Are All Taxonomic Groups Uniquely Named? The Linnaean classification system classifies and groups organisms into taxonomic groups: Kingdom, Phylum, Class, etc. Obviously, a clade at any taxonomic level is uniquely determined by its classification at this level and all its parents in the hierarchy, e.g., Kingdom = Bacteria, Phylum = Firmicutes, Class = Clostridia uniquely identifies a group of bacteria. But is this group also uniquely identified by just Clostridia? Or are there situations where two Phylums might both contain Classes with the same name?

Since Genus & Species are typically used to identify organisms, I would assume that combinations of these at least are unique. As @Jam pointed out in the comments, Species alone is not enough. Note, however, that I am not asking about the binomial name for a species - I am asking about uniqueness among higher levels of aggregation, such as Class, Order, and Family.

There are quite a few biological homonyms (especially at the genus level, which apparently you aren't asking about).  At the family taxonomic level, the Interim Register of Marine and Nonmarine Genera (IRMNG) currently lists 100 family names which are used for two or more distinct taxa.


Passing virus/diseases immunity to newborn From my understanding, our white blood cells 'learn' to fight off viruses and other pathogens that make us sick (or that they encounter because of vaccination) so that the subsequent encounters with same strain will not make us as sick; our immune system is able to fend off much better.

Newborns are protected with mother's antibodies via placenta and breast milk. My question is, can immunity be passed from mother to child via hereditary mechanisms, or does the child have a completely fresh set of 'default' defenses? Is that the reason why we get sick so easily when young?

Newborn mammals get something called "passive immunity", in which the mother's antibodies are passed across to the fetus or newborn. Depending on the species, this can happen by the antibodies crossing the placenta, or more commonly by being transferred in the first milk the mother forms, "colostrum", which is very rich in antibodies. (At the same time, the newborn has special adaptations to absorb antibodies from the colostrum into its body; this only works for a short period after birth.)

Passive immunity
IgG Placental Transfer in Healthy and Pathological Pregnancies
Colostrum

This allows the newborn to have a temporary resistance to whatever pathogens happen to be common in its immediate environment (because presumably the mother would have been exposed to them). It's very much temporary, lasting typically a few weeks or so before the transferred antibodies half-life away. During this time, the newborn has a chance to start developing its own active immunity, which is dynamic and lasts much longer.

Edit to add:

Are there other modes of heritable immunity? Sort of but probably not what you're thinking of. Innate immune responses are often triggered through recognition of molecular patterns that are common to many different pathogens ("Pathogen-associated molecular patterns" or PAMPS). The receptors that recognize these patterns are inherited, and they are essential for starting innate immune responses which are in turn very important for starting acquired immune responses. So yes, every newborn mammal, and reptile, fish, sea urchin, arthropod, nematode, etc. inherits mechanisms for recognizing pathogens.

However, it's important to understand that these don't change during the mother's lifetime. This system doesn't provide any inheritance of recognition of pathogens that are locally important, or that the mother has met during her lifetime. This is the basic toolkit that every individual of the species (often, that every individual in the genus, or kingdom) has, that's needed to answer the general question "Is this a dangerous situation? Should I activate the immune response?"

In other words, as far as the innate system is concerned, "the child has a completely fresh set of 'default' defenses"; the only non-default information that's passed from mother to newborn is via the passive immunity described above.


Can crossing over between X and Y chromosome of sex chromosomes take place? Can it? If no, what would happen if it did?

Yes, it can, but it is rare, and typically only in the pseudoautosomal region, meaning those sections on the X and Y chromosome that have homologous genes.
The reason it's rare and more difficult is that the DNA does not match as well, so the chromosomes have trouble interacting along the length of the chromosome.  Furthermore, there are less recombinant zones available.

Sources:

Kauppi, Liisa, Marco Barchi, Frédéric Baudat, Peter J. Romanienko, Scott Keeney, and Maria Jasin. 2011. Distinct properties of the XY pseudoautosomal region crucial for male meiosis. Science 331 (6019): 916-20.
Hinch, AG, N. Altemose, N. Noor, P. Donnelly, and SR Myers. 2014. Recombination in the human pseudoautosomal region PAR1. Plos Genetics 10 (7): e1004503.


THYROGLOBULIN (19S) comes to a heavier position than ferritin (51S). Why? Sedimentation values of thyroglobulin and ferritin containing iron are 19S
[1] and 51S [2], respectively. But, by density gradient centrifuge, it seems thyroglobulin (19S) migrates faster than ferritin (51S). Could anyone explain this?

Figure 3 in this article shows a migration pattern of GE High molecular weight marker containing ferritin and thyroglobulin. Thyroglobulin comes almost at the bottom but ferritin, in the middle, which I did not expect.

PS
I asked GE and confirmed ferritin in the marker contains Fe ions.

Ferritin and iron-containing ferritin are different and the latter
would of course be heavier; it will therefore sediment faster.
Figure 3 of the third article uses thyroglobulin and ferritin as molecular weight markers. For your information thyroglobulin is 650kDa whereas ferritin is 440kDa. Also note that apoferritin i.e. ferritin that is not bound with iron has a sedimentation rate of 18S (from the same article that measures the sedimentation rate of iron bound ferritin - ref#2).

There seems to be some confusion regarding the sedimentation rate of ferritin. From this article:

  One molecule of ferritin can bind up to 4500 Fe2+ ions.
  When fully loaded with iron, the ferritin can increase in mass up to
  ca 900 kDa; it then has a sedimentation coefficient of 24S (Chasteen &
  Harrison 1999).

55S for ferritin seems dubious.


Giga base or Giga byte "we reported ~2.66- Gb genome sequence of"
"we generated 191.5 Gb high quality reads"

I am very confused with these two quoted lines and I am not sure about giga byte or giga base pair.
and an additional question: How to count base pairs from a FASTQ file?
I have read numbers and length.

This refers to base pairs.

File size has no particular meaning beyond practical considerations, given that it depends on the format. (For example, 2bit files use 2 bits per base, as the name indicates, compared to the 8 bits necessary for each letter in a plain text format like FASTA & derivatives.)

For your additional question, (number of reads * length of each read) gives the total length of sequence contained in the file. It is not really a property of the file format, but a parameter of the sequencing run.


Identify this indoor plant with strange stem-like leaves It appears that this plant branches multiple times from the base of its stem; however, I'm not sure if the base stems are from one organism. It becomes yellowish in color at the tip each stem-like leaves; one node can branch 3-4 leaves at a time.

Additional information:
As for the specimen location- I am currently living in Japan and this plant was bought as a gift for me. It probably is imported from other countries since it doesn't seem to be native here. For maintenance; I was told to just cut the tip of the leaves if it began to fade in color and die; and water the plant at least once a week.

Looks like a Pencil Tree (Euphorbia tirucalli), sometimes called "pencil plant", "pencil cactus" or "milkbush." This "leafless-looking" plant is not actually a cactus, but actually a "Euphorbia" (i.e., member of the Euphorbiaceae family), and should present a white "milky" liquid latex when broken.

CAUTION: THIS IS A POISONOUS PLANT [See symptoms here].

Description: A succulent, spineless shrub with round, green branches; leaves clustered at the tip of the branches and soon dropping

Although it eventually can grow into a small-sized tree in its natural habitat, this plant is found more commonly as a medium-sized house plant or landscaping "shrub."

Range: Tropical Africa and India

Euphorbia tirucalli is very well adapted to semi-arid conditions, but also occurs in both dry and moist forest, savanna and shrub land, and withstands salt stress associated with coastal conditions, but no frost. It occurs from sea-level up to 2500 m altitude. It grows well on a wide variety of light-textured, neutral to acidic soils. It is commonly associated with human settlements and becomes naturalized rapidly. It is locally common and often occurs in groups. [Source].


Function of heparin and dextran sulfate for removing proteins From this article :

  The reaction was terminated and the histones, and most nonhistones,
  were removed by adding the nuclease-treated chromosomes to a solution
  containing dextran sulfate (2 mg/ml) (Pharmacia), heparin (0.2 mg/ml)
  (Sigma), 10 mM Tris (pH 9.0), 10 mM EDTA, 0.1% Nonidet P40, and 1 mM
  phenylmethylsulfonyl fluoride (PMSF) at a ratio of 1 volume of
  chromosomes to 3 volumes of solution.

What is the function of  dextran sulfate and heparin in removing the proteins ?

See here.

Histones are basic proteins (cationic, high pI) because they are required to interact with polyanionic DNA at physiological pH. Heparin and dextran are polyanions which form insoluble salts with the cationic histones.(Dextran is a polymer of glucose. In dextran sulphate it is derivatised with sulphonate groups creating a polyanionic material.)

Immobilised heparin is sometimes used as an affinity matrix for purification of DNA-binding proteins like transcription factors.


Do non-green flower colors have any functional interactions with the sun? I always hear the pseudo-evolutionary claim "plants are green because they need to use red and blue light".  If this premise to my question is true,

What (if any) other functional relationship occur between the color of the blossom of the flower or the color of the leaves in the fall, and the spectrum of the sun.  Could it be said that plants are actively absorbing a particular spectrum for a particular purpose by expressing particular colors other than green?

Some functions of non-green flower colors:

#1: plant-animal interaction. Flower colors act as signals received by animals with eyes (e.g., pollinators, which many plants need to attract in order to reproduce).

However, it sounds from your question as if you're looking for other physiological effects. Two that come to mind are:

#2: heat. Flower color and opacity have a great effect on flower temperature.

This can be especially important for arctic and alpine flowers. Many of these are not only shaped like satellite dishes, but even pivot to follow the sun. This creates a warmer micro-environment which can be important to attracting pollinators and to increasing/speeding seed production. (See, e.g. Mølgaard 1989)

#3: UV protection. Certain pigments can be more effective at filtering UV.

I work in the alpine and occasionally encounter "glasshouse" plants, which have translucent floral parts that act to create warmer microenvironments, with the same effects as above. In addition, these floral parts have been shown to be more effective at UV filtering than green floral parts (Tsukaya 2002)

*edit: as these papers are behind paywalls, I'll also point out that the Wikipedia pages on Heliotropism and Rheum nobile contain similar information.

