text:
Why do we weigh less in the morning?
At first I thought it may be related to physics.  You know, in one half of the day, the gravity changes, and the scale shows a different weight than the other.  Then at night, gravity intensifies, and you become slightly heavier.
But I'm a bit skeptical about that. Is that true?  That it's somehow related to gravitational fields?

Gravity changes over the course of the day? Why should it?

Gravity (at a given location at a given height) doesn't change.  A simple google search would answer your question: respiration releases carbon and water, you sweat, releasing water, and you spent eight hours not eating to boot.  http://www.businessinsider.com/weight-morning-skinnier-2014-7

Veritasium: Are you lightest in the morning?

There is a related question: Physics SE: Are we slightly lighter during the day and slightly heavier at night, owing to the force of the Sun's gravity?, which might be what you mean by "gravity changes", though the commonly held misconception of why you should loose weight during the night is due to digesting food and burning calories (and debunked in the answers below).

Veritasium created an excellent video just on this topic, which I would recommend watching, but will summarize here.
A common misconception is that we lose weight when we digest food or burn calories. Keep in mind that that broken down food and those calories* aren't "going anywhere", so technically you shouldn't loose any mass (unless you get rid of the molecules by going to the restroom).
However, in the "informal" tests done by Derek Muller, he lost about 250 grams each night. Since during the night you sweat (which evaporates or gets absorbed into the sheets and blankets), he estimated that about 150 grams was lost through perspiration and breathing out water vapor.
The more surprising loss of mass, was 0.012 grams of carbon lost with each breath when breathing in oxygen, and then breathing out carbon dioxide. Although this seems like a tiny loss, assuming you breathe in and out about 7,680 times each night, that tiny mass loss adds up to almost 100 grams of weight loss through breathing alone.
I guess health magazines should start running articles like "Top way to lose more weight? Researchers say breathe more!"

* Technically calorie is a unit of energy and not an item that can be "burned". What we mean when we use the word is the process of molecules being broken apart, which releases energy that can be used by the body; however, the pieces of the "broken up" molecules still weigh the same as the molecule as a whole, so we don't loose weight just from "burning calories".

It's not really so surprising. Carbon is converted to Carbon dioxide which is exhaled. A quick back-of-the envelope calculation shows this makes sense: 1kg of fat has about 38000kJ, that's a bit over 3 times the energy used in a day, so if we don't eat, we convert about 300g fat into CO2 in a day, or 100g during sleep (1/3 day).

There is indeed a slight weight variation during the day. About 2 - 4 lbs (approx. 1 - 2 kg) [1, 2].
Some causes are:

water loss through respiration, perspiration or urination [1].
the relative long period without eating and drinking [2].
metabolic processing of food and drinks during sleep.

References:

Cindy Banyai. http://www.livestrong.com/article/483853-how-much-can-weight-fluctuate-from-morning-to-night/
http://www.weightlossforall.com/weighing-less-morning.htm

Not eating or drinking and Metabolic processing does not change your weight/mass, that violates conservation of mass. The only thing that affects body mass are excrements (from urine, sweat, and faeces), respiration, and very small amount of debris from your skin/hair.

Mass can be converted into engergy. Setting something on fire does change the weight/mass of for instance your house, doesn't it? This is what your body does when you "burn" calories. You don't eat (add something), but your body stays 37 degrees -> the energy to keep it that temperature (even ignoring things like heartbeat and other processes like your brain) has to come from somewhere. Apart from that, the law of conseveration of mass deals with closed systems (also closed for energy!) which you body certainly isn't.

@Nanne Mass isn't "converted to energy", at least not in our human body (unless we go thermonuclear, which would be awesome, but just doesn't happen). What we do when we "burn" calories is break the chemical bonds between glucose(?) molecules; the breaking of these bonds releases the small amount of energy stored in them by the plants that spent that same amount of energy in order to produce those bonds. The combined mass of the "broken apart" molecules is still the same as the "complete" C6H12O6 molecule.

(If a biologist or chemist could double-check my comment, I wasn't sure if it was glucose or sucrose that gets broken apart. Moreover, as I only have a basic understanding in the field, I may have other minor flaws in my comment)

@Nanne Setting something on fire does change the weight/mass of for instance your house, doesn't it? > It doesn't; if you measure the increased weight of the air (the smoke particles in it) and the remaining ashes, there is no difference in weight. Technically there is a loss of mass, but it is unmeasurable by any equipment you could buy at a store.

There is only one way to gain weight, consume things. Thus after any period of time not consuming anything (i.e. sleeping) we must necessarily weigh <= what we weighted at the start of that time period. Add in respiration, and that becomes a strict inequality!


text:
What is the effect of extra-cellular potassium concentration on heart rate and conduction velocity?
If the extracellular potassium concentration surrounding a myocyte increases, then the potassium gradient accross the cell membrane decreases, and therefore the resting membrane potential will become more positive.  Similarly, if extracellular potassium decreases, the resting membrane potential will be more negative.
With this in mind, how does the heart rate change when extracellular potassium concentration increases/decreases?

Pathological potassium concentration promotes arrhythmia.
Increased extracellular potassium inactivates $Na^+$ channels and opens $K^+$ channels, causing the cells to become refractory [1]:

Increased extracellular potassium levels result in depolarization of the membrane potentials of cells due to the increase in the equilibrium potential of potassium. This depolarization opens some voltage-gated sodium channels, but also increases the inactivation at the same time. Since depolarization due to concentration change is slow, it never generates an action potential by itself instead, it results in accommodation. Above a certain level of potassium the depolarization inactivates sodium channels, opens potassium channels, thus the cells become refractory. This leads to the impairment of neuromuscular, cardiac, and gastrointestinal organ systems. Of most concern is the impairment of cardiac conduction which can result in ventricular fibrillation or asystole.

Decreased extracellular potassium leads to hyperpolarization [2]:

Lower potassium levels in the extracellular space will cause hyperpolarization of the resting membrane potential. As a result, a greater than normal stimulus is required for depolarization of the membrane in order to initiate an action potential.
In the heart, hypokalemia causes hyperpolarization in the myocytes' resting membrane potential. The more negative membrane potentials in the atrium may cause arrhythmias because of more complete recovery from sodium-channel inactivation, making the triggering of an action potential less likely. In addition, the reduced extracellular potassium (paradoxically) inhibits the activity of the $I_{Kr}$ potassium current and delays ventricular repolarization. This delayed repolarization may promote reentrant arrhythmias.

References:

Wikipedia contributors, "Hyperkalemia," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Hyperkalemia&oldid=612096441 (accessed July 12, 2014).
Wikipedia contributors, "Hypokalemia," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Hypokalemia&oldid=612818488 (accessed July 12, 2014).

source: Stack Exchange

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

sort: votes


text:
How do taenia form a species?
I know that there are many hermaphrodite animals and plants. But many of them seem to still exchange genes by mating with another member of their species.
I now happened to read the Wikipedia article on Beef tapeworm, and it turns out that there normally is one worm per host, and it self-fertilizes. Which makes some sense - if I were a large internal parasite, I wouldn't want to wait around for my host to pick up a second member of my species before I can reproduce.
But this means that there is no gene exchange when taenia reproduce. Does it mean that they are all clones of each other, barring spontaneous mutations? How does evolution function in taenia when they don't mate? How comes there are different taenia species if they can't evolutionary adapt to new environments by producing offspring with mixed-up genes?

There's inter-segment fertilization, which should help a little bit with genetic monoculture. If another tapeworm colonizes the same bit of gut, I imagine they reproduce sexually while they can. Curiously few resources on tapeworm sex out there.

You may want to have a look to the various existing definitions of species on the wiki page and eventually this post about ring species

This question has a related issue that should be addressed first: what is a species? To some extent, if you want to understand how speciation can occur, then you have to consider how you are going to define a species. There is no species concept that applies to all species, past or present. The most widely applied concept is the biological species concept (Mayr 1942), which applies (imperfectly) to sexually reproducing species. Of course, Taenia does not always reproduce sexually. I think the discussion of species concepts is beyond this question but I encourage those that are interested to check out references [2-4] as well as a series of papers published in Systematic Zoology in the mid-70s. Here, I'll focus on genetic differentiation with a subtext of reproductive isolation.
Genetic differences can accumulate between populations$^1$ of Taenia in two different ways. The first is non-adaptive evolution via genetic drift. Drift is when allele frequencies change by random processes. For example, just by chance, tapeworms in a particular host may not live very long because the host was killed in a mudslide. Those tapeworms don't produce as many proglottids over their interrupted life so they don't leave as many copies of their alleles. Tapeworms in a host that lives a long time produces lots of proglottids and therefore produce many more copies of their alleles.  The key point here is that the process of genetic drift is random. Allele frequency changes in one population of Taenia will be different from allele frequency changes in another population. Thus, over time, different populations of Taenia can become genetically different solely by chance. It's called non-adaptive evolution because natural selection is not evolved.
Adaptive evolution by natural selection can still occur on individuals that are asexually reproducing. Genetic differences will accumulate in a population over time to due mutations. Some mutations may be beneficial, some may not. Selection can increase the frequency of beneficial mutations and decrease the frequency of very mutations. Note that non-lethal but harmful mutations can accumulate in asexually reproducing species (see Muller's Ratchet) but I am assuming survivorship is decreased by harmful mutations for this example. If we assume that Taenia in different populations are subject to different selective pressures, then genetic differences can accumulate, leading to speciation. Note that drift will also affect the allele frequencies of both beneficial and harmful alleles because drift is random.
That brings us to the "mixed-up genes". I assume you mean the new genetic combinations that occur via sexual reproduction. Even if a host typically has only one individual of Taenia (not always the case), I suspect the opportunities for sexual reproduction in a population of Taenia are frequent, especially over evolutionary time. Consider places where tapeworm infestation of humans is high. Such places often have poor sanitary conditions so the opportunity for mixing of fecal material from different human hosts is high, and therefore the opportunity for mating among different individuals of Taenia is also high. If you have many humans living in squalor over long periods of time, then you have conditions very favorable for sexual reproduction of Taenia. Remember too that Taenia produce lots of proglottids, each with the chance for reproduction. Each reproductive opportunity creates new genetic combinations potentially subject to natural selection.
The final point to consider is population size. If the population size of Taenia is small (relatively few individuals) then genetic differences can accumulate fairly rapidly by genetic drift but the accumulation of beneficial mutations in the population will be low. If the population size is large then new mutations including beneficial ones can occur relatively often, increasing the rate of adaptive evolution among different populations.
Footnote

I'm assuming some sexual reproduction among individuals of the same population and individuals from different populations do not interbreed. Without sexual reproduction, we have to think about the individual as the species and that makes my head hurt.

