Dissection techniques for fruits and seeds

I will answer my own question for anyone that's interested in doing something similar. First, a great reference for seed morphology is A. C. Martin's The Comparative Internal Morphology of Seeds (1954), available on JSTOR and from sci-hub.
To dissect a seed, you’ll probably want to have a good dissection microscope, two pairs of sharp tweezers, a razor blade, and a pin. Begin by opening the fruit to expose the seeds; for a silique, it’s very easy to peel the valves open. Be careful not to crush any seeds. Using the tweezers (and optionally the razor blade) separate a seed from the fruit by breaking or cutting the funiculus. Do this for at least a few seeds, more is better. The seed coats will protect the seeds from drying out, but be aware, once the seed coat is removed, the embryo will only last a minute or two before becoming completely dried out. You'll figure this out pretty quickly, if it's a problem, otherwise don't worry.

Seeds in the silique, all still in their seed coats.
Use the tweezers to position a seed so you can cut it with the razor blade. To get a good idea of how the embryo is arranged requires several dissections, cutting the seed in different ways (vertically, horizontally, parallel to the work surface); seeds are cheap so just experiment. Cut the seed open and you should have something that looks like the image below.

Seed of Cardamine hirsuta cut in half.
What you’re seeing is (a) the seed coat, and (b) the embryo. Use the tweezers and/or the pin to get the seed coat away from the embryo with as little movement as possible to preserve the formation.

Using a pin, separate the embryo from the seed case. Note that the distinct features of the embryo are becoming visible.

With the seed coat (pale green part) removed, the radicle and the cotyledons become visible and distinct. This seed is accumbent.

The two cotyledons are pressed together in this example, but you can still see a separating line between them when you hold the embryo at the proper angle.
When dissecting seeds, do yourself a favor and select the most mature fruit available. Your life will be much easier if you have a larger specimen. These stills were taken from a video I made, available on YouTube here.


Would BMP7 introduced to a Petri dish with cartilage cause chondrocytes to replicate?

Hello and welcome Delaney Fitzpatrick.
BMP7 - Bone morphogenetic protein 7 - Plays a role in cartilage homeostasis.
Chondrocytes - A cell which has secreted the matrix of cartilage and become embedded in it.
Chondrocytes therefore make cartilage. Cartilage unfortunately has a poor regeneration capacity.
BMP7 stimulates Chondrocyte division
Naturally the question then becomes, does BMP7 also increase cartilage production?
A paper from 2009 - Chondrocytes that expressed increased levels of BMP7 in defected rabbit knees showed statistically significant repair when compared to controls.
Although an early study, it does suggest that BMP7 may improve cartilage repair.


Does the hepatic portal system form capillary beds?

In anatomy, a "portal circulation" is simply when you have a capillary bed that is interposed between two venous circulations BEFORE blood flows back to the heart. There are a couple of places in the body where this occurs, including the liver (hepatic portal system) and the pituitary (hypophyseal portal system).

To answer your question... yes, the hepatic portal circulation drains into the liver sinusoids, which is one large capillary circulation.

The hepatic arteries and portal vein give off branches that make up the portal triad which delivers blood (both arterial and venous blood) to the functional units of the liver which are the hepatic lobules.

The hepatic portal system drains into the liver and forms a highly fenestrated network of capillary beds within the liver parenchyma. In the case of the hepatic portal circulation, the flow through the liver sinusoids is considered this capillary bed. In humans, the flow of blood that makes up the hepatic portal circulation is mostly venous blood from the gastrointestinal tract.  This allows blood to flow through the liver for clearance of substances like drugs and hormones before those substances reach the peripheral circulation. Specifically, arterial blood flows to the majority of the stomach, small intestine and colon from the celiac, superior and inferior mesenteric arteries. This arterial blood flows through the capillary beds in the mesenteric circulation (i.e. the capillary beds around the intestinal enterocytes) and then into the major veins that drain the intestinal tract. There are two major veins that drain the intestinal tract, the superior and inferior mesenteric veins. The inferior mesenteric vein drains into the splenic vein and then the splenic vein and superior mesenteric veins merge to form the portal vein of the liver. Once blood flows into the portal vein it flows through the hepatic sinusoids (another capillary bed) before flowing out of the hepatic veins into the inferior vena cava, and then back into the heart.

The figure below is a picture of the intestinal veins from Gray's Anatomy  (wikipedia) that form the hepatic portal vein, the superior and inferior mesenteric as well as the splenic vein. In the figure the older term lienal vein is used instead of splenic vein. The latin word for spleen is lineal.

The picture below is a schematic of the hepatic lobule that receives its blood from a portal triad. In the center of the lobule is the "central vein". The blood flows from the portal triad to the central vein, and then the central veins coalesce to form the hepatic veins (which then drain into the inferior vena cava). The picture below is available from this website, along with some other text and picture for more information.

And another nice picture from wikipedia on "hepatic lobules".
.

As for a "freely available review" that you asked for, I can't find any with better pictures from PubMed that what is already in this answer.


Would it not then make more sense for the latter substance to simply be actively transported to its destination, as opposed to involving another substance which has no net movement at the end of the process?

But where would the energy for the transport come from! Thermodynamics tells us that the universe tends to increase the amount of disorder (Entropy). If we have active transport of a solute, then by definition, this is going against a concentration gradient. So we could end up with a substance being entirely on one side of a plasma membrane, which wouldn't be disordered at all - clearly thermodynamics wouldn't let this happen by itself since we would be reducing entropy.
This is why energy is needed for active transport. We need to put in the leg-work by using some energy to locally reduce entropy, and ultimately move something to one side of the plasma membrane. Think of the concentration gradient like the pent up energy of a spring. We can release this energy when we want, in order to make it thermodynamically feasible to move a solute against its concentration gradient.

  What is the evolutionary advantage of co-transport?

We've established that we need an energy source to drive active transport. But indeed, why would we use a concentration gradient? Couldn't we equivalently use a different energy source? Well yes, we could use ATP (for instance in Na$^+$/K$^+$-ATPase). But a concentration gradient might already be established over a plasma membrane, so its already there as an existing source of energy. Perhaps this is why co-transport evolved with this mechanism.


Can I estimate leaf temperature from air temperature? What other information would be required?

One way to do this is to use the "humid operative temperature" equation, or something similar. A variant of this equation, specifically for estimating leaf temperature, is derived using a leaf energy balance equation in chapter 14.1 of the Environmental Biophysics book (cited below).

I'll let you look up the actual equation since I'm not sure how to do math symbols here. But, in addition to air temperature, you will need to know a few pieces of information:

Vapor pressure deficit - calculated from humidity and temperature.
Incoming radiation - Measured, or you could model this using time of day, latitude, etc.
Emissivity of your leaves - you can probably look this up for your species or a similar one.
Windspeed
Characteristic dimension of leaves - measure, or look up a value for your species (Use this with windspeed to calculate boundary layer heat conductance).
Leaf vapor conductance - a combination of stomatal and boundary layer conductance to water vapor. You must know something about where the stomata are on your leaf (both sides or one side), but you can often look this value up for a given species.
A few other constants that are easy to look up.

That's about it - its a somewhat hairy calculation, but if you have standard weather data and a little knowledge of the plants you are estimating the leaf temperature of, it should be manageable.

This equation and other relevant info are in this book:

Campbell, G.S. and Norman, J.M. An Introduction to Environmental Biophysics. Springer Science, 1998


Protein binding interactions are usually referred to by how easily the binding partner can be displaced by something other than the preferred substrate. Usually, this is in reference to the concentration of the binding partner required such that the average occupancy of the protein (in this case RAS) to the binding partner is ~ 50%.

If the affinity protein for a given binding partner is in the picomolar range, that means that it binds so tightly that very very little substrate is needed to achieve 50% occupancy. In order to interfere with RAS's preference for GTP, you would have to design something that RAS likes to bind to with even greater preference that would be able to displace GTP. This has proven quite challenging.

Other kinases, whose affinity for their substrate is not nearly as high, have been easier to design molecules that displace their endogenous ligands and hence interfere with their function.

I know it is Wiki, but the activation/deactivation section of this Page provides some insight into how RAS binds GTP and turned on, how GAP functions to help RAS hydrolyze GTP->GDP, resulting in turning off RAS downstream signalling. RAS signalling is actually a balance between Guanine nucleotide exchange factors causing RAS to drop GDP for GTP (turning RAS on) and GTPase activating proteins mentioned above (GAP).

Mutated RAS in cancer often involves a coding change such that the ability to hydrolyze GTP->GDP is mitigated, thus leaving RAS in the ON state.

For your initial question of inhibitors (and more general). Cellular signalling involves the interaction of proteins with other proteins and/or signalling molecules and/or DNA/RNA. Very generically, inhibitors interfere with this interaction.

Example: Kinases add a phosphate group to another protein, that can among other things change the affinity of that protein for its binding partners, and thus set off a downstream signalling cascade. If kinase A phosphorylates protein 1, and you inhibit kinase A from doing this, you have inhibited downstream effects from protein 1's signalling cascade.

Take a look at this picture:  The two drugs in red interfere with downstream signalling cascades in B-cell receptor signalling by preventing endogenous binding/signalling events.


How does CO₂ concentration affect photosynthesis?

The rate-limiting step of photosynthesis is the CO2 assimilating enzyme Rubisco (short for ribulose-1,5-bisphosphate carboxylase/oxygenase) (Jensen, 2000). It uses ribulose-1,5-bisphosphate and CO2 as substrates to generate glucose.

Given that Rubisco is the rate limiting step in photosynthesis, an increase in its substrate CO2 would expectedly lead to an increase in photosynthesis. However, the regulation of Rubisco is complex and is influenced not only by CO2, but also by O2 (which competes with CO2 for the active site), Mg2+ and a regulating enzyme called Rubisco activase (Jensen, 2000). Hence, the effects of an increase in atmospheric CO2 may be more complex than simply enhancing photosynthesis by increasing Rubisco activity.