 Mølgaard P. 1989. Temperature Relations of Yellow and White Flowered Papaver radicatum in North Greenland. Arctic and Alpine Research 21: 83–90.
 Tsukaya H. 2002. Optical and anatomical characteristics of bracts from the Chinese “glasshouse” plant, Rheum alexandrae Batalin (Polygonaceae), in Yunnan, China. J Plant Res 115: 59–63.


If evolution is not about increased complexity, why does so much complexity evolve? In my last question I asked why we don't see increased complexity in artificial life simulations of evolution. It seems I had fallen for a common misconception, that evolution was about improvement by increasing complexity. One comment discussing that post read

  "... he [David Deutsch] is falling for one of the biggest
  misconceptions about evolution that you can, that evolution is about
  improvement. Evolution has simply only ever been about change..."

However, when you look at the history of life you see increases in complexity. You see this increasing complexity evolving over billions of years, suggesting that it requires an explanation.

My question
If evolution is not about increasing complexity then how does so much complexity evolve?

I think possibly the problem here is the way you're approaching the issue.

You're considering improvement as anything that increases the abilities or complexity of the organism—that isn't necessarily what an improvement is though. The outcome of natural selection is that the organism best equipped to survive/reproduce in a certain environment is the most successful. So, for example, thermophillic archaea do much better in 60°C-plus pools of water than humans do. Our capacity to process information, use tools, etc. doesn't actually confer much advantage in that situation. And there can be downsides to that kind of complexity as well, requiring more energy and longer developmental periods. So, natural selection in 60°C-plus pools of water gives you archaea, and in (presumably) the plains of East Africa, it gives you humans.

The comment you quote mentions sickle-cell anaemia, which is a different example. While there is little benefit to having the sickle-cell anaemia allele in a temperate region, in those regions where malaria is endemic, heterozygosity can provide a survival advantage, and so the allele is maintained in the population. If you're someone living in a malaria-endemic region, and you don't have access to antimalarials, heterozygosity for the sickle-cell anaemia allele is arguably an improvement. It depends entirely on how you define the word.

The fundamental principal of natural selection is that it favours the organism most suited to a particular environment. But, that isn't always the most complex organism. It's important not to confuse human-like with better. It isn't the universal endpoint of evolution to produce an organism similar to us, just the organism most suited to the environment in question.

Also, to briefly address the previous question you asked—you asserted that we must be missing something from the process of evolution because we were unable to simulate it. You also pointed out that (in your opinion) we have sufficient computing power to simulate the kinds of organisms you're referring to. But natural selection is intrinsically linked to the environment it occurs in, so the simulation wouldn't just have to accurately simulate the biological processes of the organism, but also all of the external pressures the organism faces. I'd imagine that, in simulating evolution, that would be the real obstacle.


Could we breed a dog to the size of a thumb? We've gotten from a wolf to a small breed such as a chihuahua. So the question is: can we go even further and have a dog as small as a thumb (adult dog)?

If not, what are the factors that limit the smallest size of a dog breed? Is it limitations in genetics, or some physiological reasons which would prevent such small dog to survive?

As mentioned above the inbreeding required to select smaller and smaller dogs would be problematic because of the myriad of health problems that would be associated with it (see inbreeding depression).
The question about physiological limitations is interesting. The main reason biological organisms often don't scale is the fact that length, area, and volume don't scale in the same way. E.g. if something is twice as big L to 2L the surface area is L to L^2 and the volume is L to L^3 which means that many systems no longer work or require more energy (see Allometry) . For example in insects the distance for oxygen to diffuse to cells is short enough that simple diffusion is possible, in humans that is no longer the case so we have whole circulatory and respiratory systems to, in effect, help reduce the diffusion distance for oxygen.
I haven't used this kind of analysis in a while so am not very confident applying it here but I would suggest that some issues that could arise due to things scaling with length versus area or volume are:

required heart rate
maintaining body temperature - many small mammals deal with this by falling into periods of cold torpor (sort of like hibernation) where metabolic rate is suppressed
fragility of bones (as Cort Ammon mentions this is actually not a problem: https://jeb.biologists.org/content/207/9/1577)


Vegetation Monitoring - Why permanent plots Why do most vegetation monitoring programs rely on permanent plots?

Take the context of a single ecological restoration site, for example.  Let's say the variable of interest is cover by plant species, and monitoring is conducted throughout several seasons to track the relative/total cover of multiple species.

If plots are randomly sampled within homogeneous vegetation assemblages, why not just establish new plots each sampling period, rather than locating and re-sampling the same plots over and over again?

If the goal of sampling the is to represent characteristics of the population (i.e. the homogeneous area of vegetation), then why do researchers always sample permanent monitoring plots again and again rather than using a new set of randomly selected plots each time?

The answer boils down to statistics rather than anything particular about this type of experiment.

If you have a sample of plots, and then take repeated measurements in that same sample over time, the variance in the values you record is a function of the variance of the time-dependent process causing changes.

If you take future measurements from a new sample of plots, you have additional variance to account for due to choosing a new sample. That is, even if you would have measured no change at all in the same plots, you expect the second sample will be different from the first just because of sampling. Because of this additional variance, you have less ability to detect smaller changes over time: less statistical power.


What is the biological limit on hearing resolution? I sometimes wonder how many different individual musical scales could be perceived by human ears. I define a musical scale as a collection of notes that relate to some fundamental frequency by specific ratios. For instance

do $2^{0}f$
re $2^{\frac{1}{6}}f$
mi $2^{\frac{1}{3}}f$
fa $2^{\frac{5}{12}}f$
sol $2^{\frac{7}{12}}f$
la $2^{\frac{9}{12}}f$
ti $2^{\frac{11}{12}}f$
do $2^{1}f$

I once did an experiment where I took various sine waves at different frequencies and multiplied them by the appropriate ratios. I found for the ones I tried that I did indeed heard the major scale. But a mathematician will look at the positive real numbers $\Bbb{R}^+$ and say there are an infinite, uncountable number of possible frequencies. However, Biologically I cannot imagine the human ear is capable of distinguishing between an infinite number of frequencies.

What is the biological limit on hearing resolution? Is there a way to estimate how many different major scales one can hear? In other words, how many different frequencies can be heard?

Short answer
The main limitation to frequency discrimination is loudness.

Background
The cochlea is tonotopically organized - it basically acts as a Fourier transformer, where different frequencies are analyzed on a place map  (Fig. 1). Frequency tuning of cochlear hair cells is mainly limited by sound intensity. The louder a pure-tone sound stimulus gets, the larger the area on the basilar membrane that is activated and hence the wider the range of cochlear hair cells that is activated, and hence the worse the frequency resolution becomes (Fig. 2).

Fig. 1. Cochlear tonotopy. Source: Cochlear Implant Help

Auditory nerve fiber tuning. The louder the stimulus, the worse the tuning to frequency. Source: - Fettiplace & Hackney, 2006

As to the quantitative aspect of this question, namely what the frequency difference limen is, and an indication how many frequency bands can be distinguished I refer you to below linked question. Both depend highly on the method used to determine the just-noticeable-difference, and as said also on the sound intensity applied. Moreover, it is dependent on the frequency under consideration. The higher the frequency, the larger the frequency band becomes expressed in Hz. This is an example of Weber-Fechner's law (Hecht, 1924). The cochlea is organized in octaves, meaning that higher frequencies have less cochlear space devoted to them and hence less hair cells to code a particular frequency range.

Further Readings
- What's the frequency resolution of the human ear?

Reference
- Hecht, J General Physiol (1924): 235-67
- Fettiplace & Hackney, Nature Rev Neurosci (2006); 7: 19-29


Are insects capable of gliding on the air with their wings spread, similar to birds? Sometimes birds can use the air to float on with their spread wings. Now, the wings of insects are too small to see if they can do that too. So is it possible for insects to do this also, or can't they hold their wings spread or is the air drag not enough?

It's worth mentioning that insects' flight is somehow different from birds' one, mainly because of the Reynolds number.

However, there is evidence of (some) insects gliding. For instance, Walkeling and Ellington (1997) have filmed gliding in dragonflies and damselflies:

  The free gliding flight of the dragonfly Sympetrum sanguineum was filmed in a large flight enclosure. Reconstruction of the glide paths showed the flights to involve accelerations. Where the acceleration could be considered constant, the lift and drag forces acting on the dragonfly were calculated. The maximum lift coefficient (CL) recorded from these glides was 0.93; however, this is not necessarily the maximum possible from the wings. Lift and drag forces were additionally measured from isolated wings and bodies of S. sanguineum and the damselfly Calopteryx splendens in a steady air flow at Reynolds numbers of 700-2400 for the wings and 2500-15 000 for the bodies. The maximum lift coefficients (CL,max) were 1.07 for S. sanguineum and 1.15 for C. splendens, which are greater than those recorded for all other insects except the locust. The drag coefficient at zero angle of attack ranged between 0.07 and 0.14, being little more than the Blassius value predicted for flat plates. Dragonfly wings thus show exceptional steady-state aerodynamic properties in comparison with the wings of other insects. A resolved-flow model was tested on the body drag data. The parasite drag is significantly affected by viscous forces normal to the longitudinal body axis. The linear dependence of drag on velocity must thus be included in models to predict the parasite drag on dragonflies at non-zero body angles. (emphasis mine)

Source:

JM Wakeling, CP Ellington, Dragonfly flight. I. Gliding flight and steady-state aerodynamic forces. Journal of Experimental Biology 1997 200: 543-556.


(How) do horizontal pupils dialate? I was looking at mongoose eyes in particular, but my understanding is:

Circular (human-like) pupils simply get larger/smaller depending on light levels, no change in "shape"
Vertical slit (cat-like) eyes get wider or narrower, from "almost a line" to "almost a circle".
Goats, mongooses, etc. have horizontal "bar" pupils — more-or-less straight edged across the top and bottom, with rounded (semicircular?) sides.

Do horizontal bar pupils, like those of a mongoose, change size in varying light levels? If so, how does their shape change? Do they get taller or narrower? Do the top and bottom become convex or concave? Does the radius of the sides increase? Does anyone have good reference pictures or diagrams?