References

Mayr, E. 1942. Systematics and the origin of speceis from the
viewpoint of a zoologist. Columbia University Press, New York, USA.
Howard, D.J. and S.H. Berlocher (eds.). 1998. Endless forms:
Species and speciation. Oxford University Press, Oxford, England.
Wheeler, Q.D. and Meier, R. (eds.). 2000. Species concepts and
phylogenetic theory: A debate.  Columbia University Press, New
York, USA.
Coyne, J.A. and H.A. Orr. 2004. Speciation. Sinauer Associates,
Inc., Sunderland, Massachusetts, USA.

Extension of Question
Beef tapeworm or Taenia saginata
Beef tapeworm or Taenia saginata shows both asexual and sexual reproduction. As you have mentioned if any other partner is not available then it will carry on asexual reproduction.
Now,

Scolex or the hook attahes to the host.
Scolex reproduce asexually by budding.
One tapeworm segment or proglottid takes around 10-12 weeks to mature.
There can be 1000-2000 Proglottids in the worm body.
Proglottids are Hermaphrodite when mature.
Each of these proglottids will produce around 100s of eggs.

That means,

A full grown tapeworm can produce from 1,000 to 2,000,000 eggs a day. They survive up to 20-25 years
Any mutation can be exponentially magnified in the generations as mostly the reproductions are sexual type(after the initial budding or occasional self sexual)

Update
According to wikipedia:

Because each proglottid contains the male and female reproductive
  structures, they can reproduce independently. Some biologists have
  suggested that each should be considered a single organism, and that
  the tapeworm is actually a colony of proglottids.[3]

Source:
[1] http://en.wikipedia.org/wiki/Beef_tapeworm
[2] http://animaldiversity.ummz.umich.edu/accounts/Taenia_saginata/
[3] http://en.wikipedia.org/wiki/Cestoda

Maybe I got something wrong, but in my understanding, a proglottid is not an animal, but a piece of the animal. The scolex buds asexually, passing its complete gene set to each proglottid. This means all proglottids of the same worm have the same set of genes. Now, a proglottid can fertilize itself or the neighbour proglottid, but it doesn't matter, because the genes of the mother proglottid and the father proglottid are still the same. This doesn't lead to new gene mixes. Or did I misunderstand the budding mechanism?

male and female taenia don't exist. A taenia is a hermaphrodite. So each proglottid can be like the other one, no difference in chromosomes needed.

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Regarding apoptosis and turning it 'back on'
Is there some chemical or chemicals or even special molecules that can be 'injected' into cancer cells that will turn any Apoptosis mechanisms 'back on'?
Or maybe chemicals and/or molecules that might cause a certain gene or set of genes to switch to a configuration favorable to apoptosis?

There are many. The two main problems are 1. regulatory network in cancer cell is different from normal cell, 2. Specific delivery of the killing molecules to cancer cells

If the regulatory network in a cancer cell is different from a normal cell could some of these differences be 'marked' by some chemical so as to identify a cancerous cell? Could such a cellular difference being marked with a biological marker be a useful target for a modified 'mild' virus?

Yes, tons of things induce apoptosis. Here is a good list that you can get for research grade
Sigma-Aldrich
Even your immune system can tell cells to "commit suicide." Now the trick is, getting drugs, proteins, pathways, and your immune system to selectively target cancer cells.

If it is tricky to selectively target cancer cells does this mean they are hard to detect by the host body? Are they almost invisible to medicine? Could cancer cells emit or give off chemical signals that make them hard to detect?

Yes to all of those questions. They are especially tricky to the immune system. Usually what chemotherapy targets is rapidly dividing cells, which coincidentally also non-specifically targeting hair root folicles.

I heard on the radio some Biologist named Michel Fossil who wrote about 'Reversing Aging' had researched about increasing Tellomeres or 'resetting' them to a state similar to how they used to be actually improved cellular functions as if they were 'younger'. Could improving the Tellomere 'length' or functioning in a cancer cell make the apoptosis mechanisms in the cell 'turn back on' or start functioning as 'they' used to before the cell became cancerous?

Do cancer cells have telomeres and would they be 'extra durable' ( as a cancer cell keeps functioning indefinitely)?


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Differentiating Taenia solium and Taenia saginata Infections
I have been told that both are spread by pigs and cattle, respectively. I would like to know the complications caused by Taenia solium and Taenia saginata. Also elaborate how dangerous is one as compared to the other, as well as preventive measure.
I googled , and found no relative comparison between these two.
Thank you.

Taenia solium is more dangerous:

T. saginata is relatively innocuous, since only the intestinal tapeworm phase occurs in man, whereas infection with T. solium has major health effects due to extraintestinal infection by the larval or cyst phase in the CNS [1].

The most feared complication of Taenia solium is cysticercosis. Taenia saginata can lead in extreme cases to intestinal obstruction.
Preventive measures:

improved hygiene
adequate thermal processing of meat [2]
preventing contamination of animals (pigs and cattle) [3]

Differential diagnosis:

PCR [1, 4]
Hematoxylin-Eosin Staining [1]

References:

Mayta H, Talley A, Gilman RH, Jimenez J, Verastegui M, Ruiz M, Garcia HH, Gonzalez AE. Differentiating Taenia solium and Taenia saginata infections by simple hematoxylin-eosin staining and PCR-restriction enzyme analysis. J. Clin. Microbiol. 2000 Jan;38(1):133-7. PubMed PMID: 10618076. Cited text is from full text article available from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC86038/
Wikipedia contributors, "Taenia saginata," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Taenia_saginata&oldid=618599196 (accessed July 28, 2014).
Wikipedia contributors, "Taenia solium," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Taenia_solium&oldid=618599210 (accessed July 28, 2014).
Luis Miguel González, Estrella Montero, Leslie J. S. Harrison, R. Michael E. Parkhouse, and Teresa Garate. Differential Diagnosis of Taenia saginata and Taenia solium Infection by PCR. J. Clin. Microbiol. February 2000 vol. 38 no. 2 737-744


text:
What are good sources of free-to-use images and diagrams
I am looking for good image repositories for biology teaching. Photos and textbook-like diagrams.
I am interested  in images that can be used commercially without payment, or, at least, that require a small one-time payment. They would be used in videos, not only on lectures, hence the worry about copyright.

i take it you mean on biology?

I'm guessing the videos are for a flipped/online course and posted on YouTube or Coursera?  I've done this. Biology is hard -- perhaps because I am picky and really want good images.
I used Wikimedia.com to search for many free images. I also contacted the publishers of the free online version of Molecular Biology of the Cell and asked if I could use up to 20 for my free online course, and they agreed.
My university was also able to work out an agreement with the textbook publisher to use 200 of the textbook images for the Coursera course as long as they were credited, and a link to purchasing the textbook was available on the site. They want to keep my university happy as our students buy a truckload of books every year.
I've also gotten somewhat decent at using a drawing tablet and powerpoint image (boxes, circles) manipulation to make some of my own cell processes and chromosomes and such.
Lastly, OpenStaxCollege.org has a wonderful collection of free textbooks for students, and they make their images available to faculty as free powerpoints. They aren't usually "good" enough to satisfy me, but definitely check them out.

You could use CC Search. It allows you to find Creative Commons licensed content that you can use commercially.

Another interesting source is somersault18:24.

An excellent source for images is the wellcome collections image library http://wellcomeimages.org/. You can negotiate commercial use with them, they are very reasonable, especially if it's for teaching purposes.


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Are trees the only source of large amounts of oxygen?
Trees use carbon dioxide and produce oxygen in the presence of sunlight.
But is there any other source?
If yes, are trees the most important source of oxygen, or is there any other source which produce more than trees do?

Like I mentioned in your previous post— did you google something about it? Did you check about photosynthetic organisms other than land plants?

Yeah, I found that water molecules are split apart after being struck with ultraviolet radiation and oxygen called photolysis and many other chemical reactions which happens in earth atmosphere. I didn't mentioned as it will be quite off topic.

Why trees? They represent a very small part of the plant population of the planet. They just happen to be big.

@terdon - in terms of biomass trees do account for a lot of vegetation, and yes, because they are big. It's not about numbers, but mass.

@AliceD in terms of biomass, I'm pretty sure they represent a very small fraction when compared to photosynthesizing algae and phytoplankton as you point out in your answer. Let alone the grasses.  Individual trees are big, yes, but there are not that may of them. In any case, 1) I only mentioned the plant population, not biomass and 2) only a very small part of a tree's biomass is actually photosynthesizing so biomass is not really relevant anyway.

Unfortunately, this, as a relatively highly upvoted question, doesn't show research effort whatsoever. It seriously doesn't take more than a few Googlings to find out what 'aquatic' organisms can photosynthesize.