Indeed, a review by Poorter (1993) showed that a doubling of CO2 lead to an average increase in photosynthesis of only 37% across more than 150 plant species. He describes various factors that determine photosynthesis rates other than CO2:

One factor that limited photosynthesis under high CO2 was nitrogen (N). Since Rubisco is an enzyme, it has to be synthesized from amino acids. As Rubisco constitutes about 30% of the total protein in a plant leaf, Rubisco is probably the most abundant protein on earth and a major sink for plant nitrogen (Jensen, 2000). For example, C3 species capable of symbiosis with N2-fixing organisms had higher growth increases compared to other C3 species under high CO2;
Certain plants utilize CO2 better than others. CAM species were the least responsive, followed by C4 plants, while C3 plants increased their photosynthesis rates the most under high CO2. Examples of C3 plants are herbaceous crop plants (Poorter, 1993);
Plants with a large intrinsic growth rate may benefit more from high CO2. These plants are said to have a high sink strength, as they rapidly convert additional photosynthesis products into outgrowth.

References
- Jensen, PNAS (2000); 97(24): 12937–38
- Poorter, Veg (1993);104/105: 77-97


What is the "lifecycle" of an average eschar and what types of cells are involved in each stage?

Response to cutaneous tissue damage occurs is several distinct but overlapping phases. First an scab is formed as the blood is 'allowed' to clot. A matrix is formed as the platelets adhere to one another, which contracts and 'dries' (forces out the serum) to form a scab. This process clearly happens prior to tissue regeneration/formation to reduce further blood loss.

Fibrinogen

In response to damage to blood vessels a signaling cascade is initated that results in the massive production of fibrin, which is deposited at the site of wounding and subsequently forms blood clots by activating platelets and stabilising the matrix by cross-linking (see PDB's protein of the month 2006).

So this is why clots do not appear to be attached to the surrounding tissue; the fibrin causes the blood to form a matrix that is very tightly bound to itself. Only after clot formation does the tissue remodeling occur, and it is during this stage that the scab will 'bind' more stongly to the surrounding tissue.

The Cell Types and Processes of Wound Healing

This figure (from (Li, 2007)) shows the various stages that occur and cells that are involved in acute wound healing  (wounds such as burns and cuts that heal "in a timely fashion");


What information do bipolar cells encode?

Recent nature neuroscience review on bipolar cells says that bipolar cells are classified into 13 (12 cone bipolar + 1 rod bipolar) different types.

Depending on the polarity of their light response, bipolar cells can be grouped into ON and OFF cells.

Answering your question, what are on bipolar cells used for ? ON bipolar cells predominantly depolarize at light-onset and stratify in the Inner Plexiform layer (ON).

Considering rod - rod bipolar path way: Eyes are sensitive to very low light level. Imagine you are seeing a star during night. As the number of photon reaching retinal layer will be very small. It reaches order of few rod photo receptors (receptive field) & then converge to rod bipolar cell for efficient signal processing. It makes vision at dim light really interesting and promising.

In case with central surround organization, It is one of the classical stimulus study which has been explored further in detail with various complex stimuli.
I recommend you to go through The Neuronal Organization of the Retina for more details.

I am absolute beginner in visual neuroscience field. Please correct me if am wrong.

-Sathish


Sex Determination System

Birds have a ZW sex determination system meaning that males are the homogametic sex. Or yet, in other words, males have two Z chromosomes while females have one Z and one W chromosome. You might want to have a look at Do males of all sexual species have Y chromosomes? for a short review of the diversity of sex determination system.

Dosage compensation

In birds dosage compensation exist but appear quite different than in mammals (Mank and Ellegren, 2009; Mank et al., 2011; Uebening et al., 2015; Naurin et al. 2009)

Sex determining locus

The DMRT1 gene on the Z chromosome appears to be important for male sex determination by affecting the testicular marker, SOX9 however it might not be the whole story (Smith et al. 2009). It is possible that several loci are involved in determining sex in birds.


Is metastatic cancer always lethal if uncured?

What you're asking is essentially to prove a negative ("Are there no ways an unchecked cancer can be non-lethal?"), which is unfortunately more of an exercise in imagination than anything else. The best way I can answer is by highlighting what about cancer actually kills, from which you can personally evaluate if a particular type of cancer fits and would be lethal.

You need to remember that it is not the metastization per se that kills something, it is the growth interfering with critical systems that causes death. Many systems in a body will prove lethal if sufficiently compromised. The brain is an obviously vulnerable point (a sample of one of its mechanisms can be found here), but even something like the lymphatic system, which is notably able to maintain its duties with some components compromised or removed, are ultimately necessary (a compromised lymphatic system will, among other things, leave one vulnerable to otherwise harmless infections). The primary checks to take away from this are "Can a body survive with this system compromised, or to what degree?".

Even in the case of a hypothetical cancer that is not particularly metastatic, but simply growing in a particular area (we'll even be generous and say the particular area is not vital to survival), tumors take resources to maintain, both chemically and mechanically (pulmonary issues are known to occur with this sort of unguided growth). Many of these effects can be highlighted in overgrowth diseases such as in Proteus syndrome (Note - My apologies, this is behind an academic paywall). Considerations for this part are "How many resources can a body afford to lose?" and "Can the heart support this extra mass?".

As an additional factor, tumors that don't allow infiltration by cells from the immune system can be prone to infections, both internally and externally. This is circumstantial, though, and not a core component of a cancer's lethality (mostly).

The mere presence of a tumor is not guarenteed to be lethal, but I would say, ultimately, any continuously-growing tumor will lead to death, simply by subverting the proper mechanisms of the body to a sufficient level.

References:

Papadopoulous et al., Neuroscience (2004);129,1009–1018
Cohen, AJMG (2005);137C,38–52


How to determine the actual flux in the human metabolic model of a cell line?

I am no expert on the field, but quantifying gene expression isn't a simple problem, although it is a possibility.

A solution I know to be used is using radioactive markers. See for example this review and particularly "The cell-cell lactate shuttle" section, which might give some insights.

This can include radioactive tracers (such as [14C]lactate), non-radioactive tracers (with [13C] or [2H]), "net exchange measurements" (I don't really know what this means here, perhaps the kind of exchange calculations they present here), and muscle biopsies (it is then possible to measure the metabolite concentration by enzymatic reaction or spectrophotometry for example).


Is there a term for a procedure in which the chromatography column is washed with 20% alcohol

Prepared or conditioned for storage would probably be perfectly acceptable.

If you're looking for a single-word equivalent, in this case, I would translate as stabilized. From dictionary.com:

  stabilize

  [stey-buh-lahyz]

  verb (used with object), stabilized, stabilizing.

  to make or hold stable, firm, or steadfast.

This seems appropriate, since one wants to ensure maintenance of the proper condition of the column for later usage, when taken out of storage.


The answer is that cabergoline does not need to enter a cell in order to function.

Cabergoline (as well as most (possibly all?) other drugs that target synapses) interact with proteins on the surfaces of the synapses. For example, the D2 receptor that you mention is a dopamine receptor which in its active form is expressed on the surface of neurons near the synaptic cleft.


Did my wildlife camera take pictures of coyotes?

Short Answer

Yes, these are likely coyotes.

 Long Answer

Your options of dog-like carnivores (i.e., Canidae) in BC include the following:

Coyote (Canis latrans)
Grey wolf

British Columbia Wolf (C. lupus columbianus)1,2
Northwestern wolf (C. lupus occidentalis)1,2

Domestic dog (C. lupus familiaris)

Siberian husky
Utonagan
Tamaskan
Alaskan malamute
Northern Inuit dog
Saarloos wolfdog
Shikoku
others...

Red fox (Vulpes vulpes)

Let's start ruling out the unlikely options:

[I'm not trying to be comprehensive, but rather just pointing out the easiest evidence we can see]

Dogs: Many of these might look wolf or coyote like, but it is very unlikely that any of these domestic breeds would be forming wild packs (as is indicated by your image containing multiple specimens). (In fact, it's unlikely you'll even see half of those breeds in BC to begin with!). I'll leave it to you to peruse the links I provided if you insist on examining and comparing their anatomies/morphologies to your specimens.
Fox: Although the largest of the true foxes, this is still a relatively small canine; they typically are less than 20 inches high and 35 inches long [source]. Without some measure of scale, we can't be sure, but your specimens certainly look larger than that relative to the tree in the background. More definitely, however, is that V. vulpes has a tail that is typically half or more of its own body length. The tail also rests nearly to the ground. The length of tail on your specimens do not match either of these length characteristics. Further, the very bushy, white-tipped tail of the fox is not represented by your specimens' only-somewhat bushy, dark-tipped tails. Red fox are also typically solitary hunters (source; unlike your shot of multiple specimens).

I know what you're thinking: "duh, get to the wolves vs coyotes already!!"

See here for a guide to differentiating wolves, coyotes, and dogs

British Columbia Wolf (C. lupus columbianus): According to Goldman (1941)3 and here, this subspecies of wolf is large with a dark (black with some cinnamon brown color) coat. No mention of a light ventral region is mentioned, which is apparent even in your night-camera shots!
Northwestern wolf (C. lupus occidentalis):

Their color does not rule them out -- This wolf subspecies is quite variable in color and can range from all dark, to mottled grey to all white. (see here for visual comparison of some wolf colorations).
This is potentially the largest of wolf subspecies (27-36+ inches tall at shoulder [source] and 4.5 - 7 feet long (nose to tail tip)! [source:i, ii). Your specimen's do not look this large, but they could be juveniles. It would be great to get a height estimate of that plant in your picture or diameter estimate of that tree...
This site suggests that the average pack size is 6-12 wolves, which is significantly more than showed up on your camera (though, obviously this could be coincidence and not a definitive way to rule out this wolf).

This leaves the coyote:

Size: Between the size of the fox and grey wolf: 21-24 inches at shoulder; 3.5 - 4.5 feet long (nose to tail tip) [source].
Color: Gray (or reddish brown), often grizzled, often with whitish/paler throat, chest, and/or belly. Black patches may be seen on the tips of tails on on feet. [[sources: Bekoff (1977)4 and CDFW].
Anatomy/morphology: Bekoff (1977)4 and CDFW compare coyotes to wolves. The snouts are thinner with smaller nose pad on coyote vs wolf, and a coyote's ears are taller and more pointed. Your images, unfortunately, don't really allow us to differentiate adequately.
Behavior: typically less social than wolves and will rarely travel in groups larger than their immediate family. Even still, they often keep their distance and practice more asynchronous activity. However, coyotes are most often observed as lone individuals or in pairs (especially during breeding season)4. This matches your camera's image.