There is a large variety of pupil shapes and ability to contract pupils in animals. The vast majority of animals can contract their pupils, including goats and mongooses. Prey animals tend to have horizontally slit pupil, like goats. Mongooses (carnivores) seem to be an exception in that respect. Here is a picture of a sheep's pupil fully dilated and fully contracted:

As you are particularly interested in mongooses, the paper "Characteristics of  the eye of the Indian mongoose (Herpestes auropunctatus)" reports the following concerning pupils dilation induced by topical application of pilocarpine: "The dilated pupil is approximately 3.80 mm in diameter and  slightly oval,  the long  axis  being  horizontal. [...] The constricted pupil is teardrop-shaped, with horizontal  and  vertical  dimensions of 2.5 and 1.1 mm, respectively,  the  narrow end of the  aperture being the nasal end." However that shape seems specific to Indian mongooses because if you search for images of mongooses you'll see that most of them have oblong pupils when contracted. But all of them seem to have almost circular pupils when dilated. Here you can compare the pupil of a mongoose during the day (strongly contracted) and at night (mostly dilated, the color comes from the night photograph):

Nellis, D. W., Sivak, J. G., McFarland, W. N., & Howland, H. C. (1989). Characteristics of the eye of the Indian mongoose (Herpestes auropunctatus). Canadian journal of zoology, 67(11), 2814-2820.


What is (probably) the closest living relative of the trilobite? The trilobites vanished from the fossil record many millions of years ago, but they were obviously arthropods of some sort. Do we know which animals are their closest living relatives? I've heard both Armadillidiidae and horseshoe crabs. Can we tell which is right (or if there is a different answer), and how?

There were so many species of trilobites for 300 million years, so perhaps some trilobites species are closer to horseshoe crabs whilst others are closer to woodlice, some trilobites were amphibious and could walk onto the seashore.

If you check this research about horseshoe crabs, there are a dozen fossils that are hybrids between a trilobite and a horseshoe crab, i.e. bellinatus trilobitoides.

 From the family tree you can see some early horseshoe crabs:

this is a harpetida trilobite:

The morphology of the fossils is mostly saved as dorsal morphology and ventral morphology. from the top the are similar to horseshoe crabs, and the different legs are similar to woodlice and bathynomus and horseshoe crabs in different fossils:

There are other living animals that resemble them like Serolina Delaria:

Tadpole Shrimps:

That's from this cool page with images of lots of things like trilobites.
Silverfish:

Bathynomus, similar to woodlice:

The videos of bathynomus are cool: https://www.youtube.com/watch?v=jfnHQPkta-Q


How much time do INS1-E and MIN6 cells need after splitting? I am currently doing an experiment on cells to test the internalization of a protein.
Normally, I seeded my cells the day before the incubation. This worked well for Hela, CHL or PANC1 cells. However, when I did the same with INS1-E and MIN6 (both beta-cells) after the incubation and the washing step the majority of the cells were gone. This was better in the control where I did not put in the compound, but still a lot of cells were detached.

Therefore, I wonder if I should seed the INS1-E and MIN6 cells earlier, more like 2-3 days before. Do these cell lines need more time after splitting to attach again?

Searching literature to see what the published protocols were is the best bet. I found a simple document for INS-1 cells here. There is also this paper describing the isolation of an Ins-1-derived cell line 832/13 which my lab (though not me personally) have experience with. Cells should only be sub-cultured when nearly or fully confluent. With Ins-1 cells that would be a sub-culture ratio of 1:4 to 1:8 and will take 2-3 days. Something to note is that Ins-1 cells are poorly adherent to tissue culture plastic. That's a normal part of their characterization. I remember lab members having to take special precautions with respect to media ingredients to prevent them from detaching, as well as really delicately adding media to the dishes otherwise the force from pipetting too quickly will dislodge many cells and explain why your cells are washing away.


What's the longest transcript known? What's the longest functional transcript known?  I'm wondering about RNA length post splicing, so not including introns.


Will moth larvae pupate in response to food deprivation Context: Trying to exterminate a clothes moth infestation.

Supposing you have a room with clothes moths, or rather, with clothes moth eggs and larvae.

Suppose then, that you remove all of the soft furnishings, all of the clothes, all of the carpet, and you thoroughly clean and vaccuum to remove as much dust and hair as possible.

Would one predict that the remaining larvae would then immediately pupate into moths, in response to this food deprivation?

I know that lots of plants will suddenly flower or fruit if they perceive that they are at risk of dying, in order to reproduce before they die. I believe the moths are essentially just a reproductive phase of the moth, so I'd be unsurprised if they did pupate.

On the other hand, I imagine pupation takes a lot of energy and food reserves (not to mention needing material for the cocoon), so I can imagine that they might be unable to do this?

Which way do it go?

Will moth larvae pupate in response to food deprivation

Not officially an expert, but I have been watching clothes moths for years and haven't noticed any small ones, so dont expect early pupation. I would expect small pupae to give small moths (like with houseflies). I do see the hormone traps reduce population, but only with lots of them (2 per small room).


Theoretical Rules Governing Life in the Universe Obviously, no one can know what life on another planet would look like until we discover such life. However, scientists have speculated that (if I'm not mistaken) all living things must be carbon-based. I think it's also assumed that all life requires water.

Are you aware of a published list of theoretical "universal life guidelines"? For example, I would speculate that locomotory organs (e.g. legs) tend to evolve in pairs (one-legged animals unlikely), and that microscopic creatures have no legs at all (replaced by cilia, tentacles, etc.).

Again, this isn't hard science; I'm just interested in knowing about the speculations of various scientists.

Let me add a few details to make my question more clear. On Earth, most life can be divided into a handful of kingdoms (e.g. plants and animals), and animals are commonly divided between invertebrates and vertebrates. Vertebrates are generally bigger and are bilaterally symmetrical (as are some invertebrates).

I would speculate that the laws of physics dictate that really tiny organisms have locomotory organs like cilia, and some may have just one cilia.

However, larger, more complex animals possess bilateral symmetry. This includes not just vertebrates but arthropods and even some mollusks (e.g cephalopods). There are some obvious advantages to bilateral symmetry among larger life forms.

So, if we discovered a planet with a similar size to Earth, we probably would not expect to find fifty-feet amoebas crawling on land. We might speculate that most large terrestrial creatures would have paired leg-like organs - and probably one or two pairs, not 100. Similarly, paired eyes help with navigation and depth perception.

But those are just very general personal guesses. Lots of alien life forms have been created for science fiction movies, but I wondered if the scientific community has created some more rigorous theories about what alien life forms would really be like.

On Earth, many animals only have one locomotory organ (such as the tail of a fish or a legless lizard). Some have five limbs (starfish). It just happens that the presently dominant group of large animals has bilateral symmetry (a distinct head and tail, underside and back, and medial and lateral, but usually no left and right distinction, except in internal organs), and hence often has paired anatomical features.


There are linear and rotary molecular motors in the cells. Do any of them have a fixed or stable frequency or speed? Are there any linear, rotary or oscillatory molecular motors in the cells which can have fixed frequeny and which can be used as a reference for elapsed time timer? This question is with relevence to my earlier question 'Is there a realtime molecular clock within the genome to co-ordinate the developmental sequences in an embryo?'

There are molecular motors but the frequency is a function of energy input (ATP); similar to the angular velocity dependence on amount of current in electrical motors.

The concept of molecular motor may not be suitable for a clock like device. There are clocks based on genetic circuits, which produce stable oscillations. Examples include the circadian clock, cell division, menstrual cycle etc.

Developmental events involve checkpoints and the timing is regulated by several factors such as number of cells, concentration of some protein etc. However, I haven't come across a master clock that integrates and synchronizes all these signals for precise developmental timing. That makes it an interesting area of research.


Why are male gametes and female gametes not equally sized Why is it that male gametes are smaller and produced in larger quantities than female gametes that are large and lesser in number. Why aren't the gametes equally sized, or their sizes the other way around. Is there an evolutionary advantage to this, or is it just how things evolved and would it not have mattered if the sizes and quantities were reversed?

Gerardo is correct that female designates the bigger gamete, so there's nothing important about the terms "male" and "female" here.  But I'd like to also respond to your initial question of how the difference in size would've evolved because I don't think it's trivial.

I can provide a rough summary of one explanation that was summarized in Dawkin's The Selfish Gene which was summarized from G. A. Parker's 1972 paper "The origin and evolution of gametic dimorphism and the male-female phenomenon."

It goes something like this:

The asymmetry could have evolved from originally equal sized gametes through the evolution of two divergent sexual strategies - a large investment strategy which opened the way for a small-investment exploitative strategy. The idea is that when gametes were all roughly the same size, some would have happened to be bigger than others. There may have been some advantage to this because the larger gamete could provide a larger initial food supply. However, this also could have created a condition for exploitation by individuals producing smaller than average gametes, especially if they could ensure their smaller gametes fused with the larger than average ones. This could be achieved by making the small ones more mobile and able to actively seek out the larger ones. Making smaller gametes would have allowed that individual to make more of them and potentially have more descendants, as they're not investing as much energy into any one gamete. The interplay of these two strategies would've continued in a runaway fashion, with the larger gametes evolving larger and larger to compensate for the ever-smaller contributions by the exploiters.  Eventually the larger gamete could become immobile since it's being sought out by the smaller gametes anyway. You can see where this is going, with the larger gamete becoming what we know of as eggs and the smaller as sperms.


What information can Uniprot give me about phosphorylated forms of proteins? I have a list of proteins formatted like this:

Protein Name        Gene Name
4E-BPI              EIF4EBP1
4E-BPI_pS65         EIF4EBP1
4E-BPI_PT37_T46     EIF4EBP1
53BP1               TP53BP1

Its my job to pull the following from Uniprot:

Subcellular Location information (this is easy)
Information about phosphorylated forms

The first thing I did was compile a list of Uniprot IDs for each gene's human form that I could plug into the Upload List function.

Next, I used Uniprot's "Customize Results Table" page, to add the "Subcellular Location" column to the output. Do you know columns will provide information about the phosphorylated forms of these proteins? I added columns PTM > PhosSite and PTM > PhosphoSite but they return the Uniprot ID or nothing at all.

