my literature, the sympathetic nervous system accelerates heart rate and modulates < 0.1 Hz, whereas the parasympathetic nervous system decelerates heart rate and is modulated 0.04 - 0.5 Hz.
According to this, heart rate accelerates in sympathetic which means the frequency should be higher than that compared to Parasympathetic. Though Parasympathetic starts with 0.04 it goes up to a value higher than 0.1Hz. Why so?
Here is the source (Physiological Sensing of Emotion by Jennifer Healey in the Oxford Handbook of Affective Computing):

Since it is known that the parasympathetic nervous system is able to
  modulate heart rate effectively at all frequencies between 0.04 and
  0.5 Hz, whereas the sympathetic system modulates heart rate with significant gain only below 0.1Hz (Akselrod, Gordon, Ubel, Shannon, &
  Cohen, 1981; Berntson, et al., 1997), the relative strengths of the
  sympathetic and parasympathetic influence on HRV can be discriminated
  in the spectral domain.

Can you cite and quote from your source? Your logic doesn't make much sense but it would be helpful to see what is actually said to help you understand it.

@BryanKrause I have added the source


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Would it be more genetically efficient to have shorter lifespans?
If, for example, humans had an average lifespan of, say, 30 years, and we reached sexual maturity at age 10, then we could "evolve" more quickly and theoretically "weed-out" more genetic diseases because we would live for shorter times, hence more natural selection.

Why don't we continually evolve for shorter lifespans (or do we)?

possible duplicate of Why does evolution not make our life longer?

@Remi.b, The linked 'duplicate' asks for the opposite. This is not a duplicate from my point of view.

This question is conceptually similar: Why are the fertility rates of large predators kept low? (~why isn't trait X evolving since it should have a positive effect), and the issue of life history tradeoffs found in the answers is relevant here as well.

Extremely briefly, we do not evolve shorter lifespans because natural selection does not act for the good of the species.
As an interesting historical aside, August Weismann proposed essentially the idea you are suggesting in 1889, in his Essays upon heredity and kindred biological problems. Within a few years, however, he backed away from this hypothesis.


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How long does conception take?
I know that conception is a multi-step process. A sperm fuses with an egg. Its contents diffuse into the cytoplasm.
Dad's DNA is transported to the nucleus. Proteins are gradually made from Dad's DNA. Do we know how long that process takes?
I'm most curious about conception in humans, but information about other species is welcome too.
EDIT:  The time I'm interested in is between the fusing of sperm and egg, and the first transcription of the newly incorporated paternal DNA within the zygote's nucleus. However, if conception is better defined by different events, feel free to correct me. I'm far from a specialist in the subject.

Can you define exactly which timespan you're interested in? Ejaculation to DNA entering nucleus? Sperm contacting egg to DNA nuclear entry? Some point until the first cell division? Please [edit] your question to clarify it, otherwise it is rather unclear.

Done. I figured there might be a research project somewhere that dealt with early embryonic growth, so I guess I was pretty general.

There is research showing that spermatozoa contain a number of RNA species, including mRNA, so theoretically translation could begin almost immediately. The Wikipedia articles on human fertilization and fertilization in general contain lots of other information, if you haven't read them already. Unfortunately, there's nothing in them about timing that I could find. I'm sure it's out there, though.


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Why do vaccines sometimes induce a fever?
How does a vaccine cause an immune response such as fever? Why do only some people experience these reactions? Why might those reactions change upon subsequent doses of the same or similar vaccines?

Does this related question help?: https://biology.stackexchange.com/questions/855/how-does-the-immune-system-learn-from-a-vaccine?rq=1

Yes, that's a useful link!  Wish there were something about side-effects like fevers, though.


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How do we know Neanderthals DNA?
According to this article, a small amount of Neanderthal DNA was introduced into the modern human gene pool. How do biologists even know what the Neanderthals' DNA look like?
The article doesn't mention how the science recognize what the Neanderthals' DNA actually is at the first place. So how do we know what the Neanderthals' DNA is if I'm guessing we never tested Neanderthals body cell samples?
If you say "From their bones/skull" but how do you know they are actually Neanderthals and not modern humans with some rare gene mutation or something else?