Coyotes are most active in the early evening, but their activity can be variable. Many coyote have become quite nocturnal (especially near humans), but they are known to also be sporadically active throughout the day and showing peaks of activity at dawn and dusk. [sources: Bekoff (1977)4 and Wikipedia. Wolves, though, are also active during evening and night...

Summary

So, based on the the few number of individuals, coloration, and perceived relative size of your specimens, it seems most likely that these are coyote. If you can get us estimates of height and diameter of the foliage in the background, this could be stated more definitively.

You could always go back to the site and photograph and compare the tracks, too (try starting here and here to compare)....

...

Though of course, it could always be a "coywolf" (also see here) :p.

 Citations

 1. Nowak, R. M. (1995). Another look at wolf taxonomy. In Carbyn, L. N.; Fritts, S. H.; D. R. Seip (eds.). Ecology and conservation of wolves in a changing world: proceedings of the second North American symposium on wolves. Edmonton, Canada: Canadian Circumpolar Institute, University of Alberta. pp. 375–397. [see map on p 376 here]

 2. Goldman, E. A. (1941). Three new Wolves from North America. Proceedings of the Biological Society of Washington. 54: 109–113. [See HERE for a map]

 3. Goldman, E.A. (1941). Three new wolves from North America. Proc. Biol. Soc. Wash, 54: 109-13. [available here]

 4. Bekoff, M. (1977). The coyote Canis latrans. Mammal. Spec, 79:1-9.[see here]


Are there any other animals that become attached to a non-living object?

So, this is psychological attachment. From the question alone, I thought of physical attachment.

If you provide stuffed animals and human children, then I'd offer the television remote, a chair/sofa and the cellphone for human adults. In general, many adults are far too sedentary for their own health.

Some non-human primates have exhibited behavior similar to that which you describe with the stuffed animals-children example.

In terms of an inanimate object, you can add the Internet. Certain behaviors like over-indulgence in alcohol, sex, gambling, hand-washing, and the like, could, broadly speaking, fit within the question as posed.


The -CO₂H groups are carboxylic acid groups, better represented as -COOH. These, being acidic, have a lower pKₐ than the -NH₃⁺ group and so as the pH increases these -COOH groups lose their protons first.

The pKₐ values for the three are shown below the arrows: as you can see the α carboxylic acid is more acidic than that in the side chain, but they are both much more acidic than the protonated amino group.


In principle, Meiosis is only the process in which the haploid egg or sperm are generated. Have a look at this figure, which shows Meiosis I and II (from the Wikipedia):

During Meiosis I homologous recombination between homologous chromosomes can happen, the chromosomes are then distributed normally among the daughter cells. In Meiosis II the cells split again and here the sister chromatids are divided and the haploid gametes form.

In the oocytes the process is in principle the same, but the cells get arrested in the so-called diplotene stage of Meiosis I (picture from here):

In the diplotene stage the chromatin is decondensated and transcriptionally active, this helps maintaining a correct chromosome structure, as the diplotene stage can last up to 50 years. When the cell receives the hormonal signal to enter the fallopian tube, Meiosis I is finished. The resulting cells are not divided symmetrical, building one big oocyte and one polar body containing the second set of chromosomes. Most vertebrate cells are arrested in this stage again until they are fertilized. Then another asymmetrical division is done, leading to a haploid cell with two polar bodies. This oocyte is then fertilized.

This process can happen almost at the same time in a lot of vertebrate species, including humans. This is probably what was meant by your textbook.

For further reading I can recommend: Meiosis and Fertilization from the NIH bookshelf.


Like other Corvids (Jays, Crows, and Ravens), Blue Jays are omnivorous and can eat and digest both animal and plant matter. Animal matter can include insects, carrion, small birds and mammals, and the eggs of other birds. Then there is plant matter including corn, seeds, etc. Your catfood was not only convenient but contains a good source of both animal and plant matter and the opportunistic tendencies of Blue Jays allowed them to take advantage.


Well, even though most people presume that it appears blue (reference) is due to the blood being deoxygenated, it is actually not the truth because blood is never blue whether it is deoxygenated or not. In a paper by Dr Alwin Kienle titled Why do veins appear blue? A new look at an old question, the authors measured how much light of various wavelengths was reflected from both real blood vessels in skin and imitation vessels in a skin-like environment. The synthetic vessel (which was a capillary tube filled with blood and placed in a milky substance with optical properties similar to skin) allowed the authors to experiment with a variety of parameters (particularly vessel depth and diameter), and they were then able to validate their results by taking measurements on actual vessels in skin. They eventually came to the conclusion that the optical properties of skin and blood is what makes the veins appear blue.

I quote from the paper as to the reason of blood appearing blue.

  "Blue light does not penetrate as deeply into tissue as red light.
  Therefore, if the vessel is sufficiently deep, the reflectance in the
  blue will be affected to a lesser extent. Deoxygenated venous blood
  has a greater absorption coefficient than oxygenated arterial blood in
  the red spectral region, and this difference of two, rather small,
  values is amplified because of the long path length of red light in
  scattering tissue. As a result, veins are more likely to look blue
  than arteries at the same diameter and depth. Often arteries are not
  seen at all because they are generally smaller than veins and have
  thicker vessel walls. It has been shown that a small vessel will look
  red when close to the surface. However, if a superficial vessel is
  large it can still look bluish, particularly in the case of the vein.
  On the other hand, if the depth of a vessel is large, even red
  remitted light will not be influenced by the vessel, and it will not
  be seen."

So in short, the blue appearance could be attributed more to the location of the vein than just the deoxygenation.


Why warfarin is given as racemic mixture?

In general, it's more difficult to produce a specific stereoisomer of a compound than it is to produce the racemate. Producing a pure S- or R- sample of a particular compound requires either enantioselective synthesis, or racemic synthesis followed by a purification step such as chiral chromatography. This tends to be expensive - especially for an older drug like warfarin where it would likely imply either chiral purification (throw away half your product) or redesigning the synthesis to be chiral.

For some drugs it makes sense to do this - some reasons might include adverse effects of the undesired stereoisomer, or taking a drug that's about to go off-patent and re-branding an enantiopure preparation for further patent protection. I think the latter is what happened with Citalopram -> Escitalopram (Lexapro) although this is speculation.

Most likely in the case of warfarin there is no strong argument for producing a pure enantiomer. It has been off-patent for a while, there likely aren't major adverse effects related to the less potent isomer, and most likely economics dictate that producing and selling the racemate is cheaper / more profitable than retooling to produce and sell an enantiopure version. That latter option would only make sense if they could sell the pure S-warfarin for enough to recoup the development / purification costs, and this is unlikely for a drug with such a long history of use in its racemic form.


Where can I find DNA decryption research?

I can think of several possible terms for what you could mean (with my interpretation of what people in those fields do):

Computational biology (the study of biological topics using computation)
Bioinformatics (the study of biological topics using computation)
Mathematical biology (the study of biological topics using mathematics)
Sequence analysis (the study of patterns in nucleotide [DNA] and protein sequences)
Genomics (the study of genomes or more generally large quantities of nucleotide sequence)

These all bleed into each other and doubtless other people have different interpretations.

There has been a ton of work in these areas, so they probably cover what you mean, but without some more concrete examples it's a little hard to say which is most appropriate.

As an aside, "DNA decryption" will be interpreted by most people in light of attempts to encode non-biological data in DNA and then decode it (see e.g. george church's stunts). However, based on what you say I think this is not really what you are interested in.

If you are looking for the technical literature for such fields, you could see the following journals, which are some of the better-known peer-reviewed journals focusing on these areas:

Bioinformatics
PLOS Computational Biology
Genome Research
BMC Bioinformatics
Molecular Biology and Evolution


What have the L-systems (Lindenmayer systems) been actually used for in biology?

Are these models important? Still taught?

Yes!! These models are extremely important, however, the application of L-systems most definitely isn't confined to just the scope of Biology. I myself first came across L-systems when taking Calculus in university, and then later in several Computer Science courses (I study Bioinformatics).

What's (probably) most significant to mention about L-systems is that they produce fractals, which is acheived by defining a substitution system and utilizing recursion.

Fractal mathematics can be used to describe extremely complex phenomena, starting with just a few simple rules and initial conditions (which is why it's so powerful/attractive to study). Also, fractals have the nickname of, "God's Thumbprint", or, "The Fingerprint of God", just from where they're found so prevalently in nature. To name a few, fractals can "easily" model:

Coastlines
Blood vessels
Brain structure (neuronal connectivity)
Plant foliage
Lightning bolts
Diamonds
Snowflakes

  I tried to find biological research that has actually used this system but I could not find any.

As you can see, some of these examples are biologically related, however, the use of L-Systems have been broadened to many other fields of science, such as mathematics (coding theory) and theoretical computer science.

Unfortunately, very rarely do biologists have the mathematical or algorithmic backgrounds to work with L-systems, since L-systems are more related to mathematics, algorithms and logic, than they are with (practiced) biology.


How does translational coupling work in prokaryotes?

Translational coupling describes in how some cases an mRNA will code from more than one protein (i.e. will be polycistronic).  Translational coupling is thought to be mostly used as a way to make a set of genes are translated at roughly the same amount in the cell.

Translational coupling is very common in prokaryotes and nearly half of e coli genes are found in a polycistronic operon.  What we know about them is revealing.  There are some fancy mechanisms to adjust the ratios of these adjacent genes, which are still coupled, but with ratios that are not just 1:1.  Its shown that the later genes are often translated at somewhat lower frequency because the first genes are available more quickly before the mRNA degrades.

Eric Alm @ MIT wrote this great paper on how operons evolve.

I've only been able to find this reference to a eukaryotic case of "translational coupling" which is very rare, but does exist.  The most common cases of translationally coupled genes in eukaryotes are RNA viruses which usually contain only a single full length mRNA which codes for all the genes in the virus.  The selective pressures to keep the viral genome small and constrain the ratios of these genes, will cause these genes to even overlap, starting the next one before the current gene finishes.