71% of the earth's surface is taken up by water. Not surprisingly therefore, the seas are an important source of oxygen. National Geographic claims that photosynthesis by phytoplankton (mostly single-celled phototrophs, such as cyanobacteria, green algae and diatoms) account for half of the earth's oxygen production. The other half, they claim, is produced on land by trees, shrubs, grasses, and other plants.
The Ecology Global Network takes it a step further and claims that all marine plants (including phytoplankton) together produce 70 to 80 percent of the oxygen in the atmosphere.
Based on these reports, hence, marine phototrophs account for 50 - 80% of the earth's oxygen production.
With regard to terrestrial oxygen production, NASA reports that 30% of the land is covered by trees, and as much as 45 percent of the carbon stored on land is tied up in forests. So on land, trees are definitely large contributors to oxygen production.

Not to mention that natural forests are going to be almost entirely oxygen-neutral on average; your typical natural forest will produce as much oxygen as it consumes (the dead trees will eventually decompose, consuming oxygen and releasing carbon dioxide among other things). To make them an oxygen-positive system, you need to prevent the decomposition - for example, in a bog (as in the trees we now mine as coal), or by cutting the trees down and making stuff out of the wood. So it's actually the industrial forests that consume more carbon dioxide on average than they produce. Now.

It's worth adding that trees are a very recent addition to the planet's oxygen budget. It was the evolution of cyanobacteria in the early oceans that produced all that oxygen in the first place!

I am not sure which class of organisms have the highest contribution in oxygen production but diatoms do have a significant contribution. The introduction in this paper says that diatoms account for 40% of marine photosynthesis which according to this site is "1/4 of the oxygen we breathe."

Trees are definitely not the only source of oxygen. First, all green plants do photosynthesis, not only trees. Moreover, about half of all photosynthesis on earth is done by microorganisms in the oceans known as phytoplankton.

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


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Do cows produce milk excessively?
Do cows produce more milk than it is required for their calves? It seems like cows are able to provide milk all the time (all year around). Is it so? Or do they, like other mammals, produce milk only in ammounts requeired by their offspring?

milk cows have millenium of selective breeding for milk production. they produce 2-3 times more than normal cows and have crazy sized udders. In the wild, can baby animals risk drinking too much milk? not really! Mammal milk production is normally decided by A/birth and B/the babies appetite and then weaning.

Dairy cows are bred, or selected to give milk.  So they do produce excessively.  The normal bovine wild type, like other mammals, not only produce less milk, but also will tend to stop lactating when the calf is not nursing.
I would be interested to know if dairy cows stop giving milk if they are not milked every day.  I understand they can get very uncomfortable if they are not milked, but i don't know if they stop giving milk or if they are injured in some way.

Can you please provide a reference for the fact that if you milk a wild cow (good luck with that) every day, after removing its calf, it will stop producing milk at some point? Alo, if they are selected to produce more milk they do not produce it excessively. If you select a plant to have bigger fruits, its fruits are bigger, sure, but they do not grow excessively, they just grow the right size for that particular plant, which happens to be bigger than other plants.

@nico "The calf is not nursing" I think he means after the calf is weaned. Also, 'excessive' is a relative term. A cow producing 4 1/2 gallons per day would be considered poor by the farmer, but is excessive in terms of her calf's needs.

@jmusser: that is what I am saying. If you get a wild cow and continue to milk it after weaning its calf it will most certainly continue to produce milk.

The average domesticated dairy cow produces far more milk than would be required to feed their calf. All cows, wild and domesticated, will only lactate in the period between their calf's birth and weaning. Milk is calf-food, and when there's no calf, there's no evolutionary advantage in producing milk.
On dairy farms, cows are milked twice daily, from spring (when they give birth) until late autumn. This mechanical milking 'fools' the cow into continuing to lactate. When a cow has stopped lactating, they will only start again after giving birth. This means that you can't just start milking a cow and expect to get milk.
Generally farmers milk their cows from spring (birth) until late autumn. The reason for stopping in autumn is simply because the grass grows much slower in winter, so there isn't enough food to support lactating cows. However, it is entirely possible to milk longer than a year; I know of farmers who milk their cows continuously for two years. These farmers will have to purchase a lot of supplimental food (like hay or silage) during winter. The advantage of milking for longer than one season is that the cows do not have to give birth every spring, but instead only every second spring.
I believe (but can't guarantee) that in winter, most milk purchased in a shop comes from the opposite hemisphere. I do know that here in New Zealand, we export a lot of milk to northern-hemisphere countries.
If you were to suddenly stop milking a cow, they might get sick but generally they will survive. It's still something to avoid!
Although if the calf is left with their mother then the cow would be relieved.
I do not have an 'official' source for these facts. However, I grew up on a dairy farm, so this was my life.

Thank you very much. This answer seems most informative and real-life applicable.

I was under the impression that certain breeds (holsteins for one) have been so over bred for the milk producing trait that there are periods where there milk production is so high, not being milked can actually cause the udder to tear allowing them to die from sepis.  Note: that's anecdotal I don't have information confirming or denying it.

Cows only produce milk after a calf is born and their lactation period lasts approximately 10 months. In many instances, farmers have given growth hormone (GH)¹ to cows in order for them to produce more milk. It must be noted that there are many side effects associated with this, not to mention the residual effects it may have on us humans as consumers. Primarily though, the cows would have decreased immune efficiency and this would leave them vulnerable to all types of parasitic infections or disease.

Welcome to Bio.SE. Can you give a reference to the GH use? The calf-bit is pretty much common sense So reference not needed there :) Thanks for your contribution!

Thank you for the welcome ^ ^ (is there a specific format for references) this is a scholarly article on the subject: http://goo.gl/MDvaDL ..also the wiki is found here: http://goo.gl/thQnmE

If you click the link icon (the chain shaped icon) in the question window, it allows you to insert web links to articles etc. However - the wiki page you refer to is about sex hormones (estradiol, progesterone etc) and the article link is on antibiotics. I have downvoted your answer as it needs work since your claims about GH may be unsupported in the literature. After edits I am happy to upvote, don't worry.

Thank you for explaining this AliceD, I have added a GH reference now.


text:
Why is post-vaccination fever for 4CMenB so frequent?
When considering the introduction of 4CMenB vaccine, the Joint Committee on Vaccination and Immunisation said:

The sub-committee noted that the clinical trials data suggest that
  when  4CMenB vaccine is given concomitantly with other routine
  childhood  immunisations a substantially increased frequency of
  vaccine-induced  fevers should be expected. Vaccine-induced fever
  rates may be similar to  those associated with whole cell pertussis
  vaccine used in the past.

What is the likely explanation for the higher rate of fever for 4CMenB in comparison with other vaccines?


text:
Is it possible to combine live attenuated and non-live vaccines?
There are many combination vaccines available but I've noticed that there don't seem to be any with both live and non-live components, e.g. DTaP/IPV/MMR. Such combinations could be useful in some cases, since most developed countries give a second dose of MMR (or MMRV) at the same time as DTaP/IPV. Is there a biological reason that this is difficult?

by live, do you mean attenuated vaccines?

@The Last Word: Yes

typically the manufacture and storage of live (attenuated) and inactive (killed, dead, kaput) vaccines is rather different, and the effective shelf lives can vary significantly. For example, inactive vaccines often have preservatives in them, which may be incompatible with live viruses. A killed vaccine may be stored at room temp, while an attenuated one may require refrigeration.

+1 It's not actually difficult, it's more a question of practicality (when the vaccinations are given), and which vaccines actually work (live attenuated almost always elicits a stronger immune response, but can have more complications).  Working on a detailed answer now.

I'll make the comments into one nice answer.

@Chris thanks for that.  Sorry I went AWOL.  Turns out I had to have surgery on myself for once.  Truncated the answer I was going to write to what's below.

@AtlLED I hope you are fine. I was browsing through unanswered questions....

First let me point out that for the US, I'm not knowledgeable enough to speak for the rest of the world, you are correct.

There are no approved live attenuated vaccines mixed with componet/subunit/inactivated vaccines.

Background:
Before we go into why that's true, let's work a little to show that's true.  The FDA publishes a wonderful list of every approved vaccine for use in the US.  Of the 78 vaccines listed (and there is a lot of redundancy due to different manufacturers etc), only 16 are live attenuated (or about 20%).
Another thing to notice is that we have vaccines to both viruses and bacteria.   Technically, some of the vaccines are to bacterial toxins, not bacteria themselves, but for the sake of simplicity, we're going to group all bacterial component, subunit, and inactivated vaccine preparations together in one group.
First you will note that there is only one live attenuated vaccine for bacteria, Mycobacterium bovis (more on this exception later).  There are several reasons for this, but as a general rule, you don't want to put a foreign object capable of self replication inside a person.  Viruses cannot self replicate, they are obligate parasites by definition, so they don't fall under this rule.  One could, however engineer bacteria that were sufficiently deficient in replication that this might not be an issue.  Another safety concern with live attenuated bacteria is sepsis.  Again by choosing a delivery route that doesn't involve injections, you might be able to mitigate this risk.
I also want to be clear that I think live attenuated bacterial/fungal (yeast mostly) vaccines can work more broadly, and are likely to be used in innovative vaccine strategies.
The main obstacle to a live attenuated bacteria vaccine is that the component and subunit vaccines work.  Sometimes they work even better by only supply the part of an organism that is known to provide broad neutralization (getting rid of) of the pathogen.  And if you know that you can provide protection with out the risk of putting the live organism in a person, why would you take that risk?
Quite simply you don't.  Back to M. bovis.  For the most part, humans are not vaccinated with M. bovis (BCG) to prevent M. Bovis infection (though zoonotic infections can occur).  Instead it is to prevent M. tuberculosis (MTB) infection.  Attenuation of MTB is difficult, and not complete.  Indeed we don't have a subunit or component vaccine that has worked for MTB, and an inactivated MTB has more safety concerns than BCG.  Thus we choose a related organism, M. Bovis, which naturally doesn't cause disease in humans (or rarely), but can provide some protection against TB.  Even the product insert admits that efficacy of the vaccine is in question.
The same pattern of necessity holds true for viral live attenuated vaccines.  They are used when you need a more immunogenic vaccine, and where we haven't been able to make safe and effective, inactivated, subunit, or VLP vaccines.  Thus when you need a live attenuated vaccine, you really do need it to be alive for it work.