If you want the full story I highly recommend Svante Pääbo's excellent book, "Neanderthal Man: In Search of Lost Genomes"  https://en.wikipedia.org/wiki/Neanderthal_Man:_In_Search_of_Lost_Genomes.  Here's the amazon link: https://www.amazon.com/Neanderthal-Man-Search-Lost-Genomes/dp/0465054951.

Neandertal DNA has been completely sequenced multiple times now, using DNA from bone and tooth samples found in cool or cold environments.  The first Neanderthal genome sequence was described in 2010:
A Draft Sequence of the Neandertal Genome
Since then, as well as higher-quality sequence, more genomes have been completed; at least 6 individuals have been sequenced (perhaps more; I've lost track a little).  As well, complete genome sequences from several Denisovans -- a Homo species that were approximately contemporary with Neandertals, but a distinct species -- have been recovered.
The science of recovering ancient DNA has advanced very rapidly in the last decade, and while it isn't routine to sequence 50,000-year-old DNA it isn't as magical as it used to be.  The current record for sequencing ancient DNA is 700,000 years, which is earlier than the sapiens/neandertalis split.

but how do they know they were not merely modern humans, deformed by diseases such as rickets, arthritis or syphilis?

For one thing, the genomes are distinct and clearly well outside the range of the human species. For another, Neanderthal skeletons don't show signs of disease -- indeed, far from being diseased, Neanderthal skeletons are vastly more powerful and robust than puny humans.  For a third, Neanderthal skeletons, of which many are known, are consistently the same as each other and consistently different from sapiens skeletons. All lines of evidence showing that they are separate species are extremely strong; taken together they are indisputable.

the mt DNA sequence differences among modern humans range from 1 to 24 substitutions, with an average of eight substitutions, whereas, the mt DNA sequence differences between modern man and the Neanderthal specimen range from 22 to 36 substitutions, placing Neanderthals, at worst, on the fringes of the modern range.

no, I don't understand it. I'm just finding arguments against it in order for me to know more about the subject. Thanks anyway for the answer!

Suggest asking a separate question, then; comments are not a good place to raise a completely new issue

Just in case anyone is taken in: Note that the comment by @Grasper above about mtDNA is copied directly (though without attribution) from the notorious "Institute for Creation Research", and as is typical from them is deliberately obfuscatory (i.e. what we call "a lie"). Genomic DNA, not mtDNA, shows that Neanderthals are a distinct species.  Starting point for reality-based understanding: Strong reproductive isolation between humans and Neanderthals inferred from observed patterns of introgression.

The answers here give you reference to the first draft genome. Take a look at these papers for high-quality sequences: Prufer et al., 2014 for Altai Neandertal, Meyer et al., 2012 for the Denisova individual. A third one, the Vindija Neandertal has been sequenced and the sequence is already available (though not published, yet) here. However, one thing has not been mentioned. The presence of ancient DNA can be confirmed by identifying specific damage patterns in the DNA molecules, i.e. mainly deamination. That is used to ensure that the DNA is old and does not result from contamination of present-day humans. Additionally, modern human contamination levels are estimated by two or three independent methods in the papers given above. These methods exploit the uniqueness of Neandertal mitochondria and Y-chromosomes, i.e. the fact that these variants have never been seen in present-day humans.
This answers the sequence part, but my answer focuses on the second part of your question and the issue your raise in the comment sections:

If you say "From their bones/skull" but how do you know they are actually Neanderthals and not Humans with some rare gene mutation or something else?