Is there somewhere else in Uniprot that I can look for information about phosphorylated forms of proteins?

You were looking in the wrong spot. The PTM section you clicked on is for post-translational modification databases such as PhosphoSite. To get the actual modified residues, click on "PTM/Processsing" (sic) further up the page and then select "Modified Residue", and in your results table you'll get a list of all phosphorylations, glycosylations, acetylations, etc.


What are all possible vectors for unicellular human parasites? I got the given question. They want the following pieces of information about protozoological human parasites:

  disease - parasite - vector.

There are 10 proteogenic diseases at the Wikipedia. I added the corresponding parasite and the vector next to them:

Malaria - Plasmodium - Apicomplexa
Amoebiasis - Entamoeba histolytica - sarcomastigophora
Giardiasis - Giardia lamblia - no vector
Toxoplasmosis - Toxoplasma gondii - no vector
Cryptosporidiosis - Cryptosporidium - Apicomplexa
Trichomoniasis - Trichomonas vaginalis - no vector
Chagas disease - Trypanosoma cruci - insect
Leismaniasis - Leishmania donovani - sand fly vector
Sleeping sickness - Trypanosoma brucei gambiense - tsetse fly vector
Dysentery - Entamoeba histolytica - sarcomastigophora

I am unsure what I should answer to the question since it is asking "all" possible vectors for unicellular human parasites.
There are many possible diseases, much more than the given ten in my opinion.
It seems also that there are many possible ways of getting the infection for each disease.

I hope that I am wrong in my statements.
It is my first course in Parasitology.

What would you answer to the given question?

Based on my course material, I managed to get the following list:

Malaria - Plasmodium falciparum, p. malariae, p. vivax, p. ovale - female anopheline mosquito
Babesiosis - Babesia devergens, babesia microti - tick ixodes ricinus
Balantidiasis - Balantidium coli - waterborne
Coccidiosis & toxoplasmosis - Eimeria species - waterborne
Toxoplasmosis - Toxoplasma gondii - waterborne
Amoebic dysentery - Entamoeba histolytica - waterborne
Periodentitis - Entamoeba gingivalis - oral-oral contact
PAM - Naegleria fowleri - waterborne
GAM - Acanthamoeba species - waterborne
BAE - Balamuthia mandrillaris - waterborne
Trichomoniasis - Trichomonas vaginalis - sexual contact
Trypanosomiasis - Trypanosoma brucei gambiense, trypanosoma brucei rhodesiense - bite of a tsetse fly
Leukopenia - Leishmaniasis specieses - different genera of sandflies: Plebotonus & Lutzomyia

Waterborne means that the parasite is transmitted to the host through contaminated food, water or hands, or by swimming in warm pools or mud pools, for instance.


What physiological processes give rise to a linear cell survival curve? If we plot the number of surviving cells in a structure over time (assuming no replacement), the shape of that curve should imply something about the underlying process responsible for cell death. For example, if surrounding conditions mean that each cell has a constant probability of dying within a given interval, then an exponential decay curve should be seen. If the cell has a characteristic lifetime (with say a gaussian distribution about that mean lifetime), then (I guess) we might expect something like a logistic S-shaped curve.

In Parkinson's disease, the onset of motor symptoms is related to the number of dopaminergic neurons in the substantia nigra pars compacta, a small structure of just several hundred thousand neurons. The decline in cell numbers due to the disease process is indeed usually modelled as something like an exponential decay.

But there is also a normal age-related decline in substantia nigra neuron numbers. This decline is usually modelled as a linear decrease from birth through to old age, at something like 0.5% to 1% per year (Rudow et. al., 2008. Morphometry of the human substantia nigra in ageing and Parkinson’s disease. Acta Neuropathologica, 115(4), 461-470 http://dacemirror.sci-hub.tw/journal-article/fc4e7854ee0cef0146d60756536b2a88/rudow2008.pdf )

Note that this percentage decline per year is not a percentage of the surviving number (which would yield an exponential curve), but of the original total. In effect, it is perhaps best to think of it as a decline by a constant absolute number of neurons per year, yielding a straight line survival curve.

Exponential decline is memoryless (conditions simply conspire such that the probability of any cell's death is constant in a given interval, uninfluenced by the history of that cell or any other). The death of a cell with a characteristic lifespan, meanwhile, does have memory, as the probability of a given cell dying increases as that cell ages and deteriorates. But the death of a constant number of cells in a given interval somehow implies a sort of memory across cells, such that the number dying in a given interval is related to the initial number, and not to the current surviving population level.

My question is what general physiological processes are consistent with such a linear decline? i.e. is a linear decline a common pattern for neurons or any other sort of cell death, and in general, what sort of process governs it?

Progressive cell death along a spatial dimension would be consistent with this. For example, imagine a cylinder of tissue in which cells at one face die, inducing adjacent cells to die. This would yield linear decay in viability to 0.


Is there a specific terms to describe variant of existing genes in bacteria? I have a question regarding a specific term that describes the variant of existing genes. I am analyzing whole-genome sequencing of a bacterial isolate. I found there are a large number of genes that have partial sequence identity or subject/query coverage to the known reference genes.

Now I know that by looking at sequence identity and coverage may not be enough to analyze the genes. I know some gene can have 30% sequence identity and still folded the same way as the original genes. However, let's say these genes are truly variant of the existing genes based off sequence identity. What is the term to call them?

My PI told me they are rapidly evolving genes. I searched some paper and found rapidly evolving genes are genes that are subjected to positive selection. While I agree for some of these are rapidly evolving genes as they probably subject to positive selection, I cannot see that all of the genes actually undergoes selection at same time. I am wondering if there is another term to call these gene variants. If there is any paper to define them that will be great.

Thanks

Allele

From wikipedia > allele

  An allele is a variant form of a given gene

I somewhat disagree with this definition in the sense that it is not general enough. An allele is a variant at any locus (locus = position in the genome). You can talk about allele at non-coding sequences. Also, if you are talking about a coding sequence, you can define different sequences as belonging to different alleles whether or not their protein products differ in function or not. The proteins might even be the exact same one for two different alleles if the only difference between these alleles concerns a synonymous mutation (or a mutation in an intron).

You can feel free to define that different sequences as being different alleles by any kind of arbitrary threshold measure. You will just need to define it. For example, you can define that different sequences are different alleles only if they have at least 5% pairwise differences or if you found out by some biophysics computation that they ought to fold differently or for whatever another arbitrary measure.

The term allele is used very often in evolutionary biology and you'll find its usage in any intro course to evolutionary biology.

Rapidly evolving genes

As far as I know, there are no commonly agreed upon definition for what a rapidly evolving gene is. To me, a rapidly evolving gene is simply a coding sequence which evolved more rapidly than other reference sequences. Per se, although it would very likely involve positive selection, I don't think it is a requisite by the definition of rapidly evolving genes. It could, for example, be caused by a very high mutation rate at this particular sequence or by balancing selection causing any new rare alleles to be beneficial.


Can qPCR primer with several mismatch works? I am designing primers for qPCR from conserved regions of a few different fish species.This is because gene sequence for my fish species are yet unavailable in NCBI database.

Is it OK (can the primer anneal to the target sequence) if the primers have several mismatch at the interior and towards it 5’ end? At the 3’ end, I can only design primer with maximum 5 conserved bases.

Thank you.

QPCR is extremely sensitive, so I would not do this. Instead I would get those primers you mention in your question and instead sequence using them instead of doing qpcr with them. Then I would make new primers specific for the region you want to do qpcr on based on the sequence.The advantage of this is that you would now know the sequence and so you would have better primers for qpcr.


Why are aminoglycoside antibiotics particularly effective for aerobic gram negative bacteria? Aminoglycosides are short chains of sugar molecules with some -OH groups substituted with amine groups. As far as I understand they function by causing bacterial ribosomes to misread RNA and create non-functioning proteins. These proteins both stop providing essential functions of the cell and increase permeability of the cell to aminoglycosides, eventually leading to the death of the cell. What I don't understand is why this mechanism is specific to aerobic, gram-negative bacteria. Surely membrane permeability would be roughly the same for both classes? And also ribosome structure? Any help would be much appreciated.

Anaerobiosis is incompatible  with effective intracellular accumulation of aminoglycoside antibiotics such as streptomycin and gentamycin.

After an initial binding step involving outer membrane lipopolysaccharide the kinetics of the uptake of aminoglycosides exhibit two energy-dependent processes (EDP I AND II). EDP I  is the slow, rate-limiting stage and is dependent upon the membrane potential ΔΨ, but the details of the process are unclear. EDP II is more rapid and may be triggered by membrane changes arising as a result of translation errors caused by the antibiotic accumulated in EDP I since protein synthesis inhibitors block the transition from EDP I to EDP II.

EDP I requires  a threshold value of ΔΨ, and there is evidence that this threshold often cannot be achieved under anaerobic conditions.

This summary is based on information in this review from 1987.  I haven't been able to find any more recent information.


Recessive is Dominant to Dominant? If a gene has for instance three alleles, p, q, and r, then could p be dominant to q, q be dominant to r, but r be dominant to p? Can a gene that is recessive to one allele not be dominant to another allele that is dominant to the second? If it can, what are some examples of traits that do this?

Dominance by silencing the other allele

The mechanisms by which dominance work are still very much unknown. One type of mechanism that will be of particular interest to this question is the modifier of dominance where the protein product of an allele silence the expression of the other allele in order to cause dominance relationship.

Is the pattern you describe possible?

In such system, I can imagine a case where allele A1 would silence A2 which would silence A3 which would silence A1. I can't think of any reason such a pattern should not exist. However, I am not aware of evidence of such pattern.

The interesting case of SI in Arabidopsis thaliana

This type of dominance (dominance through silencing the other allele) has been reported in the self-incomtability locus of Arabidospsis theliana (Durand et al. 2014). At this specific locus there are 6 alleles but they have a very hierchical relationship where A1 silences all other alleles, A2 silences all alleles but A1, A3 silences all other alleles but A1 and A2 etc..

Related posts

Evolution of dominance of alleles
What determines if a gene is dominant or recessive?