Answering the core question:
As @MattDMo pointed out, the storage conditions are very different for live attenuated vaccines.  Not only that, but most of the preservatives used in many inactivated vaccines cause titer loss (though there is work to find alternatives).
On the theory that a picture is worth a thousand words, I did a little experiment just for this post (and also I was cleaning out an -80).  I took a high titer stock of measles virus that has a protein tag on one of the proteins so we can easily detect it (F is Flag tagged).  Then I spiked 3 different tubes of virus in ether PBS (saline) or DTaP (an actual dose, just past expiration), and left them in the refrigerator (4oC) for 8h.  Note that Merk thinks you should toss the measles vaccine if you don't use it within 8/hours (also note their comment on preservatives).  Then I infected some cells that grow up measles, and harvested the cells in a total cell lysate.  Finally I ran equal amounts of total protein form each preparation on a gel for a western blot:

You should notice the three pairs of bands, in each case the lighter band (indicating less protein) belongs to the DTaP group.  That is to say less measles F protein (something you want to make antibodies to) came from the samples that were put into the DTaP vaccine compared to PBS.
Another serious problem is cold chain:
Again we need the virus to be "alive" when we give a person a vaccine.  This almost always means that we have to keep it frozen or at least refrigerated from the manufacturer, all the way up until moments before it goes into a person's arm.  There are many good reviews on cold chain to be found.  Quite simply, inactivated and component vaccines do not have the thermo-stability requirements that live vaccines do.  It would be a waste of energy in most cases to chill all of the vaccines which could be left at room temperature, and it would remove one of their clear advantages.
As far as the immunology is concerned, there is probably not a real limit on what the body can react to.  Indeed, as you point out, they are often administered at the same time in developed countries.  It is merely a question of how you can keep live-attenuated vaccines "alive" in the same preparation.  It is certainly possible that there is a solution to this, and vaccine stability is an active field of research.  Hopefully in 10-20 years we will be able to adjust this answer to say that such a vaccine has been made, and that it's safe enough for approval.

It would be interesting to see, how these mixed vaccines perform in tests.

The major reason for this are differences in the preparation methods. Live (attenuated) vaccines need permanent cooling, which makes their use in third world countries difficult.
Inactivated vaccines are inactivated either by heat, radiation of chemicals and are often freeze-dried after purification (removal of chemicals used for killing). In this condition, they have a very long shelf-life and need no cooling. Before use they are dissolved in water and then administered.
There is another problem with mixing these vaccines: Live vaccines can not be given to anybody, people which have a weakened immune system (because of an infection like HIV, chemotherapy or the adimistration of drugs, which downregulate the immune system after an organ transplantation) are not able to receive them. The attenuated pathogen which replicates usually only slowly would still be a possible danger for these people. So they can still be vaccinated with inactivated vaccines to provide at least some protection.
For more information on this topic see the chapter on immunization in "Microbiology and Immunology online" and this information from the National Institute of Health.


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X-recessive disorders and genetic markers
Please observe the following pedigree of a family with a x-recessive disease (bleeder disease).

The A's are genetic markers so close to the disease gene that recombination is negligible.
I understand it like this: They place markers that cut the DNA at the locus of the diseased gene. If you have the disease, your gene snip will be different in size than someone who does NOT have the disease and this will be visible on a gel.
So if A1 is the disease marker, how come II:1 is not affected? He only has 1 X-chromosome and has the A1 marker?
EDIT: Another problem:

Is the coming child affected? Here I don't understand how the mother A1,A1 is NOT affected when the child A1 is?! Obviously A1 is the diseased marker and the mother has two of them...So she should be sick? Unless it's spontaneous?
Am I misunderstanding something fundamentally?

You might also want to read this: http://genome.wellcome.ac.uk/doc_WTD020778.html

Genetic markers don't cut the DNA. They're simply regions of DNA sequence that happen to be variable between individuals (see my answer to your previous question). They might be measured using restriction enzymes (i.e. RFLP) to identify the exact difference, but it's not the marker that's cutting DNA. Furthermore, they don't necessarily cause disease. They're used in pedigree analysis to find regions that are linked with various phenotypes, among which is disease. However, linkage does not imply causation, especially with so few individuals.
To answer your first question II:1 isn't in the affected family - he married into it. In the affected family, A1 has become linked with the disease mutation. It is not necessarily linked with the disease in other families.
This is also the answer to your second question. I:2 has A1 marker on one chromosome associated with the disease allele, and one that's not. II:3 presumably inherited an X chromosome with the disease allele.

So the unaffected individual who is married into the family has the same marker on the gene, called marker A1, in other words, if there's a sequence AGTAGTAGTAGT in the affected family and it is called marker A1, this means they have a disease, but he also has this sequence but not the disease because he doesn't have other traits the family members have? Am I finally understanding this right? (I'm really trying!)

Almost, but not quite. There is a marker A1 that has sequence AGTAGTAGTAGT where individuals with A2 with have sequence AGTAGTAAAAGT at the same A locus. Some very short distance away from the A locus, there is a disease locus - when individuals have only the m allele instead of the M allele, they have the disease. Because the A locus and the M locus are so close together (i.e. linked), meiotic recombination is very unlikely. So if the M locus becomes mutated on one chromosome that happens to have the A1 allele, the disease m allele becomes linked to the A1 allele +

(cont'd) and you will see that the disease goes along with the A1 allele in successive generations. However, it could have just as easily been the M locus becoming mutated on a chromosome that has the A2 allele - and in some other families, this might be true for the same disease. In that case, the disease will be associated with the A2 allele for that family, for the very same disease. The marker allele is only informative within the context of a single pedigree - you don't know which allele is associated for unrelated families. What you do know is that the marker is linked to the disease +

(cont'd) because the two loci are so close by -- it could just be a different allele in different families. Does that make sense?

It all makes sense and I'm drawing it up right now but it would help if you clarified what you mean by "m" and "M" allele as it is the only thing confusing me and I need that information to read the rest of the answer.

m = disease-causing allele, M = wild type allele.


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How does frame-shift mutation not absolutely ruin the organism?
I'm a bit curious as to how frame-shift mutation works. If you shift one amino acid towards another. How does this not affect the entire chromosome? Wouldn't this mean that the organism would be absolutely "scrambled" as it would essentially be "missing" a whole chromosome...Or having a chromosome that did all kinds of wrong things at least?
Thanks.

have you read at least wiki article on frame-shift mutations? Basic structure of genome is blocks of (Promoter:gene) type sequences. So what happens inside gene sequence is isolated for that gene only

For transcription, the cell uses different signals from start- or stop- codons to determine the start and end of a transcript (see this wiki page). Codons (and hence frameshifts) are only relevant at translation of the mRNA to protein. Frameshift mutations occur in coding sequence, so the promoter and termination signals for transcription are unaffected.
Genes which are further downstream will be transcribed normally from their own promoter and their coding sequence is still in-frame with their own start-codon.
When a frameshift occurs in coding sequence, the genetic code downstream can indeed be considered 'scrambled', much alike random nucleotide sequence. In random sequence, three nucleotides have a 3/64 chance of being a stop codon. So one would not expect translation to go on beyond about 20 amino acids from the mutation. Additionally, non-sense mediated mRNA decay will detect these premature stop codons and destroy the mRNA.

The untranslated region (UTR) isn't translated by the ribosomes (hence its name), and therefore contains no reading frames, because it is never "read."  Without a frame, the term "frameshift" mutation does not have a clear sense.  Perhaps you mean a small indel in the 5'-UTR could affect the translation initiation site? By definition a frameshift can only occur in the region of the mRNA downstream of the initiation codon and upstream of the termination codon. Well, in the DNA that encodes that region of the mRNA.

Also, any single frameshift (i,e., downstream of the ATG) HAS to throw the STOP codon out of frame.  There is nothing special about proximity to the translational termination signal (e.g., "the terminal exon").

terdon, my first point is about transcription, not translation

Oh good grief. I was really on fire that day. I also had a stupid error in my own answer. Sorry about that, Sleepses, @mdperry, comment deleted.

First of all, for a frame shift mutation to occur nucleotides (not amino acids) are either deleted or inserted into the sequence.  Read about details on this wiki page. Here's an image about frame shifts.
On panel A a new stop codon is formed  (TAG is trasncribed to UAG that is serves as stop codon during translation) thus the result is an abnormally short protein.
On panel B the codon 37 is swapped to a G thus the TA from the codon 38 is shifted left by two resulting in the new codon GTA.
On panel C exactly 3 nuleotides are deleted thus codon boundaries do not change, but a codon and the amino acid encoded by it is completely deleted.
On panel D 4 bases are deleted thus the T form codon 171 and the C from 172 are merged with the G from 170.

source: the linked wiki page.
It does not affect the choromosome in the way you describe because genes are separated and are independently transcribed (with some simplification). Every gene has its own translation  start that determines the correct frame in that gene If you think of a chormosome as a chapter of a book and the genes are paragraphs, you can see that deleting letters or words may scrable one paragraph, but the others are not affected by this because they have their own boundaries.
EDIT:
During translation the ribosome reads the mRNA in the form of triplets. When a single nucleotide is deleted then the whole sequence from that point shifts to the left by one thus the first letter of the subsequent triplet gets mixed into the frame where the mutation happened (the same goes for insertion but the sequence is shifted to the right). This causes the change in the meaning of the triplet, and can ruin stop codons that would affect the translation of the mRNA but not the transcription of the gene to mRNA.It is important to understand that transcription is a countinous process and the DNA is transcribed from base to base not in triplets, and that transcriptions stop is not encoded in the from of stop codon.