This can mainly be answered on two different levels. The first level is a parsimony argument: there are a lot of those skeletons (far more than the ones that have been sequenced) and it would be too unlikely they all suffered from the same disease. Additionally, skeletons of present-day humans with the diseases you mention do not at all look like Neandertal skeletons.
The second level is a bit more scientific: bones from the spanish cave Sima de los Huesos have been sequenced as well (Meyer et al. (2014) for a mitochondrial genome and Meyer et al. (2016) for nuclear sequences - not full genome!). Bones from this cave has been dated to approx 430,000 years ago which means that those bones may not even be Neandertal bones but rather Homo heidelbergensis. This makes a strong point against your suspicion as at that times modern humans did not even exist anywhere on the planet and it took another about 200,000 years until the first anatomically modern humans evolved in Africa (and then another 150,000 years until they set foot to Europe).

The sequence of the neanderthal genome is known because it has been sequenced and could then be compared to the human reference genome. The DNA was extracted from a toe bone found in Siberia, as described in reference 1.
The sequencing was done as described in reference 2. The researchers where sure that the bones came from Neanderthals because of anthropologic differences in the built of the bones they found. They are distinct from homo sapiens bones.
References:

A proximal pedal phalanx of a Paleolithic hominin from denisova
cave, Altai
A Draft Sequence of the Neandertal Genome

but how do they know they were not merely modern humans, deformed by diseases such as rickets, arthritis or syphilis?

You can carbon date such bones - the result is pretty clear.

I thought carbon dating is only reliable up to 5,730 years. Neandertals lived 350,000–600,000 years ago.

@Grasper First: 5730 years is one half-life of C14, dating works for at least 10 half-lifes - with special preparations to exclude contaminations even longer. Then the neanderthal lived from about 230.000 to about 30.000 years, which is at least partly in this range.

@Grasper There are also other isotopes besides carbon that you can use to date bones and fossils; you can also use entirely different methods, such as analyzing amino acids. It's just that carbon-dating is the most common for human-age artifacts because its half-life and range tend to cover most modern and immediately prehistoric human artifacts.


text:
What is the difference between a mechanistic and a statistical predictive model?
The simplest description of the difference between these two approaches that I have found are on this site who summarise the difference as:
Mechanistic model: a hypothesized relationship between the variables in the data set where the nature of the relationship is specified in terms of the biological processes that are thought to have given rise to the data. The parameters in the mechanistic model all have biological definitions and so they can be measured independently of the data set referenced above.
Phenomenological/Statistical model: a hypothesized relationship between the variables in the data set, where the relationship seeks only to best describe the data.
Could someone exemplify this difference with a short example. I have used and understand the principals of a statistical model (multiple regression etc) but haven't come across any simplistic examples of a mechanistic model and I don't understand what the difference would be in practice.
Edit: I am leaving the question open for a week to see if anyone wants to create a very small 'MWE' of the two types to illustrate what the difference would look like in practice, if not I will accept Memmings answer

If you are interested in mechanistic models a great resource comes from books on statistical thermodynamics and in general anything coming out of physically motivated biological research. A good reference is "Physical Biology of the Cell" which is supposed to be a physics driven equivalent to the Alberts et al "Molecular Biology of the Cell" book.

The question is interesting (+1) and on-topic here. However, I think that you might want to consider asking such question on Philosophy.SE.

Mechanistic model answers the how question. These models are usually biophysically detailed, and designed to be causal. Say you discovered a linear relation between blood pressure drug and heart rate. This would be a statistical model. It doesn't tell you how the two are related biophysically. One could build a detailed model that describes intermediate processes from the drug entering the system, to binding to receptors, and modulating levels of hormones, and acting as a signal to the heart rate modulation system. This model would have more parameters, and if it predicts the phenomena and generalizes well, then it might be a good approximation of the system. Moreover, it generates hypotheses and is more interpretable.
That being said, I do not think the two concepts are mutually exclusive. Some mechanistic/biophysical models can also be statistical at the same time. It's a matter of having enough data and constraints to be able to fit the model or not.

Thank you for your answer. So for the mechanistic model lets say that the processes you mentioned are the only ones (enter the system, bind to receptor, modulate levels of hormones, signal to the heart rate modulation system). So for the first stage the mechanistic model would take into account amount of drug and work out absorption relating to the concentration gradient? While a statistical approach would look at marginal increases in drug absorption given a set increase in drug administered?

