What is the difference between a species tree, a gene tree and a phylogenetic tree? I have found websites and text books disagreeing over this. For example,

  Phylogenies are also known as “species trees”...

http://biologos.org/blogs/dennis-venema-letters-to-the-duchess/evolution-basics-species-trees-gene-trees-and-incomplete-lineage-sorting/

and

  It is well known that a phylogenetic tree (gene tree) constructed from DNA sequences for a genetic locus does not necessarily agree with the tree that represents the actual evolutionary pathway of the species involved (species tree)...

http://mbe.oxfordjournals.org/content/5/5/568.abstract

Although the second source, being from a journal, would seem to be more reliable, my original thought was that phylogenetic trees do show the evolutionary relationships between species and thus are species trees as opposed to gene trees.

Any clarification on the issue would be much appreciated.

Phylogenetic tree

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

gene tree vs species tree

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

Why would a gene tree not match a species tree?

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

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

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

What is a species tree exactly?

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


What is Peter's rule in neuroscience? I have heard and read about Peter's rule informally in the past, but never saw a formal definition or description.

Informally I have learned to understand Peter's rule as the assumed correlation between the amount of overlap between axons and dendrites and the post synaptic density in the synapse. Here is a sample of the search results in Google.

Is my interpretation correct? Is there a more rigorous, perhaps quantitative,  definition of Peter's rule?

I think that your interpretation is correct, although Principles of Neural Science (Kandel et al.) doesn't mention Peter's rule (which is where I would have hoped to find a simple explanation).

According to Binzegger et al. (2004), the idea behind Peter's rule dates back to Peters and Feldman (1976) and Peters and Payne (1993), though the Rule per se may have been coined by Braitenberg and Schultz (1991; at which point it was still called Peters' rule). Binzegger et al. describe it as:

  They assumed that axons simply connect in direct proportion to the
  occurrence of all synaptic targets in the neuropil. The rule can be
  extended to provide more precise estimates by taking into account the
  detailed morphometrics of the dendritic and axonal trees of the
  different neuronal types.

To paraphrase Binzegger et al., in the simplest form of Peter's rule, the number of synapses in a cortical layer are evenly distributed across the potential target neurons. So there would be a direct proportionality between synapses and targets.

The second sentence of the quote above is the meat of the Binzegger paper. They also present a mathematical model of a more complex and realistic variation of Peter's rule which takes into account different types of postsynaptic neurons and the fact that not all cells receive synapses.

Braitenberg V, Schüz A (1991) Peters' Rule and White's Exceptions. In: Anatomy of the Cortex, pp 109–112. Berlin: Springer.

Peters A, Feldman ML (1976) The projection of the lateral geniculate nucleus to area 17 of the rat cerebral cortex. I. General description. J Neurocytol 5:63–84.

Peters A, Payne BR (1993) Numerical relationships between geniculocortical afferents and pyramidal cell modules in cat primary visual cortex. Cereb Cortex 3:69–78.


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

First of all, as you mentioned, there are a lot of membrane / transport proteins with very nice, well defined tunnels. But you're looking for a soluble / cytosolic enzyme.

Some oxygen-dependent enzymes have quite long tunnels that oxygen is using. For example this one: http://www.jbc.org/content/283/36/24738.short or this one: http://europepmc.org/articles/PMC2698890

Then there are some enzyme with just deep active sites, I think the p450 BM3 is quite known for that, but any enzyme with a reasonable specificity (and especially those that have very reactive cofactors) will have a "tunnel".

You can also find long "tunnels" in enzymes that accept long substrates. I like this example of squalene synthase: http://science.sciencemag.org/content/277/5333/1811.full. The substrate first has to go deep into the enzyme to find the proton it needs to start a quite interesting reaction.

If you want to find new tunnels in your enzyme there are also tools available, such as CAVER: http://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1002708 If you look at the papers citing this tool you might also find some cavities.


Gene frequency — database/site Is there any free database when one can check the gene frequency in a healthy population? For example I would like to check it for genes like BIN1, CLU or CR1. On the English Wikipedia I found a gene frequency for APOE gene (for example: 79% for e4 and 7% for e2), and it was linked to the specific publication. I wonder if one need to look for specific publication when looking for information like that or there is any database with such information available?