What is the function of Xylem parenchyma?

I would like to aswer your question. First definition, function is from this web:

  The xylem parenchyma is comprised of parenchyma cells. Parenchyma cells are the only living cells in the xylem. They have thin cell walls, large vacuoles, prominent nucleus, and protoplasts. They have differing shapes although they are usually cylindrical and lobed in form. In the trunks of woody plants, the xylem parenchyma cells are colourless and are believed to be involved chiefly in storing starch, oils, and other ergastic substances. The inclusions in xylem parenchyma cells may contain tanninferous compounds.

And from this article:

  Xylem parenchyma cells in contact with xylem conduits are assumed to simultaneously generate the energy gradient (deposition of solutes in the form of sugars, ions or a combination of both) that allows water to flow into empty vessels/tracheids, and supply water for refilling (Zwieniecki & Holbrook, 2009). Regarding the first task, the initial research focus has been on finding the source of osmoticum through analysis of carbohydrates in the parenchyma cells and the role of phloem in the delivery of sugars to sustain refilling. Both enzymatic analysis and visualization techniques have demonstrated that starch levels in living parenchyma cells adjacent to xylem vessels decrease on a timescale coincident with embolism refilling (Bucci et al., 2003, Nardini et al., 2011a, Sakr et al., 2003, Salleo et al., 2009, Secchi & Zwieniecki, 2011).


Why are bugs attracted to light bulbs but not flames?

It has nothing to do with temperature, but with the color of the light. Insects are especially attracted to lights with short wavelenghts, especially Ultraviolet (UV) light. Yellow and red light attract far less insects. (Rich & Longcore 2006). PDF

White light, like the one emitted by an average light bulb, consists of a broad spectrum, that includes UV. Halogen lights also emit UV. Flames on the other hand emit mostly red and yellow light.

Unless the flames burn at a very high temperature, then the flames turn blue. To illustrate this, my parents used to have a candlelight on gas they used during camping. This light burnt at a very high temperature, and hence the flame had a bluish color. And it did attract insects, especially moths.


What is the mechanism behind ventilatory acclimatization?

@Michael Kunh Carbonic anhydrase is used in the human body to tip the balance of the reaction  $H_2CO_3\rightleftharpoons H^++HCO_3^-$ to the right side, and is an important player in acidobasic homeostasis.

To answer the question:

$HCO_3^-$ is excreted through the kidneys. This represents the metabolic compensation to respiratory alkalosis that appears in altitude.

To summarize:

ascension leaves us in with a lower partial pressure of oxygen. This will stimulate the peripheral chemoreceptors of the carotid bodies and aortic arch to increase ventilation (hypoxic ventilatory response). In consequence, an acute respiratory alkalosis develops.
renal adaptation begins after more or less 8 hours, and reestablishes homeostasis after 24-48h. To do that, the kidney will excrete $HCO_3^-$, which will tend to acidify blood (metabolic acidosis to counterbalance respiratory alcalosis). To accelerate this phase, one could take some acetazolamide, a diuretic drug that causes $HCO_3^-$ excretion.


Would it be correct to say that before the chromosome divides, there are simply 23 of them?

No, in a normal, non-dividing cell of the human body there are 46 chromosomes in the cell's nucleus. The 46 chromosomes are separate, but are often considered as 23 pairs of chromosomes.  The two chromosomes of a pair are called homologous chromosomes because they contain very similar, but not quite identical, information.  One member of each pair comes from the mother and one from the father.

Each of these non-dividing chromosomes effectively consists of a single chromatid, but because there is only one, indistinguishable from the chromosome as a whole, it is not talked about.

  Why not just describe the chromosome before it replicates for simplicity sake.

It is often described in that form (as one very long molecule of double-helix DNA).  However, a chromosome is also very commonly illustrated in the mid-replication form where it has two chromatids and takes an X-like shape.  One  reason for this is that chromosomes can be seen in a light microscope only in this mid-replication form, and that is the form in which they
were first observed and first shown to be the basis of heredity (long before they were known to be composed of DNA).


Is there a reproductive barrier between Khoisan and other humans?

Check the book "Genetic Nature/Culture: Anthropology and Science Beyond the Two-Culture Divide" edited by Alan H. Goodman, Deborah Heath, M. Susan Lindee. Page 205 states that that is a myth started by geneticist F Lenz of Gottingen that has been disproven.


Zickefoose et al. did a study, and showed that while you might improve while playing the game, it called into question if you actually improved outside of just getting better at the game.

Redick et al. also reported that when they did a double blind study in brain games like Luminosity that you improved in the games, but they didn't see any transfer from game to every-day life.

Also see my previous answer on the topic: Cognitive Science Forum


What does conditional analysis of a SNP in a GWA study entail?

In GWA studies you tend to analyze your "lead" SNPs in regions where genotypes are correlated (known as linkage disequilibrium).

If you find an association between another SNP with the outcome, and this SNP is correlated with the original variant, you can perform a conditional analysis where you adjust for the original SNP in the model. This is to test if the association between the 2nd SNP is independent of the first, or whether it is just because they are correlated (in LD).

So performing a conditional analysis is just seeing if the association observed is an independent signal.

At least, this is how I have interpreted it perviously!

E.g. SNP-A is found to be associated with increased risk of type-2 diabetes (T2D).

SNP-B is later found to be associated with risk of T2D as well.

SNP-A and SNP-B are correlated.

To see if the association between SNP-B and T2D is independent of the first association, you would adjust for SNP-B in the model (a conditional analysis).

First model: lm( T2D  ~  SNP-A + confounders)
Second model: lm( T2D  ~  SNP-A + confounders + SNP-B)

If the association between SNP-A (and/or SNP-B) and T2D is still significant then they have some independent effect on risk of T2D. If the association disappears then they are only both associated because they are correlated in the individuals.


Did insects and arachnids diverge before or after moving to land?

Those are two very separate questions. Arachnids include terrestrial groups such as spiders, scorpions, and other arthropods. Arachnids are members of Chelicerata, which includes horseshoe crabs, Sea scorpions (extinct), and probably Trilobites (extinct). Chelicerates evolved in the marine environment, and invaded land afterwards. Arachnids and Insects evolved on land. Hexapods are nested within Crustacea, in a group called Pancrustacea. The likely sister taxon of Hexapoda (Insects, including Protura, Collembola and Diplura) are Remipedia, which are aquatic. See Misof et al. 2014 for the most complete molecular phylogeny, with dates. http://science.sciencemag.org/content/346/6210/763


Do insects with compound eyes have depth perception?

"1001 questions answered about insects" by Alexander Barrett and Elsie Broughton Klots includes the following passage:

  Do insects have depth perception? Depth perception of some sort is important to an animal who has to catch its prey; fortunately most
  insects have it to a degree.  Although they do not have binocular
  vision that can be compared with man's, it is true that when one eye
  is covered their depth perception is markedly affected.  The criterion
  of depth seems to depend on the angle of simultaneous stimulation of
  two corresponding points of the retina of the two eyes.

However it does not mention compound eyes specifically.

There may be other methods of obtaining a perception of distance rather than the binocular vision seen in humans.  This paper suggests that there is 'clear evidence' that  some insects perceive depth by moving their head to artificially create parallax, which they can then recognise and interpret as depth and distance.  They cite the Praying Mantis as an example, which does have compound eyes.


Can you knockout specific receptors in an adult?

Short answer: yes, it is possible.

But there are some requirements for your delivery system. "Gene knockout" ("gene KO") means such DNA modification that is permanent (get inherited by cell's progeny) and deleterious to gene function (e.g. protein no longer get produced).

So your system must deliver DNA "mutation agent" to all cells (of organism or small specific area). This can be done by using viruses and, for example, CRISPR/Cas9 system for genome editing. Idea  is that virus will get in the cell, start expressing component for genome editing, multiply and infect neighboring cells. Modification in virus can make it non-lethal and less harmful, so you don't kill tissue in process. Virus delivery can be site-specific (e.g. direct injection into the area), it also might be cell-type specific if virus is tailor accordingly.

Also, remember that CRISPR/Cas9 and other similar techniques have efficiency well below 100% and also that you often have two copies of the same gene. This means that total KO probability goes as square of single copy KO probability. If for one event probability is 50%, for both it will be 25%; 10% becomes 1%.

So, all principle component for such experiment already exist.


Are your finger muscles and tendons interconnected?

That's a really interesting question!  What might help you the most is reviewing hand and forearm muscle anatomy.  I have some examples that could help.  The flexor digitorum profundus and flexor digitorum superficialis are hand muscles that originate in the forearm region.  At the wrist they split into four tendons (so FDP has 4, FDP has 4) one for each non-thumb finger.  They help make a fist.  Then there are the intrinsic hand muscles.  One interesting example is the lumbricals, which originate at the FDP tendon and have a very specific action.
To answer your question, I don't see any reason why exercising the four non-thumb fingers is recommended against, other than the possibility that you could be inadvertently moving/stressing the thumb.  I don't believe there is any connection between muscles of the thumb and non-thumb fingers, other than proximity of muscle/tendons.


As a general rule, a blanket statement in Biology should always be considered false.

It so happens that bacteria do have 'introns' (or at least the intron genomic sequence has been determined) in the sense of the cis-acting autocatalytic Group I and II introns. These are sequences of RNA that adopt such a conformation to catalyze their own excision from an mRNA transcript, and thus may be considered ribozymes, enzyme made of ribonucleic acid.

Although not generally considered 'introns' segments of RNA are removed during the course of tRNA in both prokaryotes and eukaryotes.

Now introns that are removed by the action of the spliceosome are strictly found in eukaryotes, as bacteria lack the spliceosome.

There seem to be a considerable number of papers regarding the question of intron (particularly spliceosomal) phylogeny that should be relatively easy to find if you are so interested.

One example paper in which viral introns (Group I) are reported:
http://nar.oxfordjournals.org/content/22/13/2532.abstract


Why are pilots under the illusion of gaining altitude without doing so?