@PaulBarr I think you are missing the point. If you had the appropriate data, you can always use statistics to answer the how question. Mechanistic models sometimes don't have that luxury, and are pieced together from partial knowledge from here and there. Statistical modeling exploits the observed variables, in my example, those would be only the drug administration and the heart rate.

I understand that you can use statistics to answer how something works. Specifically I don't understand the difference in how the model would actually look in practice, when it has been coded in R etc. As a side question are you saying mechanistic models work best when there is partial knowledge, it appears intuitive to me that the opposite would be true. Thanks for your help

@PaulBarr Usually, you can simulate the mechanistic model, but often difficult to fit its parameters from data. To build the mechanistic model, it is often necessary to make assumptions about the dynamics and parameters which are not strongly supported by data.

Thank you, this is really helpful. Could you add to your answer a very short MWE of what two models may look like in practice at the actual code level?

@PaulBarr I can't write MWE for those, since mechanistic models are usually complex...also I don't have the time. Sorry.

No worries, I'm not looking for an actual realistic model I just would like to see the difference illustrated if possible. I will leave the question open for a week and if no-one is keen Ill accept your answer. Thanks again


text:
What is Phytogenetics?
What is Phytogenetics? I have searched google without finding a definition. Is it even a defined term? I found it in a reference relating to genetic engineering.

Have you really googled the term? If I google phytogenetics, the first 8 results are 7 definitions and 1 translation.

@Remi.b it turns out that google results can vary dramatically for each person depending on geographic location, language preference, and other things, especially if you are logged in as well. It's always good to remind people to do a search and include what they did find in their search. I get a few definitions, offers of translations into other languages (Spanish, Turkish), and an advertisement and a prospectus for two different companies. start-up

prefix. Phyto, or phyt, is defined as plant. An example of phyto used as a prefix is in the word phytol, which means an oily alcohol that comes from combining the chlorophyll of plants with other substances and is used to create synthetic vitamins. http://www.yourdictionary.com/phyto
noun. Genetics, the study of heredity and the variation of inherited characteristics. https://www.merriam-webster.com/dictionary/genetics
Try the google machine or visit a local library next time you have trouble with words. It has worked quite well for people in the past!

Phytogenetic is

adjective
Botany
      Relating to the origin and evolution of plants.

(Source: Oxford English Living Dictionary)


text:
Are Restriction Enzymes obsolete with CRISPR?
Are Restriction Enzymes obsolete with CRISPR?

No.
While CRISPR allows you cut a piece of DNA anywhere, you need to order a guide RNA to target your desired cut site. All standard plasmids still carry traditional restriction sites, and it's often convenient to use these. Using CRISPR as a restriction enzyme is probably more expensive and more complicated than using traditional restriction digest. Additionally, there are limitations about PAM sites with CRISPR. And you can always PCR a plasmid using whatever primers you want to produce a blunt end product that is "cut" where ever you want, and I'd bet the DNA oligos needed for PCR are cheaper than the guide RNA you need for CRISPR.


text:
how long do chaperone proteins take to fold a protein?
how long do chaperone proteins take to fold a protein?


text:
Enzyme with long tube leading to active site?
Are there any enzymes that force one or more of their substrates to travel a relatively long distance through a small opening/tube through the enzyme and  to the active site? (not a transport protein)

First of all, as you mentioned, there are a lot of membrane / transport proteins with very nice, well defined tunnels. But you're looking for a soluble / cytosolic enzyme.
Some oxygen-dependent enzymes have quite long tunnels that oxygen is using. For example this one: http://www.jbc.org/content/283/36/24738.short or this one: http://europepmc.org/articles/PMC2698890
Then there are some enzyme with just deep active sites, I think the p450 BM3 is quite known for that, but any enzyme with a reasonable specificity (and especially those that have very reactive cofactors) will have a "tunnel".
You can also find long "tunnels" in enzymes that accept long substrates. I like this example of squalene synthase: http://science.sciencemag.org/content/277/5333/1811.full. The substrate first has to go deep into the enzyme to find the proton it needs to start a quite interesting reaction.
If you want to find new tunnels in your enzyme there are also tools available, such as CAVER: http://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1002708 If you look at the papers citing this tool you might also find some cavities.