You can find some, but not all, gene frequencies in a range of populations at The Allele Frequency Net Database - Allele, haplotype and genotype frequencies in Worldwide Populations.

However, your question is broad genes have a lot of variation within them, the most basic being Single Nucleotide Polymorphisms (SNPs) and you've already been pointed to one source of information (SNPedia which is new to me) but you can look at the variation of allele frequency of SNPs in different populations by looking at dbSNP1.  Note they have a subset for variation associated with clinical phenotypes.

1 This may be the source on which at least some of SNPedia is based as dbSNP has been around for a very long time.


Autophagy in eukaryotic cells What is autophagy? How and under which circumstances is it used by the cell? I believe The reason for autophagy is some kind of recycling, am I right? But why does it occur in infections?

Autophagy is a cellular process that is occurring all the time, but it can be elevated during times of need (see below).

In autophagy, cargo (can be anything - mostly macromolecules but also bacteria/viruses etc) is taken up by a lipid membrane which folds on itself to form an autophagosome, which is like a vesicle but have markers on it that makes it specialized in carrying out autophagy. These autophagosomes are then transported to, and merge with, lysosomes, releasing the cargo into the lysosome to be degraded. The broken down materials are then released back into the cytosol, where other processes can make use of them. That is the "some kind of recycling" you are referring to.

There are two types of autophagy - selective and general. In selective autophagy, receptors on the membrane of the autophagosome specifically selects for ligands (e.g. p62, ndp52 selects for ubiquinylated substrates, which usually marks molecules for degradation). In general autophagy, the uptake into the autophagosome is random.

So, you can think of general autophagy as maintaining a basic level of turnover - to ensure everything in the cell is not worn out; and selective autophagy as a response to specific ligands that needs to be degraded.

By this logic, autophagy activity increases during infection because those infectious agents, once gaining entry into the cell (either through phagocytosis or by forced entry), will need the autophagy machinery to transport it to the lysosome to be degraded. Interestingly, some bacteria actualy hi-jacks this process to ensure its survival in the cell. Here's a good review to get you started if you are interested.

Note that the proteasome also recycles macromolecules, although the things it can recycle is limited by size.


What are the reasons that soap has so different smell and flavour? Everybody has tried to taste soap in their childhood. One would think that if soap has a tasty smell it would have tasty flavor too. But we know it is not true (in the common cases). But why is there is difference in the senses to our noses and tongues for the same soap?

It is possible for a substance to not smell very much, but to taste very strongly - chili peppers are a great example. They (in my experience) have a rather weak spicy odor, but the taste is much much more intense. In the case of soaps, very small amounts of essential oils are used to give soaps their odors. You may be able to slightly taste them were you to eat some of the soap (definitely NOT recommended!), but the major taste you'd experience is the actual soap - the saponified surfactants that do the cleaning.


Rules of motif forming I want to understand how a motif is present or not, can be deduced from a PDB file. Are there any rule of thumb for forming 3D motifs? Like a series of helices and sheets in some direction will lead to a particular 3D motif? Are there any such rules? If so, any resources that you can provide me with?

For example, beta-hairpin. What should be the sequence of amino acids or helix/sheet that would result in the formation of beta-hairpin motif?

A motif is a pattern that you discover in a structure by analysis. For example, common sequence motifs are short sequence fragments with parts similar to a regular expression. So, if you have a motif like "A*C" this matches to the sequences "AAC" and "ACC" but not to "ACA". You can reverse the process to discover the motif from the sequences.

Similarly with structural motifs in proteins. A beta-hairpin is :

  The motif consists of two strands that are adjacent in primary
  structure, oriented in an antiparallel direction ... and linked by a
  short loop of two to five amino acids.

So first you have to determine where the strands and loops are, then how the strands are connected into sheets, and finally recognise the hairpins. It is the definition of the motif itself that determines how you discover it.

Some resources that might be helpful are:

Motivated proteins (Small h-bonded motifs)
The protein topology graph library (Larger motifs)
The protein geometry database (Not really motifs, but interesting)
PDBeMotif (define and search for motifs in the PDB)


Why are enzyme-catalysed reactions slower at lower substrate concentration? Suppose I'm using 200 nmoles of enzyme and 2 mmoles of substrate. The enzyme should be saturated but if I use 50 mmoles of substrate, the reaction will be faster. Why?
I just can't get it! Even at lower concentration of substrate the enzyme is saturated (all enzyme molecules are engaged in the reaction) but still the reaction rate is lower.