See this link. It provides a great overview. The answer you want is in the otolith section. To paraphrase, it states that our otolith organs are designed to help us lean forward while running to maintain our center of gravity when in motion; however, in a plane this reflex can backfire by causing a pilot to believe he is going straight when in actuality he may be going downward.


How does one predict how large of an effect on antigenic drift a substitution in the amino acid sequence of a surface protein of influenza has?

Your understanding of influenza antigenic drift is, unfortunately, hypersimplified and mostly wrong. In particular, your notion that some mutations are more important for antigenic drift because of their effects on structure is at best oversimplified.

Rather than spend many paragraphs reviewing the complex patterns involved, I'd suggest you start by carefully reading papers from people who have correlated antigenic drift with sequence change, such as

Sequence-Based Antigenic Change Prediction by a Sparse Learning Method Incorporating Co-Evolutionary Information
Using Sequence Data To Infer the Antigenicity of Influenza Virus
Mapping the Antigenic and Genetic Evolution of Influenza Virus
The genomic and epidemiological dynamics of human influenza A virus
Selection of antigenically advanced variants of seasonal influenza viruses
Antibody landscapes after influenza virus infection or vaccination
Substitutions Near the Receptor Binding Site Determine Major Antigenic Change During Influenza Virus Evolution

This is a field that a lot of extremely smart people have been looking at extremely closely for many years; all the simple approaches have been tried already.


There are couple of them. First if you want to sequence analysis basic packages are :

http://www.bioconductor.org/help/workflows/high-throughput-sequencing/

Also, Maqweb seems promising.

http://maqweb.sourceforge.net


Endemic and chronic/acute are unrelated properties of a disease. Endemic is a description of the frequency of a disease in a population or in an area. Chronic/Acute is a description of the state or course of a disease in an individual.

For example, influenza is endemic in North America: the frequency goes up and down, there's always a few people who have it, but most people don't. Periodically the influenza virus mutates, and becomes much more successful at infecting people. The frequency of the disease goes way up, and influenza becomes epidemic. However, regardless of whether the disease is endemic or epidemic, the disease processes is usually acute: it comes on suddenly, it gets worse for a few days, and then it get better (or you die).

Malaria in endemic in much of Africa and SE Asia (it's always around), but the disease can be either acute (you have fever, chills, prostration), or chronic (the parasite lives in your body, and you can be a source of the disease, you don't necessarily have obvious symptoms, but may be suffering long term damage.


Can a plant be induced to accelerate transpiration?

With high(er) temperatures, especially in drier air with a bit of breeze, a plant will transpire more. While not a chemical solution, it is indeed a mechanism that serves to cool the plant.


Textbook Recommendations Covering The Adaptive Immune System

There are two books that I see as "standards" in the field:

Cellular and Molecular Immunology, 8th Ed. by Abbas et al.
Immunobiology previously by Charlie Janeway, who unfortunately has passed, so it is now authored by Kenneth Murphy. Many people just refer to it as "Janeway".

These texts can be used both at an undergraduate and graduate level (I used them in both), and are updated every few years. The latest edition of Immunobiology is from 2011, while CMI is from 2014, so you may want to start with that one first.

An earlier version of Immunobiology is also available for free on NCBI's Bookshelf, but unfortunately you can't read directly through it, you'll need to search for what you're interested in.


Why do human females have permanently prominent breasts?

You may be interested in Breast asymmetry, sexual selection, and human reproductive success.

Abstract:

  Breasts of human females are large compared to those of closely related primate species,
  and they can thus be hypothesized recently or currently to have been subject to directional
  sexual selection. Here we show that (1) large breasts have higher levels of fluctuating
  asymmetry than small breasts, (2) breast fluctuating asymmetry is higher in women without
  children than in women with at least one child, (3) breast fluctuating symmetry is
  a reliable predictor of age-independent fecundity, and (4) breast fluctuating symmetry
  appears to be associated with sexual selection. These conclusions were similar in studies
  from two cultures differing in fecundity and brenstfeeding traditions (Spain; New Mexico,
  U.S.A.). Choosy males that prefer females with symmetrical breasts may experience a
  direct fitness benefit in terms of increased fecundity and an indirect benefit in terms of
  attractive or fecund daughters.

Some quotes from the text:

  The size of breasts in human females is large compared to that of other primate
  species, and there has thus been a recent evolutionary change in breast size.
  Human breasts are characterized by their large size and rapid development prior
  to and during puberty, when growth of other body parts also reaches a high level.
  They can thus be considered costly structures in terms of energy use. …
  Heavy investment in breast development during puberty may seem puzzling
  because the functional significance of breasts is far from obvious. There is no
  or little relationship between breast size and production and composition of milk
  in current industrial societies (reviews in Anderson 1983; Cant 1981; Low et al.
  1987), and breasts have therefore been hypothesized to constitute a deceptive signal
  used by women to attract preferred mates (Low et al. 1987). In prehistoric
  human populations, conditions may have been different, when mother's milk
  was the sole source of nutrition for young children and when resources often
  may have been more limited than in present industrial societies. In this study
  we show that large breasts tend to be more asymmetric than small breasts. In
  prehistoric societies, where resources were likely to be less available or more unevenly
  distributed among women, breast asymmetries are likely to have been much
  larger than in present industrial societies with relatively easy access to resources. …

  If the relationship between breast size and fluctuating
  asymmetry is robust, we hypothesize that a directional preference for large, symmetrical
  breasts, as apparently found in some cultures (Ellis 1954), can be maintained
  in the population because selection for large breasts will be balanced by
  selection against asymmetrical breasts

  We also show that breast symmetry is a reliable predictor of age-independent
  fecundity, and that choosy males that use breast symmetry as a cue in their mate
  choice will experience an advantage in terms of reproductive success. Breast symmetry
  can thus be considered a reliable signal used in intersexual communication.


Does this equation have a typo? (Systems Biology, singular value decomposition)

You are right this is a typo. Equation 5 is just a restatement of the definition of the dot product of two vectors:
$$\mathbf{u}_k^T\cdot \mathbf{x} = \sum_{i=1}^m u_{ki}^Tx_i$$
or written in another way
$$\mathbf{u}_k^T\cdot \mathbf{x} = u_{k1}x_1+u_{k2}x_2+\cdots+u_{km}x_m.$$

In the text Equation 5 is stating that one can find a linear combination of the metabolites described in $\mathbf{x}$ whose time evolution is described simply by a linear combination of the flux rates described in $\mathbf{v}$. The coefficients of the first linear combination are given by a row vector $\mathbf{u}_k^T$ in $U^T$. From this perspective, since there are $m$ possible metabolites ($\mathbf{x}$ is a $m\times 1$ vector), there have to be $m$ coefficients, so that the indices must range from 1 to $m$ in Equation 5. You are correct that $u_{ki}^T$ might be 0 for some $i$. But that doesn't change the fact that there should be $m$ (possibly vanishing) coefficients.


Can I sterilize the equipment for experiments without an autoclave?

It certainly can be done. Tyndallisation may as discussed on labmate may work well for your situation. If not, there are many other viable alternatives suggested.

  **Tyndallisation:
  **
  Developed partway through the 19th century by English physicist, John Tyndall, the eponymous Tyndallisation was a commonly used
  technique by the microbiologists of the 1800s. Tyndall experimented
  with boiling beef broths to develop a method to sterilise liquids in a
  safe and comprehensive manner.

  His research led him to the basic principles for Tyndallisation, a process by which medias are subjected to relatively short boils at a
  regular atmospheric pressure. This relatively straightforward method
  is still suitable for small labs, or research facilities which only
  require sterilised equipment part of the time.

  It is not recommended to attempt to sterilise closed glass containers using this method, without lining them with cotton and
  capping them with foil – allowing for air to escape without being
  subjected to contaminants.

  The process involves boiling fluids for 10-15 minutes before leaving to cool to room temperature and leaving it to sit for 24
  hours. Repeat this process another three or four times, by which time
  sterilisation should have occurred.

  Naturally this method has reduced in popularity due to the requirement to continue the process for up to five days to achieve
  sterilisation.


Is a minimum size/complexity necessary for an organism to exhibit territoriality?

With some bacteria (e.g.. Bacillus subtilis) when food gets scarce they will start trying to kill their neighbors. (See this arstechnica article) This appears to be a fight to the death between children and parents. That's a kind of territorial behavior, selectively applied only when there are not enough resources to go around. As there is no "recognition" of a specific territory being defended, just wherever the bacteria is currently, this might not meet a strict definition of territorial behavior. But the only thing simpler than bacteria are viruses.

Come to think of it, I bet there are viruses that, once they infect a host cell, will change the cell's membrane or metabolism in a way that reduces its chance of being infected again by a similar virus. Such 'behavior' could be compared to defending a breeding ground. Can't find any examples though.


Excretion of small kangaroos while in the pouch

Wow! What an interesting question!

I did a bit of searching around, and here's what I found. It looks like the baby kangaroos, or joeys, do in fact produce excrement while in their mothers pouch. The mother kangaroo uses her tongue to clean her joey and her pouch.

I found this information in a couple of differently places by doing a google search for "biology of marsupial reproduction pouch excrement."

One of the first sources I found was a New York Times article titled "Marsupail Maintenance." You can find this article at this link:
http://www.nytimes.com/2012/08/14/science/how-do-female-kangaroos-keep-their-pouches-clean.html?_r=0

The article was published in a reputable news paper, and used an interview with a curator of mammals from the Bronx Zoo as a source.

Another resource I found when researching this topic was an Australian wildlife sanctuary. This wildlife sanctuary has information web pages online to help visitors learn more about the animals that live in the sanctuary. You can find their entry on Eastern Grey Kangaroos at this link:
http://billabongsanctuary.com.au/native-animals/mammals/eastern-grey-kangaroo/

This web pages gives a pretty detailed overview of the Eastern Grey Kangaroo. The information on joeys and pouch cleaning can be found in the section called "Raising the Young."

I hope this fully answered your question!


Why did evolution make people's skin dark?

It didn't, the basal condition for humans is dark skin, all other pigmentation patterns evolved from it. Additionally Dark skin is not monophyletic/homologous in humans,
 that is some darks skinned humans evolved from light skinned humans who in turn evolved from ancestral dark skinned humans, (Evolution made skin lighter then made it darker again in other regions). Skin dark/lightness is also well correlated with latitude (which is correlated with UV levels).