So the stop and start codons are not frame shifted?

I've edited my answer I hope it helps.

Okay so when does the RNA polymerase stop then? I thought it would start coding for a gene at a start codon and stop at a stop codon?

As I indicated in my answer codons only play role and make sense in terms of translation. Genes have promoters and transcription start sites to initiate transcription and transcription termination signals and polyA signals to indicate the end of transcription. All these signals are longer than 3 basepairs. I suggest reading this wiki page.http://en.wikipedia.org/wiki/Gene this covers many basic things

No, it wouldn't. In order to understand why, you must understand that

Genes are translated independently of one another. The ribosome starts translating at a start codon (ATG) and stops at one of the three stop codons (TAG,TAA and TGA). Whether another gene has a frameshift mutation or not, does not affect the current gene in any way. The ribosome will always1 start at the ATG and stop at the STOP codon.
Genes make up only a tiny portion of the total DNA, especially in eukaryotic organisms. In humans, for example, genes are ~5% of the total DNA.
The vast majority of DNA falls in intergenic regions that do not code for protein. For example:
  gene1             INTERGENIC REGION               gene2
---------|----------------------------------------|---------
ATGCCGTAGgcgtatagcgatatcgcatcgctatcgatacgctdcggcgcgATGCACTGA

While a frameshift might throw the first gene out of sync, the second will not be affected. The intergenic regions are not translated, so frameshifts are irrelevant to them.

So, a frameshift will only affect the gene it occurs in.

1 There are some exceptions to this, some alternative start codons but they are not really relevant to the discussion here.

A frameshift will affect all downstream coding sequence, regardless of what exon the mutation occurred in.

@canadianer no, it will only affect the downstream sequence of its own exon. The splicing signals are not codons and won't be affected unless the frameshift occurs in the acceptor or donor sequences themselves. How would a frameshift affect a different exon otherwise? Remember that we're discussing frameshifts that happen at the DNA level. Naturally, post transcriptional modifications/mutations are a whole different ballgame.

The reading frame of the first exon defines the reading frame for all subsequent exons since they are literally ligated together into one long coding sequence. If you have two exons, say AUGGUA and AGUUGA, they are spliced together and translated to get the peptide Met-Val-Ser. If there's an insertion in the first exon such that it becomes AUGAGUA, the peptide, after splicing with the second exon, becomes Met-Ser-Lys-Leu-… Thus the frameshift in the first exon changes the reading frame of all downstream exons.

@canadianer you're absolutely right, of course. I have no idea what I was thinking of.  I leave genomics for 5 years and I forget the basics! Answer edited,  thanks for pointing it out and my apologies for being dense.

Haha no worries. I'm sure you'll be able to return the favour for me someday ;)


text:
Pedigree problem and type of inheritance
Please observe the following pedigree and come up with a conclusion as to which type of inheritance is most likely

Now it should be obvious that it's either autosomal dominant or autosomal recessive. BUT it could also be X-recessive if the women I2 and II5 are carriers.
Anyways, if it's autosomal dominant than about 50% of children should be sick according to a punnet square.
If autosomal recessive about 25% should be sick according to the same logic.
33% of children are sick so what do you answer? My book states a very clear and only answer without explaining how it could be other forms too, autosomal dominant. Why not autosomal recessive just as likely?

1. Please read our homework policy. 2. Demanding answers generally does not go over too well. 3. Look up "incomplete penetrance". Even if a trait is autosomal dominant doesn't mean it will occur in exactly 50% of the carriers all the time. Unfortunately, Gregor Mendel fudged a lot of things, and Punnett Squares ≠ reality.

It's not really homework, I'm preparing for exams and I already have the answer as stated in the question.

That is included in the policy. Please read it.

You should use better titles... "Very easy pedigree problems annoying me heavily": what does this mean? Are you asking why some easy problems are annoying you? Keep your title to the point.

Some edits have been made. I'd prefer not to have it closed as I did receive an answer that I am satisfied with,

Let's consider all the options.
X-linked recessive:
I:2 is a carrier and II:5 is also a carrier, and I:1 is affected. Everyone who marries into this family(except for II:2, lucky guy. He better not have any sons though.) is a carrier for the same genetic disorder. While it does work, it's vastly less likely than the other options. Observe: II:4 is affected, but only because I:2 is a carrier. I:1 is entirely irrelevant.
Autosomal recessive:
I:2 and II:5 are still required to carry the same genetic disorder, but at least I:1 contributes.
Autosomal dominant: The only individual required to have the disease genotype is the affected I:1 individual, and everyone else inherits from him.
The problem asks which inheritance pattern is most likely and not which inheritance pattern is possible because of cases like this. Most genetic disorders are rare, and it's far more likely that random chance had 25% instead of 50% of four children affected than this small family inherited two sources of this genetic illness.


text:
What is a genetic marker?
In DNA sequencing and analysis, what is a genetic marker? I've heard that microsatellites are genetic markers? Those are repetitive strands of bases such as GCAGCAGCAGCA etc. Why are they markers and what defines a genetic marker?
There are many different KINDS of genetic markers as defined by wikipedia, RFLP, SNP and many more. But when you click these, you get a technique not a sequence. So I'm confused as to whether markers are techniques to find DNA sequences or if they are literally DNA sequences?
If they are literally DNA sequences, are they sequences that everyone has?
Example of RFLP:

In molecular biology, restriction fragment length polymorphism, or
  RFLP (commonly pronounced “rif-lip”), is a technique that exploits
  variations in homologous DNA sequences.

Is there something missing from Wikipedia that's confusing you?  https://en.wikipedia.org/wiki/Genetic_marker and the links on that page seem quite sufficient to me.

@WYSIWYG the OP is trying :) I asked that they break their question into smaller ones and they've done so. Paze, WYSIWIG has a point though, what is it you don't understand about markers? The first line of the WP article seems clear enough: "A genetic marker is a gene or DNA sequence with a known location on a chromosome that can be used to identify individuals or species." What more do you need?

I made some edits to my question. Hopefully it is clearer now.

Can look ask, lf you had a genetic marker say DYS392=11 and someone else had DYS392=12 because there is only one point difference between the markers will they be related to say race or ancestry ?

Genetic markers are sequences of DNA that tend to co-occur with some biological property, in a population.
Examples
E.g. Imagine you have 200 individuals in a population. 100 individuals have some sequence GGGCCCGGGCCC at some locus (position on the genome), and those 100 individuals have blue eyes. The remaining 100 individuals have AAATTTAAATTT, at the same locus and happen to have other eye colors (green, brown, etc). Then GGGCCCGGGCCC is a marker for the biological property that is "blue eyes".
Other biological properties with associated markers can include the following: (i) predisposition to having a certain disease, e.g. Alzeimers, (ii) high intelligence, (iii) and even the presence of another gene, that is you can have markers for the biological property that is "presence of gene X".
Markers of genes vs. the genes themselves
One often finds that markers for certain biological properties are the genes themselves. But this is not obvious unless one sequences the entire genomes of several individuals of a population, and doing so is expensive. It is cheaper to rely on screening for markers.
One marker to many properties, many markers to one property
You do not always have to have one marker per biological property, there may be several markers scattered across the genome that are all associated with some biological property. You can also have a marker associated with several biological properties.

As hello_there_andy (and also the Wikipedia page) has indicated, genetic markers are DNA sequences that can be used to distinguish individuals (can also be tissues, cells, etc.).
Linkage of a phenotype with genetic markers is used to identify regions of the genome that are likely causative for that phenotype, as hello_there_andy says, but there is nothing inherent to how a marker is chosen that says it has to be linked to any phenotype. Markers are typically chosen for an analysis because they are easy to measure and track, individuals differ at the locus (so you know that if your phenotype of interest segregates perfectly with the marker, it's unlikely to be chance), and they cover the genome (or the region of the genome you already know is linked) appropriately, among other things.

You put it concisely, but please be careful of using jargon like "Linkage", I will reward you upon replacing jargon with concrete analogies or clear definitions

@hello_there_andy I added a link to the Wikipedia page for linkage analysis. As genetic linkage is the topic of entire lectures in undergraduate genetics, I don't think I can summarize it in a few sentences, but that should be a starting point for the OP if he/she has further questions.

A genetic marker is, by empirical definition, something that you can unequivocally place on a genetic map.  A genetic marker may be an allele of a known gene that confers either a dominant, or a recessive phenotype. Alternatively, a genetic marker could be either a restriction fragment length polymorphism--whose segregation can be detected by either a Southern blot or a PCR experiment, or a single nucleotide polymorphism--whose segregation could be detected by a PCR experiment, or by DNA sequencing.
If two genetic markers segregate independently after a genetic cross the we say that they are unlinked--by which we mean they map to separate chromosomes. If two genetic markers do not segregate independently after a genetic cross (i.e., a mating) then we say they are linked--by which we mean the map to the same chromosome.
Knowing nothing about chromosomes, or DNA, it is still possible, given enough genetic markers, to construct a genetic map for an organism. All of the markers that map as if they are linked to each other are said to form a "linkage group".  When there are enough genetic markers to identify all of the linkage groups then the number of different linkage groups will equal the number of chromosomes (this assumes one crossover per chromosome during meiosis).
It is important to remember that chromosomes can only be seen with a microscope, cytologically, typically after fixation, and staining, whereas linkage groups, and genetic maps, do not require, or rely on, chromosomes. A genetic map, made up of different genetic markers, is an abstraction.  In some cases a genetic marker can actually be placed on the physical map of a chromosome--for example, in a species with a sequenced genome--this allows us to coordinate the genetic map with the physical map (for that locus).