Alan Boyd's answer covers the mechanistic aspects quite well, but there is another aspect he didn't quite touch on - what's going on at the molecular level. To understand this, you need to think about the actual conditions of the reaction: unless it's taking place inside a cell, which straight biochemical reactions of the kind you're talking about almost never are, then the enzyme, substrate, and product are all floating around at a certain concentration. The enzymatic reaction is proceeding nicely, and as the substrate binding pocket is freed as product dissociates from the enzyme and diffuses away, allowing another substrate molecule to take its place and the next reaction to occur. This is the situation at your 2 mmol [substrate] level. At 50 mmol, the concentration of substrate is much higher, and so even though the actual catalytic portion of the enzymatic reaction is taking place at essentially the same speed, the rate of substrate diffusing into the active pocket is somewhat higher because the local concentration of substrate is higher, allowing for an apparently slightly faster reaction rate.


How did the cardiovascular system evolve? How has evolution created our blood, lungs and the heart?

We can't exist without blood, which transports the oxygen to all areas of our body. However, the blood needs a lung, which gives it the oxygen to transport. The blood also needs something which lets it flow through the whole body, which are our veins. And in order to allow the blood to flow through our veins, an organ is needed to pump the blood, which is our heart. We also need a brain which controls all that, and the brain in turn needs the blood in order to function right.

Evolution makes very slow steps....."it just doesn't jump". So, How did evolution manage to create all that?

While others have addressed the big picture aspects of your question, I think it would be useful to look at the specifics.

Have a look at the heart (or more accurately, the hearts) of the earthworm:

They're nothing more than veins with some pumping muscles wrapped around them. It seems almost a stretch to call them hearts, they are shaped so different from what we think of as a heart proper.

Also, note the earthworm's lungs, or rather, lack of them. It doesn't have any! Why not? It doesn't need them. It gets enough oxygen through its skin via osmosis. It's only larger organisms that need dedicated systems to concentrate oxygen from the surrounding environment.

So, the worm has a simpler system (no chambered heart, no lungs) that works.

All vertebrates descended from a common ancestor that was very similar to this earthworm. It had simple hearts, and no lungs. You can follow the evolution of the human heart through fish heart:

which is a more sophisticated pumping vessel with two chambers.

Amphibians evolved from fish, reptiles from amphibians, and mammals from reptiles. In this diagram, you will find that the heart becomes more sophisticated and efficient in each:

So, this should give you a good idea of the evolution of the human heart from simpler, working system. I won't take the time to draw out the evolution of blood vessels or lungs; maybe someone else will, or you can google them yourself, the information is readily out there. But they all follow the same pattern: gradual, incremental improvements on working, simpler systems.


Is this a hawk, or an eagle? I saw this large bird gliding fairly low over the trees while hiking in the late afternoon in some hills near Taipei recently. It seemed quite large compared to what I normally see here. It's quite difficult to gauge, but I'd guess the wing span was one meter or so.

It made that shrill, descending, single "peeeew" sound that I associate with birds of prey (probably mostly from old movies or TV commercials).

Is it at all possible to guess if this is a hawk or an eagle from these cell phone snapshots? These are cropped out of the full resolution originals. A half-size original for scale is also included.

The words "hawk" and "eagle" are very confusing and may mean different things in different parts of the world. In fact, the nearly thirty species of raptors (not including owls) native to Taipei apparently include one called a mountain hawk-eagle (Nisaetus nipalensis).

If no one can answer your question, you might narrow the field with a process of elimination. I can't vouch for the accuracy of Wikipedia's list of birds native to Taipei, but it's a start.

There are apparently seven native raptors that are called eagles. If you can eliminate all seven eagles, then it presumably is not an eagle.

Your photographs are helpful insofar as they illustrate the bird's general outline, but it's very hard to distinguish its color pattern. However, the shape of the wings should help narrow the field.

Birds Native to Taiwan

EDIT

I don't know if you're familiar with the terminology, but many raptors are classified as buteos or accipiters. If I remember correctly, species with broader wings are generally buteos. Species commonly called "hawks" include both buteos and accipiters, but I believe most birds called "eagles" are buteos.

Anyway, here's another link...