First it helps if you remember skin is translucent so even very light skin absorbs a great deal of light. Additionally black also radiated heat better than white its is a double edged sword so to speak, it absorbs heat better but also sheds it better.

But the current hypothesis about why light skin evolved is due to vitamin D. The skin absorbs some UV radiation to manufacture vitamin D. Dark skin blocks more of this radiation reducing vitamin D levels. As humans migrated into higher latitudes with less UV radiation they needed lighter skin to harvest more of it. If your skin is too light you have issues with sunburn, skin cancer, and folic acid destruction darker skin protects from these. Now in modern humans clothing and diet completely swamps these effects, so studying it is difficult. the use of clothing in humans moving into colder climates may have exacerbated this effect. The later evolution of lactase persistence could further confuse the effect.

Note that this hypothesis is controversial and only weakly supported because it is extremely difficult to test and the the multiple confounding factors.

http://evolution.berkeley.edu/evolibrary/news/140305_skincolor

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3024016/

https://www.ncbi.nlm.nih.gov/pubmed/16766240

https://dl.dropboxusercontent.com/u/38568440/admixture/shriver01.pdf

https://en.wikipedia.org/wiki/Human_skin_color


Well, don't use M or B, those are already taken (C or A, and not A, respectively).  You can see the full list here: http://www.dna.affrc.go.jp/misc/MPsrch/InfoIUPAC.html (The enWiki article on Nucleobases lists a few others but I would ignore those as 1. D is present in both and 2. they are rare and inapplicable)

5-methylcytosine isn't on there.  If you want to be pedantic about it, 5-methylcytosine is an epigenetic marker and as such is by definition not a genetic sequence; that remains simply a C and, genetically, the sequence is the same, despite the fact that it may indeed make a difference.

Most of the time people use m5C, so I'd go with 5 if I were you.  That certainly isn't used for anything else and if you must use a single character most anybody will know what you are talking about.


Can you find malaria parasites in saliva?

No.
Although malaria is transmitted through the saliva of a female Anopheles mosquito, it stays in the bloodstream and doesn't pass over to the saliva of humans (otherwise it probably would be transmittable via humans directly). Once the parasites travel to the liver, it infects and bursts hepatocytes after reproducing (asexually). The burst cells then infect the bloodstream via red blood cells, where the parasites reproduce further and eventually burst their host cell, leading to a vicious cycle. This whole process only has to do with the bloodstream, since the parasites live in red blood cells.

However, there are certain markers present in the saliva which can be used to detect the presence of malaria the most known of which is called PfHRP2, or Plasmodium falciparum histadine-rich protein 2. This only applies to people infected by the type of parasite P. falciparum, however it is this parasite type which is the cause for the vast overwhelming majority of deaths and complications during malaria infection. The range of PfHRP2 values in malaria-positive patients' saliva ranged from 17 to 1167 pg/mL in one study.

References:

http://www.malariajournal.com/content/11/1/175
http://www.jstor.org/discover/10.2307/30086299?uid=3738432&uid=2&uid=4&sid=21104875852967


Where should I go for online information on animals endemic specifically in Mozambique?

Here is a large list of animals (sorted by guilds) that can be found throughout Mozambique.

Each animal in the list is linked to a page with picture and information!

Wikipedia maintains a few lists of animals found in Mozambique.

See here for  a list of mammals (sorted by order).
See here for a list of birds (sorted by order).
They also have 2 lists for mollusks (fresh-water, marine) and 1 for plants.

Gorongosa's own website provides a list of common animals found in Gorongosa:
http://www.gorongosa.org/explore-park/wildlife
As user Sudachi mentioned in a comment below,  iNaturalist and GBIF also have lots of well-managed species lists and observation data.


Can rats pass on memories of a maze to their offspring?

The phenomenon you're talking about was a fad in the 60's, called 'interanimal memory transfer'. It started out when James McConnell performed a later-discredited experiment in which he found that if you chopped up flatworms which had been exposed to some stresses, and fed them to other unexposed flatworms, the unexposed worms became wary of the source of stress quicker after eating their dead companions. He jumped to the conclusion that a 'memory molecule' was being transferred, and that the cannibal worms gained the food worms' memories of the stress.

People then started looking to see if they could:

repeat the experiments
find the same phenomenon in other animals

In the first case, nobody could replicate the experiments in worms, but because McConnell was such a PR genius he managed to convince the public that his results were valid (see Rilling, 1996 for more on this).

In the second case, Frank et al. (1970) and others tried working with rats - I think this is the experiment you're talking about in the question. They found various interesting results including that if you trained rats to run through a maze by using particularly stressful negative reinforcement (like electrocution), then those rats' children would be able to learn the new maze much faster. However, Frank et al. didn't make the same mistake as McConnell - first of all they wondered if the parent rats might be leaving a scent trail. So they used duplicate mazes with the exact same design, putting the children into clean mazes. The children of adults who had already learned the maze continued to outperform the control rats - the explanation was not scent trails.

Next they wondered whether it might be that the second generation rats had been born with a higher wariness as a result of the stress their parents suffered; i.e. it could be a hormonal transfer from mother to child (e.g. cortisol, the stress hormone).

Frank et al. tested their hypothesis by torturing some rats for a while (rules about animal welfare were not strict in the 70's). They would lock some rats in a small jar and bash them about for a long time, then kill them, chop them up, and take out their livers. They fed the livers to other rats, and found that after eating the livers the other rats learned the maze much faster. They interpreted the results in what now seems a sensible light: the stressed rats were producing high concentrations of a stress-signalling molecule. When those rats either had children or were fed to other rats, they passed on high doses of the stress molecule. This raised the alterness and wariness of the receipient rats so that they were much quicker to learn which parts of the maze were dangerous.

There is no evidence that the child rats actually 'remembered' the maze - they still had to find their way around, but they were extremely wary of the electrocution plates and so avoided them, finding the safest way to the end. This is not a case of genetic memory.

 Frank B, Stein DG, Rosen J. 1970. Interanimal “Memory” Transfer: Results from Brain and Liver Homogenates. Science 169: 399–402.
 Rilling M. 1996. The mystery of the vanished citations: James McConnell’s forgotten 1960s quest for planarian learning, a biochemical engram, and celebrity. American Psychologist 51: 589–598.


What are non-heritable changes to genomes?

I don't know what you really mean by "heritable changes to the genome". I think you will understand why this sentence makes no sense after reading what follows. I start with some background and then try to address directly what confuses you.

Short introduction to the concept of heritability

The concept of heritability may have two meanings.

Heritability is a concept defined at the population level for one given trait. The heritability ($h_B^2$) (in the broad sense) is the ratio of the genetic variance $V_p$ over the phenotypic variance $V_p$, where the phenotypic variance can itself be decomposed into environmental $V_e$ and genetic variance $V_g$ (and their covariance that we will neglect for the purpose of this question).

$$h_B^2 = \frac{V_{g}}{V_{p}} = \frac{V_{g}}{V_{e} + V_{g}}$$

When saying environmental variance $V_e$, we don't refer to the total variance in the environment (such as the variance in temperature for example) but we refer to the phenotypic variance (in a given population of a given trait of interest) that is caused by environmental variance. The same logic is true for the genetic variance.

Inheritence

While the concept of heritability applies to phenotypic traits, the concept of inheritence can apply to DNA material. A mutation is inherited if the offspring receives the sequence from his/her mother or from his/her father (assuming we are talking about a species that have sexual reproduction with 2 genders).

Somatic versus germline mutations

As pointed by @Chris in the comments. In multicellular organisms, not all mutations can be transmitted to the multicellular offspring. Most of the cells do not give rise to any other multicellular organisms. For example, imagine that while the biceps is under development at very low age, a mutation occurs that will be inherited by the daughter cells but not to the multicellular offspring. we call the line of cells that do not give rise to gametes (sperm and ovules), the soma line, by opposition to the germ line which gives rise to the gametes.

To answer your question

As soon as a given locus (position on the DNA) has some variance and that this variance explains some phenotypic variance, then the phenotypic trait it influences has a heritability greater than zero. If the variance at this locus has no effect on the phenotype, then it's heritability is zero (because $V_g = 0$, although there is some variance in the actual sequence). If the phenotypic trait of interest does not show any variance (in the population considered), then the concept of heritability is undefined for this trait!

I think you may have a confusion between "inherited trait" and "heritable trait". A mutation will necessarily be transmissible to the offspring (except if it happen to be in the somatic line in such case it will only be transmitted to daughter cells but not to the multicellular offspring) but it doesn't mean that this mutation will necessarily explain some variance in a phenotypic trait. A new much is necessarily heritable (pay attention to the soma vs germ line) but does not mean that a phenotypic will have higher heritability thanks to this mutation.


RNase AWAY is marked for Category II skin corrosion/irritation and Category II eye irritation/serious eye damage. Recommendations by the MSDS followed by definitions as follows:

Skin contact Wash off immediately with plenty of water for at least 15 minutes. Remove and wash contaminated clothing before re-use. Immediate medical attention is required.
Eye contact Rinse immediately with plenty of water, also under the eyelids, for at least 15
minutes. Immediate medical attention is required.

SOURCE
DEFINITIONS FOR GHS LABELING
More information is included in the MSDS provided.
As for any smell, RNase away is reported to be a proprietary alkali hydroxide solution, so without any additional information it's difficult to tell.


First of all, we have to think about the ecosystem in which banana exist. Obviously, the banana is in a rain forest. Rain forests are a very interesting ecosystem with lots of species. The climate is really hot and the atmosphere has high humidity.

Banana is definitely not CAM plant, because this kind of photosynthesis has usually cactuses and succulents. CAM plants usually have closed stromas during the day and open at night to protect from possible loss of water, carbon dioxide. This type of photosynthesis doesn't suite into the rain forest.

C4 plants are well known for Kranz anatomy of a leaf. They have special sheets to do secondary fixation of carbon dioxide. So according to this web I personally believe that banana is not C4 plant.

So according to this article the banana has C3 photosynthesis.