What organelles are in an onion cell? I was wondering what organelles are in an onion cell, because, based on the labs we are doing in my biology class, I only saw a nucleus and cell wall. My friends and brother say there are all the organelles that you would find in a typical plant cell, but I can't find any evidence anywhere. I need to create a model and it's due in a week.

OK, so the first thing you always do when recreating a cell microscope slide (like drawing or modelling the cell) is that you only draw or model what you see. In your case, this would just be the nucleus, the cell membrane and the cell wall.

To answer your question, onion cells (you usually use epithelial cells for this experiment) are ‘normal’ cells with all of the ‘normal’ organelles: nucleus, cytoplasm, cell wall and membrane, mitochondria, ribosomes, rough and smooth endoplasmic reticulum, centrioles, Golgi body and vacuoles. You cannot see most of these as they appear translucent as well as being too small to see under the light microscope. You need an electron microscope to view these. Note: chloroplasts are not present in an onion cell as it is not a photosynthesising cell.

This is a typical onion cell slide with labels:


Can we say that microevolution and macroevolution is fundamentally the same thing over different time scales? This Wikipedia article states:

  Macroevolution is evolution on a scale of separated gene pools. Macroevolutionary studies focus on change that occurs at or above the level of species, in contrast with microevolution, which refers to smaller evolutionary changes (typically described as changes in allele frequencies) within a species or population. ... macro and microevolution describe fundamentally identical processes on different time scales.

My question is: Is this a valid claim? Can we say that creating the genetic information for a feather is not qualitatively different from changing the colour of that feather?

You are mixing up two different things in your question:

the mechanisms (processes) that cause micro- and macroevolution, and
the genetic basis for different types of traits.

The processes of evolution (selection & drift acting on genetic variation) are the same for both micro- and macroevolution, and this what the Wikipedia article is stating. The second question is dealing with the amount of cumulative genetic change that is needed for different types of traits. This naturally differs dramatically between traits (the accumulated genetic change that is), and is also reflected by the different scopes of micro- and macroevolution. Macroevolution is usually studying problems above the species level, and therefore often larger morphological changes, while microevolution is dealing with smaller changes within species and populations. The macro/micro division is also artificial and should be seen as a continuum.


What is the role of the tissue surrounding neurons in decision making and taking control of impulses? How does the fatty tissue surrounding neurons supports and enhances the speed of electrical impulses? How does it stabilize connections that take control of impulses and decision-making? The cells surrounding the neurons in this case being either glial cells (neuroglia) which provide support and protection for neurons in the central nervous system and peripheral nervous system, or myelin an insulating sheath around many of the nerve fibers consisting of proteins and phospholipids.

Short answer
This question is pretty broad as it basically translates to "what purpose serves neuroglia in neuronal communication"? In short: next to everything.

Background
In the adult brain there are three types of glia: oligodendrocytes, astrocytes, and microglial cells (Purves, 2001). A few notable examples of their functions:

Oligodendrocytes (peripherally called Schwann cells) generate myelin sheaths around neurons, which increases conduction speeds (saltatory nerve conduction) and increases the metabolic efficiency of neural communication.
Astrocytes are a highly heterogeneic group of supportive cells. To put the impact of glia in perspective: this class of cells is considered to contain as many cell types as there are types of neurons in the brain. They are thought to mediate transfer of nutrients from blood capillaries to neurons, and they also assist in removal of neurotransmitters from the synaptic cleft and thereby speed up the recovery from synaptic activity and hence they increase the speed of information transfer (Tsacopoulos & Magistretti, 1996).
Microglia are the brain's immune cells, and are similar to peripheral macrophages. They act as the major inflammatory cell type in the brain, and respond to pathogens and injury.

References
- Purves  et al (eds). Neuroscience, 2nd edition. Sunderland (MA): Sinauer Associates (2001)
- Tsacopoulos & Magistretti, J Neurosci (1996); 76(3): 877-85


What makes white phosphorus toxic? What makes white phosphorous toxic?

I mean it causes liver and kidney damage, and altered blood coagulation, but it is hard to find anything about what biochemical mechanism this poison uses to kill liver and kidney cells and why the liver is not capable to neutralize it even in a 50mg/kg dose (LD50 in rats). It would take just a simple oxidation to convert it to phosphate, which is commonly used by living cells.

conclusion:

I think the main cause that white phosphorous is so toxic that it is not something common in the environment, so there was no evolutional pressure to adapt to it. The human body can deal with it relative fast, but it damages cellular organelles and causes possibly fatal liver and kidney damage in hours. Some of the metabolites are even more toxic and they can cause arrhythmia and disturb the CNS. Because the molecular mechanism of toxicity is still mostly unknown and there is only a short time to treat people before liver and kidney damage, currently I think there is no way to save somebody exposured to a high dose of white phosphorus.

There seems to be some difference on the development of symptoms depending on the route of uptake, but eventually poisoning with white phosphorus leads to kidney and liver damage.

Oral uptake leads to gastro-intestinal problems like abdominal cramps, nausea and vomitting, if you take up low doses chronically, this may lead to phosphorus laden stool (also called "smoking stool syndrome").

Since white phosphorus will ignite when it comes in contact with air, skin contact often leads to severe chemical burns. White phosphorus is also highly soluble in lipids and is therefore suspected to cross through our skin rather fast, leading to absorption in the body and subsequent poisoning by liver and kidney damage.

See reference 1 for a short overview and reference 2 for extensive information.

Regarding the exact molecular mechanisms is surprisingly little known and published. It is clear that poisoning with white phosphorus causes Triglycerides to accumulate in the liver, causing the fatty liver syndrome. Depending on the source it is also speculated that carbohydrate and/or protein synthesis in the liver is also affected (see for example here or here). Mostly this is explained by the high reduction potential of the phosphorus, which disturbs the fine balanced metabolic pathways. Finally this seems to leads to liver failure (see also reference 3).

According to the toxicology profile (reference 2) the damaged protein synthesis in the liver leads to fatty liver very fast.

  Liver damage in animals exposed to white phosphorus progresses
  rapidly. Four hours after receiving a single oral dose of white
  phosphorus, minimal fatty changes in hepatocytes were observed; by 12
  hours fatty changes were extensive (Ghoshal et al. 1969). Exposure to
  white phosphorus has been shown to damage the rough endoplasmic
  reticulum and cause a disaggregation of polyribosomes (Ganote and Otis
  1969; Pam et al. 1972). This damage results in impairment of protein
  synthesis, in particular, a decrease in the synthesis of the
  apolipoprotein portion of very low density lipoproteins (VLDL), which
  are required for the transport of triglycerides. A significant
  decrease in protein synthesis has been detected as early as 3 hours
  after oral exposure (Barker et al. 1963). The smooth endoplasmic
  reticulum is also involved in the formation of the VLDLs, and damage
  to the smooth endoplasmic reticulum also impairs the formation of
  VLDLs. The net result of these ultrastructural changes is an
  accumulation of triglycerides in the liver (Ghoshal et al. 1969). This
  results in steatosis and fibrosis, which is one of the mechanisms
  involved in the hepatotoxicity of white phosphorus. The mechanism
  behind the damage to the endoplasmic reticulum is not known; also, it
  is not known whether white phosphorus itself or a metabolite of white
  phosphorus is the damaging agent. In addition to these damages, white
  phosphorus or a metabolite causes damage to the mitochondria and
  nuclei in the livers of animals orally exposed to white phosphorus
  (Ghoshal et al. 1969). The damage to the mitochondria may impair the
  cell’s ability to produce ATP, thus resulting in necrosis of the cell.

Another possible (and additional) toxic effect may be traced to the (possibly enzymatic) generation of phosphines from phosphorus and water which are highly toxic to the central nervous system (here my source is only german, you can find it here). According to reference 4 phosphines are interfering with the COS gasotransmitter signaling. They can cause cardiac problems by this mechanism. Phosphines smell garlic like, this is an observation often made, when victims of white phosphorus poisonings are authopsied.

References

White Phosphorus Exposure
TOXICOLOGICAL PROFILE FOR WHITE PHOSPHORUS
Biochemical changes associated with acute phosphorus poisoning (in
humans)
Sulfurous Gases As Biological Messengers and Toxins: Comparative Genetics of Their Metabolism in Model Organisms


Is this a termite wing or flying ant wing I saw this on the bottom corner of my pantry in the Washington DC area. I can't tell whether is termite wing or something else. The wing is 3/4" long.

This appears to be the wing of a crane fly (Tipulidae).  Using this figure you can begin narrowing down the possibilities for wing venation. Searching diptera wing venation, I think, brings up this excellent diagram (see bottom left for Tipulidae) which quite closely matches your photo if rotated in a graphics program (GIMP):

 Wing photo from OP paired with wing outline image copied and rotated from Batsdiet.com
You could likely drill this down further by searching Tipulidae venation or the like on Google Scholar, which pulls up many papers with detailed information on various regions and taxa of crane flies.


Mating types in fungi (and somatogamy) I would have some related questions about the mating types of fungi.

Does a single spore generate a mycelium possessing only one mating type? If it does not in general, do Ascomycota and Basidiomycota possess only one mating type per individual mycelium?
Are homothallism and heterothallism properties of the individual mycelium or of the species? The definitions that I find in my book and on line confuse me. I understand that homothallism is the property of a mycelium (possessing only one mating type or can it possess many mating types in a similar way to hermaphrodite animals? cfr. question 1) that can mate with itself (if it can possess many mating types and it can mate with itself only by using gametes of different mating types, is it still homothallic?) and heterothallism is the property of a mycelium that is not homothallic, but I am not sure I understand, because I read of homothallic and heterothallic species too: is a homothallic species a species where at least some individual is homothallic, where all individuals are homothallic or something else?
I am sure that mating type is a property characterising at least gametes, but is it a property of indiviual cells too? As an example, I know that it is necessary, among many species of fungi, for two gametes to belong to two different mating types in order to produce a zygote. Some fungi, as it is the rule among Basidiomycota, reproduce by somatogamy, i.e. the nuclei generating the zygote are from somatic cells, other than gametes. In such cases, are there species where it is necessary for the somatic cells of a homothallic mycelium to belong to a different type than the type with which they are undergoing plasmogamy? Thank you very much for any answer!