Buteos


Properly changing the time scale of a parameter in a growth model I have a two-population model, where one of the populations is a bacterial culture with its growth described as a logistic growth, with a reported growth rate of $2 \log\hbox{bacteria hour}^{-1}$ and a death rate of $1.5 \log\hbox{bacteria hour}^{-1}$ and a carrying capacity of  $7 \log\hbox{bacteria}$. However, my model studies the interaction between bacteria and fungi in a time scale of days, but if I try to directly rescale these parameters, I get a growth rate of $48 \log\hbox{bacteria day}^{-1}$ and a death rate of $36 \log\hbox{bacteria day}^{-1}$, which is absurd, given the carrying capacity of bacteria.

Is there a standard method for properly rescaling these parameters for bacterial growth, without having to change the model? What alternatives do I have?

These values are not absurd: it's just a different unit, it does not change the reality of th phenomenon.

The fact that your population can grow by a $48$ or $36~\mathrm{log}$ factor in one day, while the carrying capacity is $10^7$ bacteria, only means that the growth happens in less than one day (once the latency phase is over). Many bacterial population can grow in less than one day, it is not shocking.

In my opinion, it is not absurd to use the growth rates in $\mathrm{log}~ \textrm{bacteria} \cdot \textrm{day}^{-1}$. There is not need to rescale values if you just want to convert hours into days.


When do most mammals mate? Is one part of the day more prevalent then other when it comes to mammal animals mating? Is there an aggregating study that has been done to see if these living beings in nature mate mostly during day or night?

Why would it evolve?

No research (that I can find) is consistent with specific time of day mating across many species. I can't think of any reason why even just a few quite different mammals (e.g. mice, bats, lions, whales, and humans) would all find a fitness benefit of mating at the same specific time of day and therefore it is highly unlikely to evolve. I would suggest that if there are consistent patterns they are no reason other than coincidence (correlation over causality).

For example, dawn and dusk peaks in activity...

I have no references to back this idea up but lets see how this goes. The majority of mammals will be awake around dawn and dusk because there is likely an over lap between nocturnal and diurnal species at these times. Given that mating (normally) requires the participants to be awake then this would be a time when more animals are awake it is therefore a more likely time for mating to occur. But, as I already mentioned it would purely be because of the increased numbers awake.

Simple statistical illustration of the dawn & dusk idea...

Imagine a raffle with 2000 winning tickets. You buy 1000 and put 500 hundred of these in a box called nocturnal and the other 500 go in a box called diurnal. The raffle is drawn 24 times (perhaps every hour). The first 14 times it is drawn you can win if the ticket is from the nocturnal box, the latter 14 times you can instead check the diurnal box. This means during the first 10 draws you have a 25% chance of winning, and likewise in the latter 10 hours, but in the middle 4 hours there is a 50% chance every draw.

This comes down to a simple statistical phenomenon, if you don't buy a ticket you can't win the raffle.


Are there ways to speed up the growth of plants? I'm interested in what humans can do to speed up the rate of growth in a plant. I'm interested in both the context of home gardening and large-scale, institution-backed projects.

Obviously, optimal growing conditions are one factor that can be modified. I imagine that there are also genetic mutations that can be done (possibly even at home!). Botany is not my field so what I'm looking for here is are the basics and some good resources for further reading.

Yes.

The research team, led by the Durham Centre for Crop Improvement Technology, and including experts at the University of Nottingham, Rothamsted Research and the University of Warwick, have discovered that plants have the natural ability to regulate their growth independently of Gibberellin, particularly during times of environmental stress.
They found that plants produce a modifier protein, called SUMO that interacts with the growth repressing proteins.
The researchers believe that by modifying the interaction between the modifier protein and the repressor proteins they can remove the brakes from plant growth, leading to higher yields, even when plants are experiencing stress.[1]

Bacterization is the process by which bacteria applied to the soil and plant parts. Under certain conditions yields were able to increase 10 to 13 percent. However, not all results were able to be reproduced so this is something you can look into more as well. [2]
Another option is to artificial increase the amount of CO$_2$:

Over the years there have been numerous laboratory experiments which conclude that increases levels of CO2 result in increased plant growth no matter how that plant growth is quantified. Sylvan Wittwer in Food, Climate and Carbon Dioxide tabulates the results. [3]

Lastly, you can look into genetically modified organisms (GMOs) which is a hotly debated topic.
With a Google search, you will see that that there are numerous articles on methods to increase plant growth, to numerous for me to give a blurb about them all. Therefore, I linked a few that seems promising as well as interesting.