I found this strange tooth in Galveston, Texas. What does it belong to?

This is a cow tooth. Your image matches above image.
https://www.flickr.com/photos/61377404@N08/12300347505


Microorganisms in Louis Pasteur's experiment of beans

So, where do microorganisms come from? Do they come from the environment?

Yes!

There is no spontaneous generations. Microorganisms (virus, bacteria, unicellular eukaryote, small multicellular eukaryotes) just like macroorganisms (big-enough to be seen by the naked eye multicellular eukaryotes) are not recreated out of nothing. Abiogenesis happened a long time ago and as far as we know, it is not happening today.

This means that if there is a micro-organism somewhere, it must have come from the environment. It did not pop up out of nowhere.


How is AMP "recharged" to become ATP in a cell?

AMP is first converted to ADP in the reaction

AMP + ATP $\leftrightarrow$ 2 ADP

catalyzed by adenylate kinase. So one phophate group is transfered from ATP to AMP, resulting in two ADP molecules. The ADP formed is then used to synthesize ATP as usual, by the mitochondrial ATP synthase or by the glycolysis enzymes.

For other nucleotides and deoxynucleotides, the monophosphate form NMP are usually phosphorylated to NDP using ATP, catalyzed by various kinases. For example, UMP and CMP is handled by the enzyme CMPK. Note that this is essentially the same type of reaction as adenylate kinase.

Regarding the energetics, the above reaction is only slightly favorable (at equal reactant concentrations) with $\Delta G=-2.6$ kJ/mol. In most cells, ATP concentration is much higher than ADP though, which helps drive the adenylate kinase reaction forward. See this site where you can investigate the energetics more closely.


Taxonomy problems on algae: Is Cryptophyta a Phylum or a Class rank?

It is not possible to tell which one is "correct" and which one is "incorrect";
Actually "ranking" itself is a bigger problem with entire classification system.

After the "sexual species concept" we have somewhat a grasp that many (but not all) species fall on "same rank"; but for supra-specific ranks it is theoretically impossible to tell whether the  grass  (said to be "family" rank) and a  compositae (said to be "family" rank) fall exactly on same "rank" or not; similarly it is theoretically impossible to tell whether the animal (said to be kingdom rank) and plants (said to be kingdom rank) are exactly on same rank.

Practically; we forcefully assign the taxa from different lineages into similar ranks somewhat based on apparent perception, and in some cases we develop fine divisions of ranks and develop some criteria, that is also based on perception of 1 or a team op people; but that is not absolute.

What we can theoretically confirm, the taxon "Plant" is certainly higher than  (superset of) the taxon "grass" (a subset). I.e. hierarchies (superset-subset relationship) exist along a lineage. But the concept of "rank"; i.e. assigning 2 taxa from different lineage into "ranks" is a highly subjective and controversial.
(Personally I confess I don't know whether the ranking system have any real advantage other than arranging information)

A routine change of rank usually does not make anything correct or incorrect. (if within the single lineage you assigned a phylum into order and simultaneously an order into phylum; then it would be a clear false, or jumble-up the subset-superset relation). But when you just change a vague and confusing sort of
 "weightage" with respect to taxa on other lineages; keeping all subset-superset relations unaltered; nothing actually changes!

N.B. Additionally, if a taxon (set) is broken into adjacent or more taxa, or 2 adjacent taxa (set) is fused, (without cutting a taxon from one lineage to another) that is also a minor change in "refinement" or "resolution", not a change in correct-or-incorrect-ness.


Can I imbibe seeds before sterilization?

Personal anecdote: Once I planned to sterilize seeds of Silene latifolia for tissue culture but after the first step (washing the seeds in water for an hour) I had to do other things and the seeds did spend the night wet in room temperature. The next day some of the seeds were showing first signs of germination - a little crack in seed coat. I decided to sterilize them anyway, since there was nothing to lose. The result: Some seeds did germinate after sterilization and were fine. Some seeds died. Interestingly, in some seeds the bleach destroyed only the exposed root meristem resulting in rootless seedlings.
I have never worked with lettuce seeds but I would consider questions:

How fast the seeds germinate and what conditions they need for germinating? You cannot sterilize seed that have already germinated.
Could the inbibition change the properties of the seed coat and make it easier for the bleach to pass through and kill the embryo? I suspect not, but cannot be sure.
Wet environment is good for bacteria and fungi growth. "Dirtier" seeds are sometimes harder to sterilize - they need longer exposure to bleach or stronger bleach concentration to completely remove contamination. Stronger bleach or longer treatment can sometimes kill some (especially small) seeds. It is hard to say weather two days of wetness can make any difference. The cold should slow down the bacterial and fungal growth.

At the end of the day I reccomend you to try with few seeds and see the result. Maybe include negative control with usual order of steps. If the survival is the same for both groops you are good to go.


For how long can a person drink sea water?

(source: free.fr)

Alain Bombard

He is a french biologist who voluntarily tested how many days a man can survive drinking seawater and how?

Biologist point of view

Sea contains ~3.5% of salt$^1$. Our kidney separates the waste from water and excrete them in urine provided the salt content is less than ~2%.$^2$
So, it will take the water already present in the body. Causing excessive thirst and dehydration, eventually cause death.

Alain's Experiment

  Just one spoon of seawater at 20 minute intervals, drinking very
  slowly and letting the saliva in your mouth reduce the saline in the
  water you have swallowed.

Though he survived 65 days (From and including: Sunday, 19 October 1952
to Tuesday, 23 December 1952, ~4,400km) of his journey and lost 25 kg of weight, this result is never successfully reproduced.

Source:

http://oceanservice.noaa.gov/facts/whysalty.html
http://paradise.docastaway.com/drinking-sea-water


As you've pictured this is a fledgling that you found which has a mixture of adult feathers and immature feathers.  This indicates that it flew to your location, and a nest is nearby.  You should either attempt to find the nest, or just leave the fledgling alone and let it make its own way home as indicated in this online resource.

Fledglings are juvenile birds who have a mix of fuzzy down and adult feathers and are learning to fly. You may come across them hopping along on the ground, perching on low-hanging branches, or hiding under bushes, but as long as they’re healthy, just let them be.
Note: Fledglings are often “rescued” from their natural environment when they don’t need to be.


Is the promoter region of a gene transcribed?

would it form the initial mRNA portion soon after attachment by reading the promoter region?

The RNA Polymerase binds to the promoter, however since it is so large the front end of it hangs off the end of the promoter.  When Transcription begins the promoter is not included, as the transcription process occurs at the front of the polymerase.

  Also, does the RNA polymerase read DNA base pairs one by one and add the RNA base pairs to the chain one by one?

The RNA polymerase adds nucleoside triphosphate (NTP) one by one.  As the picture shows below, there is only room for one NTP in the active site and once the correct NTP is placed it is added to the RNA chain.

  How does the process end just by reading the terminator region?

The question of termination is dependent on the cell.  Prokaryotes terminate in either a Rho independent or dependent process.  Independently, a hairpin occurs in the RNA that breaks off the transcript, dependently, a Rho factor binds that causes termination.  Eukaryotes are less well known, but it is generally believed that after the poly-A site there are also factors that bind and induce termination.

  So, should the promoter and terminator region of a gene be considered parts of the gene or separate entities?

This question is slightly more about definitions that biology.  The Oxford Engligh dictionary defines a gene as "The basic unit of heredity in living organisms".  Since the promoter, non-coding, and non-translating regions are still paramount in getting the protein made, I would argue that they are still part of the gene and the larger hereditary unit.


Risks of latent viruses that reside in ancient genomes under research?

First, I don't understand why you are more worried about viruses of extinct species, instead of ancient viruses of species that haven't gone extinct. Clearly the infectious potential of the latter is greater for the current species. I haven't heard a peep in published literature about the dangers of resurrecting mammoth viruses, but surely recreating (in 2005) the 1918 influenza
did stir some fairly substantial safety debates.

In general, working with ancient DNA (aDNA) does require some safety precautions, but mainly because of the risk of contaminating the aDNA (with modern DNA)-.

Furthermore, I'm not aware of any research having resurrected an ancient virus from an extinct species aDNA (your specific scenario), but one ~5-million y.o. retrovirus (dubbed Phoenix) was assembled from current human DNA (in 2006); the authors were a little worried as to its infectious potential, so they engineered it so it couldn't replicate more than once.

More commonly, the genome of less ancient virus strains is being fairly routinely reassembled from e.g. from mummies, skeletons, or even packrat middens in order to study the evolution of common viral diseases. Most of this goes on without any safety controversies, as far as I can tell. Less commonly, ancient viruses of various species are found fairly intact in permafrost which does also stir some safety discussions (regarding the handling of permafrost).

So is your scenario possible in theory? Yes. Are experts worried about it? Not that I've heard...


(How) does coppicing fundamentally alter tree growth?

According to Deckmyn et al (2004), the primary effect of coppice management is that the fraction of total biomass in roots is relatively higher after coppicing, and that a substantial fraction of carbon in roots (~20% of root mass) is reallocated aboveground to support shoot growth in the spring following coppicing.

Because of this large re-allocation, coppiced plants are able to grow more rapidly (and reach canopy closure sooner), than seedlings (Ceulemans et al 1996) it is important to consider that canopy closure (maximum leaf area index) occurrs more rapidly after coppicing

Deckman et al, 2004 Poplar growth and yield in short rotation coppice: model simulations using the process model SECRETS. Biomass and Bioenergy doi:10.1016/S0961-9534(03)00121-1

Ceulemans et al, 1996. A comparison among eucalypt, poplar and willow characteristics with particular reference to a coppice, growth-modelling approach Original Research Article
Biomass and Bioenergy, Volume 11, Issues 2–3, Pages 215-231 doi:10.1016/0961-9534(96)00035-9


Why does max heart rate decrease with age?

There are many reasons why the maximal heart rate decreases with age.
The most prevalent is the heterogenous thickening of the walls of the heart.
Cardiac output is stroke volume times heart rate.

When the wall thickens, the heart needs more energy to achieve the same pumping (bigger stroke volume) or it needs to increase heart rate at rest.
Because of physical limitation, the stroke volume cannot be increased.
Heart needs to also rest which it does before the action potential reaches the AV conduction system.
Note the long time just after the action potential reaches AV node.