Background:
Most fungi can reproduce sexually and asexually, and some even parasexually. Fungal reproduction is complicated!
Idiomorphs  are at the exact same locus (like alleles) but produce a completely different protein rather than a variant of the protein.
Heterothalic - also called outbreeding: male and female reproductive structures are in different individuals. Partners have opposite mating-types with compatible MAT idiomorphs
Homothalic - also called inbreeding: male and female reproductive structures in the same individual. Partners have the same mating type but both MAT idiomorphs are present in the same genome and used in mating-type switching.
Heterothallic species are said to be homogenic incompatible, heterogenic incompatibility occurs when the offspring of a heterothallic cross between different strainss shows negative heterosis. There are forms of heterogenic incompatibility that appear to act only in the sexual phase.
Note that mating type and sex are not the same as sex is determined by mating structure and mating type may have no effect on sexual structure only on the nucleic content.
Answers:
1. I am not certain, but my understanding is that a haploid spore will generate a haploid mycelium of the same mating type. Note that things can get more complicated because you can have bifactorial incompatible mating types (e.g. two unlinked mating loci)
2.  Homothallism and heterothallism are properties of the of the species
3.  I am not entirely sure I understand the question here. In Basidiomycota (Club Fungi) Mycelia of + or - mating type will fuse to form a dikaryotic (two nuclei) mycelium for the majority of the life cycle. Only under unfavorable conditions will karyogamy (the fusing of the haploid nuclei) occur to form diploid hyphae and fruiting bodies where meiosis will take place to create haploid spores with mating types which will generate the new mycelia. Part of what makes the lifecycle here difficult is remembering that diploid somatic cells will have both mating types. (Life Cycle)


Is epimysium same as fascia? I have read that epimysium is dense regular connective tissue made covering the a muscle like bicep brachi. at the same time we have fascia that is made of dense regular tissue and covers muscles. so are they same or different how can we describe it and differentiate it?

Epimysium is the specialized fascia located at the muscle.

  Epimysium is a layer of connective tissue, which ensheaths the entire muscle. It is composed of dense irregular connective tissue. It is continuous with fascia and other connective tissue wrappings of muscle including the endomysium, and perimysium [1].

The fascia that covers muscle is named deep fascia:

  The deep fasciae envelop all bone (periosteum and endosteum); cartilage (perichondrium), and blood vessels (tunica externa) and become specialized in muscles (epimysium, perimysium, and endomysium) and nerves (epineurium, perineurium, and endoneurium) [2].

References:

Wikipedia contributors, "Epimysium," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Epimysium&oldid=540536396 (accessed June 27, 2014).
Wikipedia contributors, "Deep fascia," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Deep_fascia&oldid=593605746 (accessed June 27, 2014).


The meaning of RNA-seq data many papers I read mentioned "RNA-seq data". While searching for the meaning of this word, I could not find any layman's definition.

As far as I understand, RNA-seq data is the complete RNA information in a cell (or all of the cells) of a species that is extracted at a certain time.

Am I correct with this definition? If yes, does this mean that by extracting all the RNA information ones knows all the RNA sequences in that species (like AUGGUCAUCAG....)? Or does it mean I have the RNA, but not the sequence?

RNA-seq data usually provides a snapshot in time of the transcriptome of that which is being sequenced. Single-cell sequencing is possible, but less common than RNA-seq on a sample (containing many cells).

You are correct that RNA-seq provides one with knowledge of RNA sequences, like AUGGUCAUCAG and so on. However, one will not necessarily have information about all possible RNA sequences from a particular species. Performing RNA-seq on the same cell type of a species at two different time points, or two different cell types at the same time point, may result in different profiles for the RNA sequences you get back. It depends on which parts of the genome are being expressed by the cells in a sample at the time of RNA extraction.

The data one gets back from RNA sequencing depends on the technology and company used. Typically, RNA-seq involves using a reverse transcription step so that the sequence data you get back is actually reported as the cDNA version of your original mRNA transcripts. Usually one gets a (very large) file of sequencing 'reads'. One can either then 'assemble' these directly to form a snapshot of the transcriptome or one can map them to a known reference genome. One of the main benefits of RNA-seq is that we learn not just what the sequences of the RNA molecules are, but also their relative abundances within the sample. Knowledge of this can be particularly useful in testing or developing a large range of biological hypotheses.


What is the second phase of photosynthesis? I really want to know what the second phase of photosynthesis (in the dark) is. I have a fair understanding of the first cycle where molecular oxygen is generated under the influence of light, but I don't understand the second cycle which can take place in the dark. It would greatly help to have a graphic of the second phase of photosynthesis.

Note: it is not for my homework, but for my own understanding. My textbook doesn't explain things very well.

Here's an overview of both the Light and Dark cycles of photosynthesis, which looked particularly useful to me as it shows that the energy-carriers ATP and NADPH2 generated through solar energy are used in the dark cycle to generate sugars.

.

Here is another one that shows more details on the precursors involved in the Calvin cycle:

As commented by others, googling 'dark cycle' or its synonyms will give thousands of optional images to choose from if these don't suffice. The first one is taken from tutorvista.com the second one from users.rcn.com.


Ion-gated ion channels Today I've heard for the first time of calcium-gated ion channels but find it hard to get an idea how they work, where they are located, and which role they play.

I assume calcium-gated ion channels are just a special form of ion-gated ion channels, which would be a fourth group of ion channels next to voltage-, lipid-, and ligand-gated ion channels (with ligands being some larger molecules). But on ion-gated ion channels even less is to be found on the internet.

One specific paper that mentions ion-gated ion channels is this (Experimental Neurology, 2001)

One paper that mentions calcium-gated ion channels is this (New England Journal of Medicine, 2015)

Where do I find a general introduction into ion-gated ion channels - if they exist?

The main families of calcium-gated channels I am aware of are the calcium-gated potassium channels and the internal ryanodine receptors involved in calcium-induced calcium release - you could start from those linked Wikipedia articles.

I wouldn't really make these a fourth category, they should either be thought of as voltage-gated channels that are modulated by intracellular calcium, or as ligand-gated channels - the ligand just happens to be a calcium ion.

Some channels in this category are not influenced by calcium directly but via calmodulin, which is a common mediator of calcium-driven intracellular influences.


Circulating factors affecting human health/longevity Circulating factors present in young mice have been shown to promote rejuvenation of aged mice, suggesting that tissues have inherent capabilities to regenerate, and circulating factors may be promoting/inhibiting this [1].

Specifically; supplementation of GDF11 (growth and differentiation factor 11) can reverse some effects of ageing (muscle tissue rejuvenates, and some degree of cognitive improvements) [2]; conversely circulating CCL11 impairs neurogenesis in aged mice and causes cognitive impairment [3]. GDF11 decreases with age, CCL11 increases with age.

(Image from Bitto et al 2014, [1])

These factors (well, GDF11 at least) are not as highly expressed in humans as in mice [4], so the specific mechanisms may differ.

What other circulating factors been shown to affect health or longevity? Particularly in humans, but other mouse (or 'higher' organisms, e.g. primates) experiments would be interesting too.

Bitto, A., and Kaeberlein, M., “Rejuvenation: it’s in our blood.,” Cell Metab., vol. 20, no. 1, pp. 2–4, Jul. 2014.
Sinha, M., et al, “Restoring systemic GDF11 levels reverses age-related dysfunction in mouse skeletal muscle.,” Science, vol. 344, no. 6184, pp. 649–52, May 2014.
Villeda, S., et al, “The ageing systemic milieu negatively regulates neurogenesis and cognitive function.,” Nature, vol. 477, no. 7362, pp. 90–4, Sep. 2011.
Souza, T., et al, “Proteomic identification and functional validation of activins and bone morphogenetic protein 11 as candidate novel muscle mass regulators.,” Mol. Endocrinol., vol. 22, no. 12, pp. 2689–702, Dec. 2008.

Oxytocin

It has been shown that oxytocin signaling helps in muscle regeneration by activating MAP Kinase/ERK pathway in skeletal muscles.[1]

Oxytocin is also known to promote adult neurogenesis.[2]

Myostatin

It is a paralog of GDF and like GDF prevents hypertrophy of cardiac muscles.[3]

Leptin

Though leptin is not really connected to ageing but it regulates appetite and thereby the metabolism [4]. It may contribute indirectly to ageing by reducing food intake and preventing obesity and other metabolic syndromes.

This review summarizes different soluble small (synthetic) molecules that have potential to induce regeneration.


Is there an 'anti-virus'? A virus spreads around and usually attaches itself to the host, multiplies & causes diseases. But is there something like an anti-virus? A single celled entity that does the opposite: spreads around 'kills' other viruses and/or cures diseases. Has anybody discovered something like it or is there any research group working on synthesizing one? If so any links to their publications?
Forgive me if I got my facts wrong, I am physical sciences person and know nothing about biology. :)

There is a "anti-virus," although many call it a virophage.In 2008, a paper in Nature was published about the observations of a new strain of a virus known as Acanthamoeba polyphaga mimivirus. This virus mainly attacks amoeba. It was discovered in 1992. It was one of the biggest viruses ever found.Later, a related virus called the mamavirus was discovered. But, after observing this specimen under an electron microscope, scientist found tiny viral particles attacking the mamavirus. It was called Sputnik. The Sputnik virus hijacks the mamvirus's machinery and depends on the mamavirus to survive. It made scientists wonder if the mamavirus is a living thing.
Here is a picture of it attacking the mamavirus:

You can see small subviral particles attacking the bigger virus. That is Sputnik.
Note that it is a virus that coinfects other organisms but needs a virus infecting an organism to survive. According to Wikipedia:

Sputnik virophage is a subviral agent that reproduces in amoeba cells that are already infected by a certain helper virus; Sputnik uses the helper virus's machinery for reproduction and inhibits replication of the helper virus.

It seems that there are more species of virophages, including one that infects the marine phagotropic flagellate Cafeteria roenbergensis in the presence of a second virus — Cafeteria roenbergensis virus and another one known as the Organic Lake virophage but not much detail is known about this virus.
Here is the link to the Nature article on the Sputnik virophage, published in 2008:
http://www.nature.com/nature/journal/v455/n7209/full/nature07218.html
It may be possible to synthesize one in the future. However using this to kill viruses would not make sense because the virophage technically still attacks the host of the virus it is hijacking, plus, from what I understand, it only uses the virus's machinery.
Hopefully this was helpful. If you have questions, you can comment on this answer...