What is Tandem repeat? After reading -

(wikipedia) Tandem repeats occur in DNA when a pattern of one or more nucleotides is repeated and the repetitions are directly adjacent to each other.
( a paper) A tandem repeat in DNA is two or more contiguous, approximate copies of a pattern of nucleotides.

I deduced that the portion of oriC containing all four 9mer-s
was to be called a tandem repeat and it together with all three 13 mer-s, two tandem repeats.
But again while reading Principles of genetics by Simmons I stumbled upon the following-

The single ori in E.coli has been characterised in considerable detail. It is 245 nucleotide pair long and contains two repeated sequences. One 13-bp is present in three tandem repeats. The three repeats are rich in ...

So here it says that each 9-mer in the series is a tandem repeat actually.
Which meaning is more accepted?

The DNA sequence "TATATATA" contains 4 repeats of the 2-mer "TA" and because these repeats are adjacent to each other, they are tandem repeats. The pattern of  nucleotides is repeated and the repetitions are next to each other.

This is what both the Wikipedia and the Simmons definitions are trying to communicate.  The statement you quote from Benson'a paper can be taken to mean the same thing (except for "approximate"), but might also be construed as saying the collection of all contiguous repeats is one tandem repeat, but that is not what was intended.

So, the oriC sequence has 4 tandem repeats of one kind (9-mers) and 3 tandem repeats of another pattern (13-mers).


Do probiotics survive digestion? Pretty much this. I've been wondering if any of the yogourt and other "health" foods containing living probiotic cultures survive digestion to populate our intestines? If so, is there peer-reviewed evidence you could point me to?

When I took Microbio we had a entire lecture on this. My professor's view was that they do not survive due to the pH of the stomach.  He told us that there are microbiologist on both sides as to whether they do make it to the intestine (or enough of them to make much difference) or that they do survive and help. I have added a link below to a article by the American Society of Microbiology. Here it is saying that it may be helpful, but that more studies are being conducted.

http://cmr.asm.org/content/16/4/658.short


Do primate RGCs have overlapping receptive fields? According to this link,

http://hubel.med.harvard.edu/book/b10.htm

retinal ganglion cells (RGCs) receive input from overlapping receptive fields (RFs). This is also an idea used in convolutional neural networks for deep learning of images.

On the other hand, this one, for the primate retina, states that there is no such overlap:
http://www.sciencedirect.com/science/article/pii/0042698995001670

So do primate RGCs have overlapping RFs? If not, how does the primate visual system deal with this sparse input? How does it fill in the blanks?

Short answer
Associated ON- and OFF-center retinal ganglion cells can show 100% overlap in their receptive field.

Background
When looking at the elementary neurophysiology of the retina, we can see that a single cone generally synapses onto two bipolars. Because photoreceptor cells hyperpolarize when illuminated, glutamate release from their synapse is inhibited. In turn, OFF-center bipolar cells are hyperpolarized and ON-center bipolars are depolarized. The OFF-center bipolar synapses onto an OFF-center retinal ganglion cell (RGC), while the ON-center synapses onto an ON-center RGC (Fig. 1).

 Retinal circuitry linking cones to bipolar cells (left panel) and bipolar cells to retinal ganglion cells (right panel). source: Washington University.

Then to your question - the basic circuitry shows that the ON- and OFF-center RGCs receive their input from a single cone and hence have 100% overlapping field. In the foveal region, bipolars link 1:1 on cones, as in Fig. 1, so in this example case, they show 100% overlap.

Note that there are an estimated 30 types of retinal ganglion cells, about half of them being not even described yet, as per a 2015 review article (Sanes & Masland, 2015). Hence, this answer is anywhere from exhaustive, but it does show there can be substantial overlap between RGCs.

Reference
- Sanes & Masland, Ann Rev Neurosci (2015); 38: 221-46


Curious what this bug is I just found this little guy crawling on me after coming in from the garden in Northern VT.  We live in a narrow grassy valley in a pretty wooded area.

This bug was crawling up my neck and when I tried to sweep him away he clung the way a tick does.  He also has a very flat profile and kind of a "hard" feeling body, but otherwise bares no resemblance to a tick.