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Are triglycerides fat?
I have a quick question: Are triglycerides essentially what we call "fats"?
I've tried reading up on it but there seems to be some conflicting information.
Thank you.

I think "fat" is a word that maybe it is not too recommended to use in an organic chemistry context. What I understand as fat is those "yellowish" and solid compounds, like margarine.
In a chemical context fat is often confused with the lipids, which are (be the definition broad) the amphipatic compounds, mainly composed by carbon and hydrogen and that fall in two groups, the ones that can undergo saponification and the ones that cannot. this is consequence of having or not the FATTY acids (C-H chains ended in a carboxy group).

If the fatty acids have a double bond in their C-H chain they are called insaturated, and are often liquid at room temperature. The ones with no double bond are saturated, and are SOLID. If you accept my definition of "fat", saturated triglycerides YES would be FAT, but the others would be not. Thats what I think, but I am not 100% sure

Fats include free fatty acids and their compounds with glycerol: mono-, di- and triglycerides.
In a cooking context, fats refer to solid fats, and oils to fats that are liquid at room temperature. Most of them contain triglycerides.
Fats belong to a broader group--lipids--, which are substances that are usually not soluble in water and usually soluble in certain organic solvents, such as ether or acetone. Besides fats, lipids include sterols (cholesterol, plant sterols), waxes, lipid-soluble vitamins (A, D, E, K) and steroid hormones (aldosterone, corticosterone, etc).
Examples of complex lipids are phospholipids, glycolipids and lipoproteins.
Fats and lipids are often used as synonyms. However, you usually say dietary fats and blood lipids.
http://www2.chemistry.msu.edu/faculty/reusch/VirtTxtJml/lipids.htm
http://biology.about.com/od/molecularbiology/ss/lipids.htm

As far as I know fats are solid lipids while oils are liquid lipids in (I guess) room temperature. So saturated triglycerides are usually fats, and unsaturated triglycerides are usually oils.
This is because saturated and trans-unsaturated fatty acid chains are linear while cis-unsaturated fatty acid chains are curly (non-linear). Forces between linear chains are stronger that's why they are solid after a length.


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Do we know the genome contains all the information necessary for embryonic development?
Since high school biology I've assumed that all information necessary for creating an organism is found in its genome.  As Nature's Scitable site says:

Deoxyribonucleic acid, more commonly known as DNA, is a complex molecule that contains all of the information necessary to build and maintain an organism.

However, I've been reading Sean Carroll's "Endless Forms Most Beautiful" and here is one passage that illustrates the question in the title.

Ultimately, the beginning of spatial information in the embryo often traces back to asymmetrically distributed molecules deposited in the egg during its production in the ovary that initiate the formation of the two main axes of the embryo (so the egg did come before the chicken).

Dr. Carroll seems to be saying that the information determining whether genetic switches are on or off ultimately does not come from the embryo's genome, but rather comes from other molecules provided by the mother.  So, my question is whether we know these molecules responsible for initializing the switches that regulate gene expression can be traced back to something in the mother's genome?  If we don't know these molecules trace back to the mother's genome, then is there some other reason we think the genome "contains all of the information necessary to build and maintain an organism"?

Comments are not for extended discussion; this conversation has been moved to chat.

The second quote is about stochastically determining which side is the "head" and which is the "tail", effectively, which occurs by positive feedback of an existing gradient. This is not really a matter of information stored in the sense that we think of information stored in DNA bases or bits on magnetic tape, the passage seems to be referring to information in the sense of a reduction in uncertainty about the state of the universe. The way a developing embryo chooses where the head is going to be is like dumping a bag of M&Ms on the table and having the head develop wherever the highest concentration of yellow M&Ms are. If you expect them to be uniformly distributed, you'd be correct statistically, but for any one iteration there will be a non-uniformity that determines what happens next: that's information, reduction in statistical uncertainty. If you, via the power of a thought experiment cousin of Maxwell's demon, were to scramble the positions of molecules in the egg cell, that would change where the "head" develops.
Yet, all of this is guided by proteins that are created and function according to the "instructions" in DNA. DNA doesn't have information about where in the future there will randomly be a concentration of yellow M&Ms, but it does have the information to synthesize proteins that react to concentrations of yellow M&Ms, causing a positive feedback loop that further concentrates them on a particular axis.
For embryonic development, these yellow M&Ms are mRNA transcripts, and at least in drosophila, these initial transcripts are indeed made in the egg cell, not post-fertilization (see https://en.wikipedia.org/wiki/Drosophila_embryogenesis#Anterior-posterior_axis_patterning_in_Drosophila). It's possible to introduce a mutation to a fly that will only affect her offspring, by interfering with transcription of these mRNAs. More generally, maternal effects are observed when the egg cell or developing environment has some influence on the offspring.
However, all those influences are coded in the DNA of the next generation, too, so it also seems reasonable to say that the genome contains all the information necessary. Containing all needed information to do X is not the same as being able to do X. To turn DNA into RNA transcripts, and to turn transcripts into proteins, requires more than information, it requires machinery. We can say the information to build those machines is also in the DNA.
Honorable mention to mitochondrial DNA, which comes entirely from the egg cell.
Generally, I think learning about biology from these grand pronouncements like "all information is in DNA" is a bad way to learn biology. Biology is not mathematics, we do not operate in the certainty of proof. Learn how things actually work, first, rather than trying to prove or disprove "truths". These statements are meant to capture wonder and convey the basic order of things, they are not dogma (even if someone regretfully calls it that).

Nice answer! Reminds me of the last line of Gunga Din. Mitochondrial DNA does deserve an honorable mention. :)

Also, and feel free to delete this, but I always thought of Watson as something of an imposter, a feeling that solidified on listening to him speak a few times at Cold Spring Harbor, and we’re chiseled in stone with his racist views.

Thanks, great answer, and your answer does illustrate why scientists tend to think all the information is ultimately stored in the DNA.  From what you say, the asymmetric concentration appears to be as informative as a coin flip.  The head formation has to start somewhere, and there has to be a concentration to get things started, but the concentration's placement is randomly distributed, so there is no specific instruction identifying a particular location where the head has to form.  I'm acquiring some books on epigenetics to see if all developmental instructions are indeed encoded in DNA.

I also just found this question https://biology.stackexchange.com/questions/30645/do-changes-in-an-organisms-cell-modify-the-genetic-information-it-uses-for-repr?rq=1, which says mutations in the gametes are heritable.  Which would be one example of heritable information that is not encoded in the DNA.  I can ask a separate question about this to see if it falsifies the statement that "all information is in the DNA".

@yters Though "epigentic" is quite broad, most of what is described as epigenetics still involves DNA, it's just outside the traditional ACGT bases. I do not understand why you think heritable mutations in gametes would not involve DNA. I don't think "all information is in the DNA" is a statement you should bother falsifying, rather, you should think about and understand what someone meant to convey by making that statement.

@BryanKrause there is a subtle distinction in my question that I'm having trouble getting across.  It can be both true that the mechanisms of transmitting epigenetic information is encoded in DNA, i.e. proteins, while the information itself may not track back to specific instructions encoded in the DNA.  I'm having trouble asking my question in the right way to get the answer.  Think of this analogy.  When I type a Word document, the document is dependent on the Word source code that generates the Word program.  However, the information in the document cannot be traced back to the source code.

@yters Part of the problem might be that you are not expressing a question of interest to biology. Most biologists only really care to understand how the biology works - there's enough stuff going on there to spend many lifetimes on figuring it out and it isn't necessary to apply it to some greater truth for it to be interesting.

It might be worth thinking about a plant...many plants are of indeterminate size. They grow according to their environment. The instructions for that growth are all encoded in their DNA, but there is a lot of external "information" that will determine the plant's final morphology. For example, if it's receiving a lot of shade early on, some plants will attempt to grow very tall very quickly to escape the shade, at the expense of growing wider. That's "information" in the universe uncertainty/entropy sense; it's not information in the sense of the first quote in your post.

Let us continue this discussion in chat.

In your Word document example, all of the environmental conditions: sunlight, soil contents, neighboring plants and any signals they release, damage from predators, these are all like the keys you strike while you have Word open, but the way that those inputs are rendered into the plant shape you see today is all in Word's source code, and to generate another plant that follows the same rules given the same external input, all you have to do is copy the Word source code.

@BryanKrause - so many attempts to teach/answer. Hence why you’re a better [person] than I am, Gunga Din.

First of all, concerning the theory of epigenetics and the concept of epigenetic modification of 'gene expression' -- or of the data encoded in DNA in the form of its base sequence and structural conformation --, it is important to realise that all the enzymes implicated in such epigenetic processes must themselves be encoded in DNA and produced through the mechanisms of transcription and translation, all of the enzymes and proteins associated with which processes, transcription factors and so on, and including histones themselves, must also be thus encoded.
Putting aside such contention about what is inevitably the self-controlling function of DNA transcription however, the conception of a genome constituted primarily by the DNA molecules comprising cell nuclear chromatin is a theoretical construct permitting a broad understanding and its more-or-less consistent experimental verification of the phenomena of heredity and of the relation between the old-fashioned ideas of the phenotype and genotype.
The derivative notion that DNA contains all the information necessary for the growth of organisms is only the imputation of the prevailing paradigm of causality to that relation: thus that the form of DNA 'causes' the intricacies of growth to occur -- and this is no doubt useful in an empirical context, particularly one in which the genome embodied in or by DNA is to be manipulated towards some end.
However, it might be helpful at times to consider the scenario from a different philosophical perspective, to put the horse before the cart as it were, and to imagine that the dynamic and evolving structure of DNA is rather a reflection, at what we define as the cellular level, of the singular process of life, growth and attendant evolutionary transition -- correspondingly understood as an orderly process -- conceived in its more essential sense, than its cause; therefore to view DNA as a theoretical instrument for describing fairly precisely and in an analytically consistent way in physico-chemical terms this singular process, notwithstanding significant gaps in the capacity for that theory generally to account for the entirety of that instrument: for example, to account for the function of non-coding DNA (which must inevitably require a revision and expansion of the philosophical perspective itself).
Clearly there is far more to this process of life and evolutionary growth than can be accounted for by the view of DNA as it currently stands in orthodox cellular biology, even if it is also true that there is no conceivable aspect of that process which will not be reflected -- which will not have its manifestation -- at some level, however subtle, of that dynamic structure and conformation of DNA.