Identify this excreta! A picture is worth a thousand words!

It's about 1.3cm (1/2") long. We rented a basement and I found this on a machine that was moved in a bit earlier.

I would like to know if there are any mice, rats, etc that could have come in.

We are on the island of Malta, in the Mediterranean sea.
The basement is below a shop that used to sell AC units and the basement was used as a storage. The walls have gaping holes where cables and pipes go in and out, etc. Clearly industrial and not made for the customer to see.

Bat is the other basement creature that comes to mind. It looks like a match as explained in this and several other videos - https://www.youtube.com/watch?v=897Fb9ndids


Does the Urea Cycle exist in invertebrates? Do invertebrates (like Drosophila and C.elegans) have a urea cycle?

Perhaps worth adding that the role of the urea cycle in terrestrial vertebrates is the disposal of excess N derived from protein metabolism. Such animals are ureotelic. Arthropods, in contrast, are uricotelic, using uric acid for N disposal, so it would make no sense for them to have a functional urea cycle. (Nematodes - I don't know.)

The importance of avoiding having a urea cycle when it is not needed is illustrated by the situation in yeast (Saccharomyces cerevisiae). In yeast some of the enzymes that would be part of the urea cycle are used in degrading arginine, while others are used in the biosynthesis of arginine. Yeast cells will carry out one or the other of these processes depending upon their metabolic status. If both processes were to be active at the same time this would result in a urea cycle that would waste ATP. This is avoided by having a multienzyme complex consisting of arginase and ornithine transcarbamoylase (in the degradative and biosynthetic pathways respectively), allowing reciprocal regulation so that only one of these is active at any time.


Which algorithm to find the evolutionary relation of 5 sequences? After Multiple Sequence Alignment (MSA), data sets are produced on which models of evolution are used. I've seen in books that if there is strong similarity between the sequences then Maximum Parsimony (MP) is used, if that is low then Minimum evolution, and if there is very weak similarity then Distance based Method is used. However, all of these have their own cons.
Since character based methods are more reliable (as book), Can these methods be used even when there is low sequence similarity?
Are there any algorithm that builds the precise tree model without considering similarity of the sequences?

If you work with protein coding sequence and on the DNA level their to divergent, then it is better to use the amino acid sequence for alignment and phylogenetic reconstruction.

Better sampling can also help you, for this you can check the online databases with BLAST to find similar sequences that would fill the gap.

The problem with sequences with low sequence similarity is that it is difficult to identify homologous positions/characters and all alignment based methods rely on the assumption that the aligned positions are homologous.

Finally, there are alignment-free algorithms as well. (https://en.wikipedia.org/wiki/Alignment-free_sequence_analysis)

In general about algorithms for phylogenetics:

Nowadays, journals usually require you to run maximum likelihood (ML) analysis or Bayesian analysis. Both of these methods are referred to as model based. The most common programs used for these are RAxML (ML) and MrBayes (Bayesian). Another common software is MEGA (Molecular Evolutionary Genetics Analysis), which can run different tree building algorithms.

Usually, for quick reference maximum parsimony or neighbour-joining trees are good. For publication a maximum likelihood tree is very useful, since it returns a single best tree. While Bayesian analysis and maximum parsimony return a collection of trees.

It is also helpful different algorithms and if all return similar trees than you can be more sure about the relationships.


Is there a human form of estrus? Now I just learn that estrus is a trait in all mammals except Humans. So does it occur significantly in Humans? Of course I'm aware of the cliched "horny", "aroused" etc., but is it a biological function in Humans too? and if so, when and what is it called?

By 'human estrus', I take it to mean that the female shows some increased desire when they are fertile.

At the height of fertility, which coincides with estrus, female behavior changes a stronger interest in sexual activity is exhibited.  In many primates in general, the female may give of a strong scent or even physically show color or swelling that indicates even to observers of other species that they are fertile, also engendering sexual behavior in the males.

For instance, baboons are well known for reddening of the female's rump and they also emit a strong scent.  Non - primates also show estrus - most of us know how dogs and cats can change their behavior.

Human signs of Estrus is of great interest to primatologists, evolutionary biologists and psychologists as it influences the biology and the social nature of people.  It has been proposed that humans do not exhibit estrus and this is still an influential idea. Certainly its difficult to look at a woman and tell whether she is ovulating and most women themselves cannot tell when that is happening.

Still, examination of behavior and appearance have shown that womens appearance does change over their monthly fertility cycle.  Women's faces may become thinner at higher fertility and this and other cues make them more desirable on the average.  While their sexual desire is not clearly higher, female perception of men's faces changes too.

While this is quite different than the typical definition of estrus, the biochemical cycle of fertility does affect human social behavior and preferences, perceptions.  The evolutionary reasons for these changes are probably adapted to the highly social nature of human existence and the fact that offspring are such a large investment.


What is the best way to calculate the biological diversity of samples from bacterial/viral OTU tables? I have a few large OTU tables of bacterial and viral datasets. The samples are across different sites and times.

I would like to visualise the community 'diversity' across the times for which I have data. For example it would be interesting to see if community diversity peaks in the summer months and falls in the winter months- in a repeating pattern.

I have not come across much advice or literature which looks at looking at diversity for large OTU datasets. Considering the OTUs are essentially arbitrary and that there are thousands of them, what is the best way to calculate and visualise the each samples diversity?

With the vegan package on R it is quite easy to calculate the Shannon/Simpsons diversity index for an OTU table. Can you simply use this on a 'raw' table of OTUs?

I mostly concur with @Nathan's answer, and in particular with the references he provided.

As Shannon & Simpson indices can be hard to interpret and can be non-intuitive, I prefer using Hill diversities as suggested by Nathan (the Jost 2006 and 2007 refs are great to read up on this). The main argument is that Hill diversities give effective number of species that are comparable between samples and follow the duplication principle.

Hill diversities rely on a unified formula (see this wikipedia article) with one parameter, q. Increasing values for q correspond to increasing weighting of taxa abundances in the diversity calculation:

D with q=0 does not account for taxon abundance, so is just the number of taxa, or richness
D with q=1 is not defined, but asymptotically approximated by e^H where H is the Shannon entropy. D_q1 is the effective number of species with abundance weights.
D with q=2 corresponds to the Inverse Simpson index (1/D_Simpson). D_q2 weighs more abundant taxa even more strongly.

One can choose any value for q (with q=1 with the limit e^H), and comparing diversity estimates for varying q can give you an idea of sample evenness. Setting q=∞ gives the Berger-Parker index (the fraction of individuals in the sample belonging to the most abundant species).

Importantly, for alpha div analyses on (16S/18S-based) OTUs, I would always generate rarefaction curves first, and then generate diversity estimates at a common, rarefied number of reads per sample.

You can do most of this using the R package vegan. The phyloseq package provides various alpha div estimates in one command, but no Hill diversities. I've written a few simple functions to perform rarefaction and calculate (rarefied or non-rarefied) Hill diversities from an OTU count table matrix:

function.rarefaction.R

function.alpha_diversity.R


Can someone identify this bird? It looks like it has a few deformities All pictures taken at Lake Roberta in Tampa, FL.
All pictures depict the same bird.
(The wing deformities can be explained by the lake water being slightly highly toxic, but the neck I can only assume to be caused by the Muscovy ducks that live in the lake.)

It's an anhinga, as@kmm commented. There's nothing wrong with it; it's not deformed in any visible (to me) way. They spread their wings to dry, as they are darting birds that do not float on the surface of the water, but beneath it.

Here's one drying itself on a turtle.


Tissue identification in vascular bundle sections I always have trouble differentiating the tissues in a vascular bundle. I specially cannot properly identify the vascular cambium and phloem. I know xylem vessel elements are large cells with thicker cell walls, that makes them clearly different from other cells in the vascular bundle. However, the difference between vascular cambium cells and phloem cells is unclear. I would like to know how I can identify these tissues accurately. A photomicrograph with marked borders would be appreciated along with explanation of cell appearance in these tissues. Thank you a lot.

Here is a single Helianthus (sunflower) vascular bundle, complements "The" Ohio State University. The xylem in a vascular bundle is generally the easiest to discern. The phloem tissues is always exterior to the xylem and the cells are generally more uniform and smaller than most of the xylem. Picking out the phloem is also more complicated by other cell types exterior to the xylem such as the "fibers" shown here. The phloem will always be interior to the sclerenchyma or collenchyma "fibers" when they are present. That is, the phloem is always adjoining, and exterior to, the cambium.
The most difficult to precisly locate is the vascular cambium since it is very thin. Notice in the diagram below, the relatively continuous line that is being pointed to by the dashed line from the label. As you go inward toward xylem and outward toward phloem, the smoothness of trying to trace a line parallel to the vascular cambium becomes much more "bumpy" as the cells are already beginning to differentiate.

To find many more images on the web, search "vascular bundle labeled photo". You should investigate further, appearance of these bundles varies between dicots, monocots, roots, shoots and species.


Better population models than the logistic equation For modelling the population of a single species in a region, the logistic equation is used

$$ \frac{dN}{dt} =kN\Big(1-\frac{N}{K}\Big) $$

where $N$ is the number of organisms, $K$ is the carrying capacity, and $k$ is a constant.

However, for most real primary consumers, in the absence of predation, the population usually deviates from the standard sigmoidal curve in two ways

The population typically overshoots the carrying capacity before decaying again to the carrying capacity
The population usually oscillates around the carrying capacity, rather then remaining constant

Are there any better mathematical models for describing growth mediated by density dependent factors of primary consumers in the absence of predation?

It is not complicated to make your own model of population growth

You can make a model with any kind of function, it is not super hard. It just happen that logistic growth offer quite a good match to observations. You can have exponential growth, linear growth, quadratic growth, ...

However, there are more possible behaviours behind those models than what you think!