According to information on the CAVER website:
The access tunnel is sometimes described as a "keyhole" in which analogy the lock is the enzyme and the substrate is the key that goes through the keyhole to the active site. The tunnels are commonly found in all six enzyme groups: Oxidoreductases,Transferases, Hydrolases, Lyases, Isomerases, and Ligases. Source: https://youtu.be/M6bW8lcM9jk

http://europepmc.org/articles/PMC2698890/figure/F2/

Other tunnel finding softwares include: (Mole, MolAxis, Hollow, etc.). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3341237/


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Why don't stem cell therapies use viruses?
Why don't stem cell therapies use a virus to deliver gene editing sequences to stem cells instead of the harvesting-transformation-transplant route.
I thought it might be because of a lack of specificity on the part of the viruses, but then I saw phage display techniques that would seem to make that a non-issue.
I thought it might be trans-cytosis or getting the phages out of the blood-stream and into contact with the stem cells. I haven't found an easy solution to this hurdle, but it doesn't seem to be insurmountable.
I think the main issue is regulatory? Perhaps a lack of precedents in this area. What do you think of my analysis? Is this idea even feasible?

There is active research in this area using animal models, which bypasses many ethical hurdles (I assume that's what you mean by regulatory). The immune system is a significant hurdle.

Phage display isn't that good at making structures that actually work in vivo. I'm not saying there are no successes, but the rate is pretty low. And any time you're delivering viruses into a patient you're likely to develop antibodies against that virus, making repeated doses harder. That's how vaccines work.

Any idea how far along the animal model viruses are?

Interesting read relating the subject.

Stem cell therapies do in fact utilise viruses. In the examples cited, the stem cells were infected by viruses in vitro, genetically modified, and then reintroduced into the target as autologous transplants. The main issue at hand is that live viruses introduced directly would be targeted and destroyed by the immune system, which greatly reduces their efficacy in causing transformation of cells.
In a recent Nature paper, zinc finger nucleases were used to target and disrupt the CCR5 or CXCR4 gene, which greatly reduces the efficiency of HIV binding to CD4+ T cells. The zinc finger nucleases were introduced into the cells using an adenovirus vector.

Generation of cxcr4 ZFN adenovirus and CGW-siX4s lentiviral vectors. The CXCR4 targeting locations of siX4s and ZFN are shown in Supplementary Figure S1.

This technique was then used in a number of clinical trials to modify hematopoietic stem cells using zinc finger nucleases, as summarised in this review paper. The recent advent of CRISPR-Cas systems will probably lead to an increase in similar techniques, due to the higher specificity and ease of engineering of Cas9-based nucleases.

This is an exciting field. I am very interested in the potential to avoid the immune system.

Thanks to you guys I googled, "stem cell virus animals" and found some promising links! I appreciate you guys emphasizing immunological response. I was hoping that the virus would be effective enough to work on the first shot and thereby avoid most of the immunological complications. However it seems that the second generation of adenovirus vectors in animal models was abandoned for just that reason: source - NCBI.
Here is a nice excerpt regarding animal models:

“third-generation adenovirus vectors”: This research focuses on the development of improved production systems for gutless adenovirus vectors and their use for the efficient introduction of large or multiple transgenes into human progenitor and stem cells with minimal vector-related toxicity. In addition to the use of regular third-generation adenovirus vectors for the transient genetic modification of target cells, we have embarked on the generation of new vector types for stable transgene expression in transduced target cells using locus/site-specific transgene integration or homologous recombination. For example, we have generated new adenovirus/adeno-associated virus vectors. These vectors stably integrate into a specific locus on human chromosome 19 and are capable of genetically complementing dystrophin-deficient human myoblasts.
-Leeds Universitair (NZ)