It’s nice that you gave an answer, but one of the top expectations on this site is that answers are supported by reliable sources. Please provide some support for your answer(even though it’s good, helpful, and a perspective as opposed to an actual answer.)

@anongoodnurse  The intention was only to proffer a reasoned response to a question which cannot really be answered in the ordinary sense, not the least because the terms are ill-defined -- 'information', 'build an organism'. Eventually, the only way to address confusion about the relation between the chemical structure of the genome and the phenomenon of living organisms, of dynamic life itself, is to adopt a view capable of putting the theoretical construct of DNA as the basis of the genome in its proper philosophical perspective. The logic of a perspective must be able to support itself.

I am only informing you about site culture, which is meant to be helpful. You have no upvotes; I hope that changes. This type of answer may be perfect on a different site. That says something about the site and about the answer. It doesn’t answer the question, that’s all. On this site, answers must do that.

The main remit of the Stack Exchange network is to exist as a repository of knowledge and solutions to problems. Whilst a fresh perspective on the underlying philosophy of an approach can be healthy and sometimes very necessary, it's not what we do here.

As you wish. The question had remained unanswered for 5 days, which should tell you something about the sort of response required -- which is one that attempts to reframe it in terms more likely to address the philosophical confusion implicit in that question itself. Perhaps I should have been more succinct: 'We' do not KNOW that DNA, considered as a 'molecule', contains ALL the 'information' etc., nor CAN we know that. At the same time, we do not NEED to know that in any meaningful empirical context. Also, the first paragraph of the answer DOES address the contention about epigenetics.

Your reasoning is appreciated, as is your willingness to help the OP. On this site, the answer is not philosophical, it’s empirical. It’s also(to me) just too broad and the OP too argumentative to bother answering the question.

Here's an example of missing information.  When scientists inserted the fly's eyeless gene into a mouse, it created mouse eye cells, not fly eye cells.  So, the gene had enough information to signal "create eye cells", but did not have the information to specify the kind of eye cell.  In the context of my question, this is an example where the eyeless gene has insufficient information to create an eye.

@yters It's also an example of the limitations of the term 'information' in such contexts; as pointed out in the answer you cite, this sort of example clearly illustrates the experimental impossibility of validating your argument in the way you suggest, which is not to say that the idea itself that there is more to the elaboration of living organisms than the physicochemical form of DNA construed as the substrate of the genome is incorrect.Consider the case in which sensory 'information' is conveyed to mechanisms of epigenetic modification of 'gene ' expression. While the origin of this data..

...while the origin of this data is exterior to the cell and even the body, it becomes 'information' relevant to the organism only within it; moreover, all the pathways of this transmission and transition of such data to epigenetic function -- including the constituents of sensory organs themselves: cilia in the nose, tension of the stapedius muscle and so on -- directly implicate enzymes and peptides, including transcription factors etc, whose production is eventually encoded as some form of 'information' within the cell, primarily in the structure of DNA, but also importantly within...

...within the whole cellular and cell nuclear context of that DNA, conceived in its dynamic entirety; meaning that this inevitably includes such information as the relation between chromosomes, and between DNA constituents of cell nuclei and of mitochondria, in cells adjacent and distant, considered at a quantum mechanical level

...considered at a quantum mechanical level. A real can of conceptual worms, especially in the empirical terms of attempting to relate specific pieces of DNA explicitly to crude phenotypical features. It is however a subject worthy of deeper contemplation than is likely pertinent to experimental scenarios; which is what ordinarily leads to some expansion or revision of 'philosophical perspective'. Good luck with that; it can get pretty scary sometimes.

What I don't understanding is why the term "information" is considered confusing in this discussion.  Information, in my programming mind, is the bits encoding instructions on how to bring about a certain result.  Take Windows, for example.  The code for Windows contains all the instructions necessary to instantiate the operating system within a particular hardware context.  However, the code does not contain all the instructions necessary to create the hardware context.  Likewise with an organism's genome...

Likewise with an organism's genome, the question is whether it is the same sort of situation.  Obviously, within the context of a cell and the womb, the genome has enough information to instantiate a particular creature.  But, is the information sufficient to create the cell and womb?  Let's imagine we have the perfect scientist, with skill and knowledge way beyond current human limits.  Can this scientist, with full knowledge of biochemistry, look at a genome and use the instructions encoded there to make the creature, womb and all?  If not, then there is further information...

If not, then there is further information necessary for the generation of the creature that is encoded elsewhere than the genome.  This has practical implications.  My prior naive understanding of genetics was that all DNA was in a sense "interchangeable".  Every genome contained a complete set of instructions to generate a creature.  Which also means that different instruction sets could be mixed and matched (at least by our perfect scientist) and generate new creatures....

and generate new creatures.  For example, our perfect scientist could graft in the wing instruction set from a bat into the genome of a walrus, and with suitable adjustments to the genome code taking into account the new environment, could produce a flying bat walrus.  On the other hand, if the genomic information is incomplete, and epigenetic information is also necessary for creation of the bat wing, then no matter what DNA from the bat genome is spliced into the walrus genome, our scientist will never be able to attach bat wings to a walrus....

bat wings to a walrus.  In a more practical context, human characteristics may not be fully reducible to the genome, and so no matter how much knowledge we gain about manipulation of the genome, we may never be able to, say, give everyone a perfect IQ, exquisite physical beauty, nor extremely long life.  Such human traits may be hereditary, but not encoded in the genome, but encoded in some other fashion...

encoded in some other fashion. That bioengineering human perfection is possible through manipulation of the genome I believe is a huge assumption of the modern biotechnology enterprise, one which no one appears to apply much of a critical eye.  Going back to my question, this sense of information as the instruction set which gives full control over all aspects of a creature seems plain to me, and I'm curious why we are confident this complete instruction set is contained within the genome.

@jeremiah I've rewritten my question with a specific example.  Hopefully this is clearer what I am asking.

@yters Quite right: more generally, sensory 'information' is modifying the existence of an organism at all times through what amount to 'epigenetic' means. However, in order to respond to this 'nurture' side of things. the state of the organism must already be open -- primed -- to respond to it; it must be able to 'hear' the data as it were, and this is the function of the dynamic condition of the DNA/genome at any moment. You must ask yourself WHY you are asking this sort of question and the answer to that is philosophical: thus the form of my answer, which as is evident is not welcome here.

All philosophical inquiry, into truth, eventually reduces to a single question: is all of this beautiful intricate reality accidental, or is it ordered? Here it is critical to concede that if universal reality is ONE INDIVISIBLE UNITY, one 'quantum field', one 'substance' etc., then it must be one or the other, totally and entirely accidental, OR totally and entirely ordered by a singular universal CAUSE. Real understanding, wisdom, flows only from the latter if the assumption of universal unity is accepted as self-evidently true. The prevailing paradigm in the sciences is based on the former.

@jeremiah I'm asking because what I was taught about DNA does not seem to be correct based on what I now know about science.  Yes, there may be some sort of teleological cause behind it all, which does seem the much more plausible explanation.  I have a lot of experience programming, and my MSc was in evolutionary algorithms, and evolutionary algorithms cannot produce anything like the intricately arranged structures we see in animals, nor the sort of code that programmers can write!

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text:
Does the minimum spanning tree tell us anything useful about evolutionary ancestry?
Question migrated from bioinformatics stackexchange due to lack of interest.
I'm new to bioinformatics and have been reading through a bioinformatics book, and it seems calculating a phylogenetic tree is quite a complicated process.
I'm wondering if generating the minimum spanning tree (MST) from a similarity matrix would provide a decent approximation to the actual phylogenetic tree, i.e. provide some information on the evolutionary ancestry of a collection of organisms?  My thinking is that animals diverging from ancient ancestors will always be farther away than animals that diverged recently, so the MST will at least show me what animals are genetically related and which are genetically distant.
I realize this is not quite the same thing as a phylogenetic tree, but it seems to give me some of the same information provided by a phylogenetic tree, namely which animals are closely genetically related and which are distant relatives.
For reference, I'm measuring similarity based on the normalized compression distance (NCD) metric.  The metric is defined in "Clustering by Compression" by Cilibrasi and Vitanyi.
Here is an example MST using the dataset from the referenced paper.  Some parts make sense from my rudimentary knowledge of biology, like the clustering of primates.  Other parts are new to me, and I'm not sure if the relationships are just an accidental feature of the metric, MST, or if real.  For instance, cows are more related to whales instead of horses according to the MST, cats and dogs appear to have evolved from seals or visa versa, and pigs are related to a wide variety of animals: ranging from bats to rabbits to whales.
Note, the 'randgen' nodes are randomly generated DNA sequences that I added to the dataset as a sanity check.  As expected, they are off on a branch by themselves instead of mixed into the population of real animal DNA sequences.  The reason why they are clustered is because I repeat each DNA sequence 40 times to amplify the signal, and repeated short random subsequences become compressible.  The random DNA sequences are probably clustered because they tend to share random subsequences, while the mammal DNA sequences are orderly and have fewer random subsequences.
Here is the repo to reproduce the tree.
https://github.com/yters/ncd

If i search for anything as distant as a mouse and a seal i get 5000 results. I did an OTT parser but i dont know what a similarity matrix is... Dont know why or how to apply similarity to phylogeny!