However, the heart cannot increase its maximal heart rate if the elasticity of the walls have decreased in ageing.
Ageing often leads to heterogenous thickening of walls of the heart.
If this is the case, then T wave gets high fast; which causes the risk of bleeding when exercising.
Doing sport or just feeling tired can cause a long-standing pain in the heart area in the chest.

Sport then again leads to dynamic hypertrophy of the heart tissue, which increases the maximal heart rate.
Ageing then again does not have such a dynamic changes.

There are secondary reasons caused by ageing

hormonal changes
decreased metabolism
decreased physical activity
...

which are associated with decreased maximal heart rate.

Why most endurance athletes reach their peak cardiovascular performance at around age 30?

Human's best age is at about 25 years old physiologically.
Muscles grow in rest.
When practicing at that age, recovery time of muscles is short.
It takes long time to improve cardiovascular performance (1-5 years), since heart muscle improves slowly.
I think the slow hypertrophy of heart musculature and the best physiological age of human are the reasons why the most successful endurance athletes are about 28-30 years old.


Yes, in this context $\gamma$ indicates phosphorylation. See e.g. "The phosphorylated form of H2AX is called $\gamma$-H2AX [18, 19]." from here, and references therein.
I am unsure of the exact basis of this, but I believe that it is because the gamma phosphate group of a nucleotide triphosphate is the one that is generally used by kinases to phosphorylate other functional groups. SEE UPDATE for derivation.
Other notations such as the $p$ prefix are more readable to me, but the usage appears to be cultural and somewhat field-specific.
Update
In response to @MattDMO comment, I read further and found that the terminology derives from this paper. They don't directly explain the terminology, but in context it's pretty clear:

At the maximum, approximately 1% of the H2AX becomes $\gamma$-phosphorylated per Gy of ionizing radiation.

In mammals, the serine in this motif is residue 139, the site of γ-phosphorylation.

When mammalian cell cultures are exposed to ionizing radiation and the acid-soluble nuclear proteins are analyzed on two-dimensional AUT-AUC gels, novel components that will be referred to as $\gamma$ (Fig. 1, A and B) are found in the H2A region of these gels.

It appears that the name probably derives from an observation that was just "whatever in this 2-D gel is $\gamma$-P32 labeled when we induce DSBs when $\gamma$-P32 ATP is present."
@MattDMO also points out that the irradiation that induces the gamma component in this context is gamma radiation. So it's all a bit of a muddle, it could also be that.


Telomeres are maintained by telomerase (in certain cell types, not all of them) at every replication. So, the answer to your questions "where did that existing telomere come from? And the telomere before that?" is: "because there was already a telomere to extend at the end of this chromosome".

Your questions boil down to "how did telomeres appear in the first place?" (because once telomeres and a maintenance mechanism have been established, they will simply remain unless some major genomic catastrophe happens), and this is a difficult question. As Whitney pointed out in the comments of your question, some hypotheses about the origin of telomeres are discussed in this article.
Interestingly, Drosophila doesn't have telomerase, and maintains telomeres by a transposition mechanism. Somehow this is a clue about how telomeres appeared: Drosophila telomeres could be an intermediate between circular chromosomes and telomerase-based maintenance of linear chromosomes.

This is a complicated topic, but the scientific literature about the appearance of telomeres is fascinating. Some bacteria (Borrelia and Streptomyces taxa) have linear chromosomes, but maintenance mechanisms that have nothing to do with transposition nor telomerase.

Here are some references:

Drosophila: https://doi.org/10.3389/fonc.2013.00112
Borrelia: https://doi.org/10.1146/annurev.micro.112408.134037
Streptomyces: http://link.springer.com/chapter/10.1007/7171_2007_090

If you can read French, you will find more info in the introduction of my PhD thesis.


Which Papaya (Lechosa) plant (male or female) bears fruit?

Male flowers have no ovary and do not produce a fruit but females need to be pollinated or the fruits will be aborted falling off when they are about golf ball size (1). Therefore, you will need at least one male or hermaphrodite plant with your female plants so you can manually pollinate the female plants. Also, note that hermaphrodites can pollinate themselves so you will not need another one or a male for fruit.

The article goes on to say that hermaphrodites are the preferred type but under certain circumstances a hermaphrodite can shift to a female.

  Cool winter weather or high soil moisture can lead to a shift toward femaleness, where the stamens fuse to the carpels or ovary wall. The re
  sulting fruits become severely ridged (carpelloid, or “cat faced”) and hence are deformed and unmarketable (1).

  Home gardeners should take steps to avoid having only a single papaya plant, in case it turns out to be a female. One way to accomplish this is have several plants in the garden, to ensure the possibility that at least one will be
  a hermaphrodite with pollen. If space is limited, allow several seedlings to grow to flowering stage in the same planting spot, and then remove all but the healthiest hermaphrodite plant (1).


What is the difference between a species tree, a gene tree and a phylogenetic tree?

Phylogenetic tree

A phylogenetic tree is a tree showing relationship between lineages. These lineages might be computed for genome-wide DNA or from only a single gene. As such the term phylogenetic tree is general.

gene tree vs species tree

If you compute a phylogenetic tree, from genome-wide DNA, then you are computing a species tree (although some sister lineages might not perfectly fit the definition of species). If the phylogenetic tree is computed from data coming from a single gene, then we are talking of gene tree.

Why would a gene tree not match a species tree?

But a gene tree is not just a species tree with fewer data. There are reasons for why a gene tree may not match a gene tree. Genes may duplicate within a given genome. The two duplicated genes are free to evolve independently since the split. All descendants lineages will then inherit these two genes but if you map the two different copies of the gene (red and green below) in two sister clade, they will be much more different then the two same copies (say the green copy) in two distantly related species. Here is a picture to show that

Also, copies of genes can be deleted later on and there might have horizontal gene transfer. For all these reasons the phylogenetic tree of a gene might well be very different than the phylogenetic tree of species.

Below is a gene tree and the associated species at the tips. Take time to make sense of what is going on on the picture.

What is a species tree exactly?

One could call a species tree as some kind of average tree among all gene trees.


How many generations does it take for one species to become a new one?

Your question is like asking about the color spectrum. A wavelength of 530nm is green; a wavelength of 580nm is yellow. So let's say it takes 60nm of wavelength change to go from green to yellow. What color does a wavelength of 579nm have, green or yellow? If it's green, then does the color shift in a single nm difference of wavelengths? If it's yellow, what color is 578nm, etc?

The answer in this case is, 579nm is yellow; so is 578nm. 570nm is more ambiguous; some people might say it's yellow, others think it's greenish-yellow, in some contexts it might look clearly green. And so on along the spectrum; the reality is that there is no hard boundary between "green" and "yellow". There are colors that are clearly green, colors that are clearly yellow, and there is a difference between those two, but there are also plenty of intermediates that are a bit like green and a bit like yellow, and those intermediates are what you go through when you go from green to yellow. There is no definite point everybody can agree on where a single shift happens.

It is the same thing with species. A species is a group of organisms that interbreed to produce fertile offspring, but "interbreeding to produce fertile offspring" isn't a on/off thing. Organisms are more or less fertile. What if organisms from two groups interbreed and produce offspring, and only half of those offspring are fertile? Or they have half as many offspring as couples within the two groups have?

The reason species are an important concept, and can be distinguished visually as being like each other and unlike members of other species, is that within a species there is widespread sharing of genes over the generation, as individuals breed with each other, but they don't share genes with other species. Meaning species will evolve as a unit; changes that happen within a species will spread between individuals of that species, but won't spread outside of it.

But because sharing genes isn't an on/off thing, you could have 100% of genes being shared from one population to another (then they're clearly the same species), or 0% (then they're clearly not), or 90%, or 70%, or 10%... That's where you find the fuzzy boundaries. The races, strains, varieties, sub-species, all those different words to describe populations that are different but aren't outright different species. And the debates on whether different groups are different species or not in the first place, in the cases where it's really ambiguous.

And the same thing is true of evolutionary change in general. You don't have a mammalian carnivore that isn't a cat, and then bam! a cat. You have a mammalian carnivore that isn't a cat (or dog, or weasel... but kind of like any of those in various ways. Like generic carnivore-ish), then a mammalian carnivore that's a bit more like a cat or a dog (and another one next to it that's a bit more like a weasel), then a mammalian carnivore that's even more like a cat (and others that are even more like a dog, and even more like a weasel), then a mammalian carnivore that's clearly feline but isn't a cat, or a lion, or a tiger; it's a different species of feline that doesn't exist today, and also looks more generic-feline-ish than any modern feline. Then there's a feline that's more like a cat (and others around it that are more like a lion, and a tiger), but also clearly isn't a modern cat. Then there are felines that are really like cats but a bit different from modern ones and it's hard to tell, maybe we should extend the definition of "cat" to include them? And then bam! a cat. But that cat isn't clearly a Jungle Cat, or a European Wildcat, or a domestic cat, or any modern species; it's its own "archaic cat" species. And then there are cats that are more like Jungle cats, or more like domestic house cats...

Also don't confuse the creation of new species with evolutionary change in general. Over the long term they are related, because once two groups are different species then they will change through evolution in independent directions, and they will end up looking different from each other as well as from their common ancestor. But over the short term you can have speciation with very little morphological or genetic change (you just need two groups that used to interbreed, to no longer do so), or morphological/genetic change without speciation (if all the change happens within one group).

Both speciation and genetic/morphological change can happen within a single generation, but usually happen over much longer timescales. But there is no hard rule for how long that is; as far as speciation goes, if groups aren't prevented from interbreeding in some way then they will keep breeding with each other and can stay a single species indefinitely (whether individual from generation 10,000 could interbreed with individual from generation 1 is a different question, but it's not like it's a situation that happens). As far as evolutionary change goes, natural selection means species change to adapt to their environment. Once they're adapted to it, if it happens their environment never changes then natural selection will push them to stay the same as they are, again indefinitely. In the real world most environments change over time so organisms do change more often than not, but just to illustrate that the timelines are a product of circumstance, not an intrinsic feature of evolution itself.