The behaviour that you describe is totally possible with a discrete time logistic model. In short, consider the recursion equation $n_{t+1} = f(n_t)$. Consider also $\hat n$ as being an equilibrium of your system (typically n=0 or n=k, where k is the carrying capacity). In other words, $\hat n$ satisfies the equation $\hat n = f(\hat n)$. And finally consider the statistics $\lambda$ which is equal to the derivative of $f(n)$ over $n$ evaluated at the equilibrium $\hat n$. If $\lambda < 0$, then you have oscillatory behaviour (and therefore overshoot) at the vicinity of the equilibrium $\hat n$. Using the correct parameters, the logistics equation gives you a lambda smaller than 0 (typically between $-1 > \lambda > 0$), and therefore you can have the oscillatory behaviour you describe.

If you have any trouble to make these basic analyses of those models, I strongly recommend that book.


Book request: biology of sensation and perception I’m interested in learning about the biological and chemical basis of human sensation and perception (on both a microscopic and macroscopic level). This includes

The mechanisms underlying our “five senses,” i.e. the eye, inner ear, tongue, nose, and nervous system, and how (chemically/physically) they are triggered
How our brain makes inferences from the raw sensory data we receive, e.g. using our depth perception to infer distance from a two-dimensional projection onto each of our eyes
Comparison with other species of animals
Experimental results relating to the three points above
An evolutionary perspective hypothesizing about why these sense-detecting organs were important for human survival

There is plenty of information about these ideas scattered throughout Wikipedia, but I was wondering if anyone knows of a single book (or perhaps another online resource) that covers most/all of the points above in an accessible and interesting way.

Any suggestions?

This is a very broad range of topics. I doubt you'll be able to find a single reference on all of it. I'm providing below some references with a focus on more introductory approaches.

  The mechanisms underlying our “five senses,” i.e. the eye, inner ear, tongue, nose, and nervous system, and how (chemically/physically) they are triggered

Bear, Connors & Paradiso "Neuroscience: Exploring the Brain" is pretty extensive. It covers chemical senses, vision, audition, the vestibular system and touch. It is not cheap, but that's the only reference that will cover most of the topics you are interested in. However it focuses mostly on the physiology of the senses, and not really about perception

Otherwise I'm afraid you'll immediately have to read specialized books such as Palmer's "Vision Science", Moore's "introduction to the psychology of hearing", Goldberg et al. "The vestibular system". Those are fairly readable introductory books. I don't know much about chemical senses.

  How our brain makes inferences from the raw sensory data we receive, e.g. using our depth perception to infer distance from a two-dimensional projection onto each of our eyes

For the topic of inference specifically a classical reference is Richard Gregory's "Eye and Brain: The Psychology of Seeing". It is dated (60s) but still very relevant. This is somewhat contradictory with your first point because inference is a behavior while you asked for more physiological references. Stereopsis specifically is a classical field of vision science so any descent book will cover it.

  Comparison with other species of animals

I cannot recommend enough Sarah Shettleworth's "Cognition, evolution, and behavior". Though focusing only on behavior, it is a very extensive and interesting book.

  Experimental results relating to the three points above

Any good book would include data and plots from classical experiments.

  An evolutionary perspective hypothesizing about why these sense-detecting organs were important for human survival

Again, Shettelworth's book.


Biological Pathway of Lipid Hypothesis I've read a lot on both sides of the debate of low carb vs low fat diets trying to make some sense of what is being proposed. The lipid hypothesis runs roughly along the lines that we have lots of observational epidemiological evidence that eating a high fat diet correlates heart disease/obesity/enter disease of choice.

An alternative hypothesis is that high carbohydrate diets cause these things. Since the studies haven't been done, there is not the correlation to point to. This hypothesis is believable (to some people) due to the well-understood biological pathway: Carbohydrates turn to glucose, which causes an insulin release, and insulin regulates fat storage, so high carbohydrate diets lead to weight gain (see a biochemsitry textbook for a more detailed explanation).

My question is: Does the lipid hypothesis have any biological pathway for which there could be proposed a causal relation rather than just a correlation? Of all the speakers/writers on this topic, the low carb advocates always clearly describe the causal relation, whereas the low fat advocates never say why eating fat should cause weight gain.

Note: I'm not interested in discussing the merits of the studies, but rather the proposed causal mechanism.

I think you're confounding two separate things.

The Lipid Hypothesis is about the creation of atherosclerosis (only atherosclerosis) and was proposed as an explanation for why plaques of cholesterol, fatty acids, and somatic cells form in arteries. It does not try to explain adipocyte behavior, which would result in weight gain.

For the Lipid Hypothesis, after the glycerol has been removed from fatty acids, they are free to diffuse into the blood and can start plaques.

Weight Gain/Loss due to adipocyte behavior is significantly more complicated. One of the weight-related regulatory hormones present in adipose tissue is Leptin: http://en.wikipedia.org/wiki/Leptin

And a more scholarly article from 1995 discussing Leptin:

http://www.nature.com/nature/journal/v395/n6704/abs/395763a0.html

Leptin helps inhibit appetite, along with Ghrelin and a host of other molecules that control hunger and keep track of nutrient levels. However, as the wiki article states, Leptin and Insulin based activities are the primary functions of adipocytes, so a high-fat diet would conceivably deal with either or both of those molecules.

One of the quirks of Leptin is that fad dieting or starvation techniques have a very undesirable affect on Leptin levels (for years after a starvation diet, sometimes) that cause adipocytes to accumulate lipids that they normally would not have.

Obesity can also cause Leptin resistance (which might be aggravated by Fructose intake: http://www.ncbi.nlm.nih.gov/pubmed/11723062 ), much the same way that a diet rich in simple sugars can cause Type II Diabetes: http://www.ncbi.nlm.nih.gov/pubmed/8532024  The Leptin levels are at the expected concentrations in obese individuals, but the proper neuro-receptor activity isn't taking place.

Come to think of it, this may be what you're after. High fat diets will result in more Leptin and thus quicker/more Leptin resistance. Once Leptin resistance occurs, the mechanisms for controlling hunger are no longer as effective as they once were, resulting in more food intake and more weight gain.

However, the actual satiatory signal of Leptin is still debated. Some researchers have proposed that it's more of a "starvation" signal than a "satiation" signal, and thus Leptin resistance might be a normal condition when energy-dense foods are widely available: http://www.ncbi.nlm.nih.gov/pubmed/19644451


What is Mendelian Segregation and how is it related to the Hardy-Weinberg equilibrium? I can't find the exact definition of Mendelian segregation. In addition, I am wondering how it is related to the Hardy-Weinberg equilibrium?

Mendelian segregation is defined on the Nature site, and I quote:

The Principle of Segregation describes how pairs of gene variants are separated into reproductive cells. The segregation of gene variants, called alleles, and their corresponding traits was first observed by Gregor Mendel in 1865. Mendel was studying genetics by performing mating crosses in pea plants. He crossed two heterozygous pea plants, which means that each plant had two different alleles at a particular genetic position He discovered that the traits in the offspring of his crosses did not always match the traits in the parental plants. This meant that the pair of alleles encoding the traits in each parental plant had separated or segregated from one another during the formation of the reproductive cells. [...] We now know that the segregation of genes occurs during meiosis in eukaryotes, which is a process that produces reproductive cells called gametes.

Likewise, the Hardy-Weinberg equilibrium is explained on Nature's website:

The Hardy-Weinberg equilibrium is a principle stating that the genetic variation in a population will remain constant from one generation to the next in the absence of disturbing factors.

So in case of Mendell's experiments, his pea plants showed no disturbance and quite perfect ratios, for example 3:1 green:yellow seed pods:

The Nature site continues on the Hardy-Weinberg principle:

When mating is random in a large population with no disruptive circumstances, the law predicts that both genotype and allele frequencies will remain constant because they are in equilibrium.
The Hardy-Weinberg equilibrium can be disturbed by a number of forces, including mutations, natural selection, nonrandom mating, genetic drift, and gene flow. [...]. This occurs because certain alleles help or harm the reproductive success of the organisms that carry them. [...]. Because [...] of these disruptive forces [...] the Hardy-Weinberg equilibrium rarely applies in reality. Therefore, the Hardy-Weinberg equilibrium describes an idealized state [...].

So to get back to your question on the relation between Mendelian segregation and the Hardy-Weinberg equilibrium: The Hardy-Weinberg equilibrium is necessary for the Mendelian segregation to become phenotypically apparent. So in Mendell's controlled experiments the 3:1 green:yellow pods became nicely apparent as both phenotypes had equal chance of survival.
And to continue the seed pod example, if there were to be introduced a disturbing factor, such as a pest that wrecks havoc in plants with yellow pods, but not in green, the Hardy-Weinberg equilibrium (i.e., Mendell's 3:1 green:yellow) would be disturbed and Mendelian segregation would become less apparent as aberrant phenotpyic ratios would emerge (>3 : <1).


Does pouring water on your skin affect the evaporation process and heat loss? Recently I've been playing football in the sun pretty hot temperatures. During the water breaks I tend to pour a lot of water over my head to cool me down, now this has an instant effect on cooling me down but in the long run would this have any affect on my body temperature? We know that the body cools itself by using heat to evaporate sweat on skin, would drenching  my head and face in cool water affect this process or not?

Drenching your head and face with cool water will both directly cool your skin (because cool water is colder than you) and contribute to evaporative cooling. Your skin doesn't care if the water that evaporates comes from sweat you made, the pool, a water bottle or a hose.

The Khan Academy video is a good review of the principle.


What is meant by electron transfer potential? I was reading a text and came across the term. What does it mean? The sentence said 'The driving force of oxidative phosphorylation is the electron transfer potential of NADH or FADH2 relative to that of O2. '

the electron transfer potential is based on the difference in the affinity of elements/molecules to bind electrons. the affinity of the element derives from it's components as shown in the elements table, just like all other characteristics. for example, oxygen has higher affinity to bind new electron than carbon. the affinity of the molecule derives from the atoms that build it, their electric potential and the connections between those atoms.

this potential between the two elements/molecules (lets say: NADH, O2, iron–sulfur clusters) holds energy that can start a reaction which will never start otherwise.

I have tried to keep it simple. for more reading about oxidation-reduction ( reactions involve the transfer of electrons between chemical species) read TERMODINAMICS AND CHEMICAL KINETICS p.255 as suggested by @Roland.