Have you tried comparing your tree to phylogeny? From a cursory look the answer seems to obviously be "no".

Whales are artiodactyls just like cows and pigs, so that actually makes sense. but from looking at it they must be using a really shallow dataset because they have some strange clustering. Also the fact all your randoms are clustering makes me wonder if they are really random.

@John the reason the randoms are clustering is because I have to repeat each string 40 times to get enough compression.  So, the repetition causes the randoms to cluster, because most other sequences don't have as many random subsequences.  Their subsequences are more orderly.

@com.prehensible similarity matrix is created by measuring similarity between each unordered pair using the NCD metric I reference.  I repeat each sequence 40 times before measuring similarity to get enough of a signal for the metric to work.

@BryanKrause that is a good suggestion, but I'm also wondering about the informativeness of a minimum spanning tree in general.  It would seem the MST should show how closely/distantly related different organisms are.  Hence my question about the weird clusterings that John mentioned.  Basically, the MST seems to be much simpler than the tree construction algorithms I've read about, so it'd be great if the MST is phylogenetically meaningful.

Well, for a start, it shows nothing about ancestry. A phylogenetic tree shows where modern species exist relative to their most recent common ancestors. That concept is completely missing here.

I agree with @BryanKrause. For species relationships, this is absolutely meaningless, showing nothing about common ancestry. It could perhaps be interpretable as, for example, an unrooted haplotype network, but if there is no explicit interpretation in number of inferred differences (and of course, given the level of divergence summarised here) this doesn't make much sense either.

@NatWH if I have organisms A, B and C, and A and B are linked on the tree, while A and C are far away, can't I infer that A and B have a recent common ancestor and A and C have an ancient common ancestor?  I think this is valid reasoning because the MST is formed from the shortest edges, i.e. most genetically similar organisms, and two organisms that share a recent common ancestor should be more genetically similar than two organisms that have an ancient common ancestor.  Is there a flaw in this logic?

@yters Take an example where A and B are closely related, and C is more distant from A and B (let's say A is a tiger, B is a lion, and C is a gorilla). In your map, A and B will be connected, sure, but where is C? It should be equally far from A and B. In your map it will instead connect to either A or B. That connection is not meaningful. It should connect hierarchically to (A and B). Phylogeny has this, your map does not.

Well yes, because rates of evolution frequently vary between lineages, and genetic (dis)similarity may not cleanly map to species relationships. So you might get some signal, but most of it is probably meaningless. For example, your figure above is telling me that fin whales are as closely related to blue whales as blue whales are to Hippopotami, but it's fairly uncontroversial that cetaceans are monophyletic. We already have fast algorithms to infer inaccurate trees.

For another example from your actual example, it looks like a chimp is connected to a platypus through a rhino? What does that even mean?

Even worse, to get from guinea pig to mouse we go through blue whale and pig?

@BryanKrause Yes, it seems to only give me one directional inferences.  If C is far away from A and B then I can infer it is from a more distant common ancestor.  But, if B and C are both connected to A, then I cannot infer much about the distance of the common ancestor in that case.  I also agree my tree has a bunch of weird paths, but I'm not sure if this means MST is meaningless or that evolution is much weirder than I first suspected.

@NatWH the branch lengths are not meaningful in my graph, so I can only make inferences based on number of nodes on the path.  This means my graph says a dormouse is more closely related to a cow than to a mouse, but it does not say a blue whale is as closely related to a fin whale as to a cow.

Actually yes, it does - because you're confusing distances for relationships. Relationships are only ever discrete, defined in terms of degrees of common ancestry. The branch lengths do not matter in terms of statements of relatedness. So your graph explicitly does say that a blue whale is as closely related to a fin whale as it is to a cow, because they each are separated by one edge. If you wanted it to say otherwise, you would have to introduce a node representing the hypothetical ancestor to the tree, and @BryanKrause points out.

Basically, any algorithm that places an extant taxon on a node, not a tip, is probably not inferring a phylogeny.

@NatWH great point.  I have updated my question to not be so attached to the phylogenetic tree aspect, but whether a MST tells us anything about the evolutionary ancestry.  The reason I'm focused on the MST is 1) it's easy, fast, understandable algorithm and 2) seems to hypothetically provide some information about evolutionary ancestry.  But, your point that evolution rates can vary dramatically would imply that the MST is meaningless.  However, then I wonder how is it possible to infer anything about lineage based on DNA sequences if the rates are so variable?

@yters there are already fast, distant-based approximations for phylogenetic trees - look up Neighbour-Joining. But they are weak for the reasons we have discussed. Instead, we use more sophisticated models which can account for variable patterns of substitutions, rates across sites, and even rates across lineages, implemented via maximum likelihood or Bayesian inference. The reason that phylogenetic inference is frequently slow is precisely because the process we are attempting to understand is intensely complicated, and short cuts are often suboptimal.

I think @NatWh has explained this very well. I also think the updated question title is a bit worthless. Can it be useful? Well, maybe if you only have a group of closely related species it could give you some hints but it's not particularly efficient and there are other better tools. I'm not sure why you are reinventing this wheel.

@NatWH simplicity is also a reason I was looking at MST because the problem with an extremely complex process is that it is easy to bake in a lot of assumptions about how evolution works.  The more complex the reconstruction the more likely we are making the data fit our model instead of the other way around.  I will look into the neighbor joining method.  A bit more complicated, but it seems straightforward to implement and the wiki page has a worked example.  Thanks!

That would be all well and good if we didn't already have solid demonstrations that attempting to oversimplify this process leads to totally erroneous results (like the ones in your network). Why are you trying to reinvent the wheel?

@NatWH mostly b/c barrier to entry and understanding for standard approaches looks quite high, and they seem to have a whole lot of assumptions built into them.  Given how frequently and significantly evolutionary theory keeps changing, the built in assumptions seem like premature optimization.  I don't want to spend months and possibly years learning an outdated theory of evolution.  And, as I mentioned, just thinking about the logic of evolutionary lineage, the simple MST seems like it should provide some insight.  At any rate, the current answer provides a good way to check the MST.

I am not sure that you have thought about the logic of evolutionary lineage, or you have fundamentally misunderstood what I and other commenters have been saying. Your diagram is not a phylogeny, and doesn't show anything about evolutionary history or even lineage, because it implies that extant taxa evolved from other extant taxa, which is false.

@NatWH the main sticking point is the rate of evolution.  But, even if there is high variance in rate, there are still certain patterns in the MST.  For instance, organisms with the highest rates should be farthest from everything else, and organisms with the slowest rates and common ancestor should be closest to each other.  Organisms like bacteria will have extremely high evolution rates, and organisms with long lifespans and few children like humans and elephants have very low evolution rates.  Thus, an MST with humans, elephants and bacteria will form three unmixed clusters.

@yters If you think the main sticking point is the rate of evolution you are definitely not understanding the criticism. The main sticking point is that you've generated something that is nothing like a phylogeny. I'm also uncertain what you mean about evolutionary theory changing...the major principles have been constant for decades. All that has changed recently are minor nitpicks.

@BryanKrause the problem is I'm not a very clear communicator :)  Yes, the MST is not a phylogenetic tree.  The initial phrasing caused this confusion, which I've corrected.  The MST seems to tell us something about evolutionary lineage, based on the simple mathematical reasoning I've offered.  My understanding of modern evolution comes from a couple books, such as the bioinformatics book I linked in my question.  I've also been reading through Koonin's 'Logic of Chance' and Kauffman's 'The Origins of Order'.  The evolution they describe is not the kind I read about in 'Origin of Species'.

Your graphic is omitting nodes of the tree, branching points, which are essential for trees and phylogeny.
When you read the data file, you should count the brackets ((( ))) because they signify where the tree has nodes, common ancestors.
You should generate simple phylogeny trees, prior to doing complex data mining for similarity. The names are in latin? there are genetic distance numbers? What format and data are you using? You have given the common animal names. you may have to use a database of common-and-latin-names to be ables to search "tiger"... that database will return "panthera tigris tigris"... And then you can start crawling up and down the tree branches to search for animals related to tigris tigris, by counting brackets and marking species close to that name.
To prevent the tree exploding to 5000 animals, you can
1/define a search depth. Depth 5, Five, will not go further than five brackets: (((((panthera_tigris_tigris)(lion)(cheetah)))))
2/represent a random fraction of the species (1/100 gives 50 animals from a 5000 tree)
3/use statistics measures to select certain animals based on data mining.
If you want to travel from whales to monkeys, you will have most of the mammalian family, and you will be able to count nodes and brackets by the dozens.
Not that parsing 5000 species has a big computational load that can take 1 hour to read through once, let alone 40 times!
Whichever statistics you are using to measure similarity, number of brackets / genetic distance numbers, you should have once represented trees as branches, nodes and leaves, because that is what tree data is meant to represent.
I'd recommend that you draw a tree using nodes and random animal selection, like 1% chance the animal is drawn in the final tree. When your tree has branches and is drawing OK, change the 1% selection line for the complex MST / MCD selection.

This is a great suggestion to run the MST on a known phylogenetic tree.  Currently, I am just using a collection of DNA sequences.  If you could provide a link to a database that has both the tree and the DNA sequences for comparison, I'll mark this as accepted.