I took this photo with my phone so it's not great.  The eyes are distinctly roundish and black. His mouth parts were visible and moving around slightly, but while I watched him he didn't appear to be trying to bite into me.

That's all I've got.

The blurry picture makes it hard to be sure, but I'm guessing it's some sort of louse fly (family Hippoboscidae). They are typically very flat, and can lack wings. They can bite humans, but the different species are dependent on their specific hosts to reproduce.

Image of a louse fly (found on someones neck) for comparison:

(image source)


Recognition of snake (image) I would like some help with the recognition of the snake shown in the image below. I was doing a fieldwork in a forest in Slovakia when I found it.

I was thinking it could be a water snake but I am no expert in snakes.
Does someone know what kind of snake is this?

Aesculapian snake (Zamenis longissimus). Common european species, non venomous, rodent/egg eater.

edit1: they can swim and can be found next to water bodies but are terrestrial.


Why do cherries sometimes grow as triplets? Usually when I think of cherries, I think of them as pairs. I think most of us imagine them that way, but recently, I stumbled on a picture of a triple cherry:

Which I found interesting, but I couldn't find any more info on this, so I hoped to find some answers here. Why do they sometimes grow like that and how often does it happen compared to their regular twin counterparts?

Why do they (cherries from a cherry tree) sometimes grow like that (in triplets) and how often does it happen compared to their regular twin counterparts?

After doing a considerable amount of research, I also wasn't able to find much of any literature that addresses your question, aside from this. From that article it says:

When you think of cherries you imagine them in pairs, don't you? It's also common to find cherries grouped in quadruplets on a single bunch of stems. This happens because of the way cherry flowers bloom -- several pink blossoms grow from a single focal point, and when those flowers wilt and become fruit, the resultant cherries are connected, too. It's smart to keep cherries attached to their stems whenever possible, as they will stay fresh for much longer. And when you're harvesting the fruits, harvest the cherries at the stem (no higher!) or you risk next year's buds snapping off along with them.

The bolded section seemed to be most revealing, and so, I was able to find a time-lapse video that depicts the various stages of the flowering & fruiting process for a cherry tree. The video is only 4 minutes long, and I highly suggest watching it.
From watching the video, it can be confirmed that the statements made by the previously quoted passage are true -- "several (pink) blossoms grow from a single focal point, and when those flowers wilt and become fruit, the resultant cherries are connected, too".
Consider the following series of images, which are screenshots from the time-lapse video. You should view these images in an alternating left to right, right to left fashion, going from top to bottom (so, snake-shaped).

As can be seen, each flower does grow from a shared focal point, and, the cherry fruit does originate out of the exact same location as where the flower was.

What's most interesting to note, and which begins to answer your question, is:
When viewing the third row (left to right), for the first two images, there are multiple cases of three cherries growing from the same stem. However, in each case, one of the three cherries are actually extremely underdeveloped. But then, if you compare the second and third image (still in the 3nd row, left to right), those underdeveloped cherries completely disappear!
It would then seem to me that, since one of the three cherries are severely underdeveloped (most likely due to limited nutrition & resources), the farmer who is tending to the tree will prune these (underdeveloped) cherries, thus leaving only pairs of two. In extreme cases, perhaps, the third (or even fourth) cherry achieves enough development for the farmer to not consider pruning it, but, this appears to be the exception.
Further supporting this idea, consider the next series of screenshots (from the same video).

When harvesting, the farmer deliberitely picks the cherries by pairs of two. There's even a time when he almost pulls off three, but then makes sure to leave the third. This process of pruning underdeveloped cherries, as well as harvesting in pairs or two, is most likely common practice amongst cherry growers.

And when you're harvesting the fruits, harvest the cherries at the stem (no higher!) or you risk next year's buds snapping off along with them.

Given that quote, it could be that picking in pairs of two is the most efficient method of harvesting that also best ensures the safety of next year's buds. So, to restate the reason, it would appear that cherries are rarely seen in groups of three (or more) due to nutritional constraints, and the pruning & harvesting methods of the farmer, or tree owner.


Which type of test tube should not be used for blood collection? The following question is presented in my biology textbook:

You are required to draw blood from patient and keep it in a test tube for analysis of blood corpuscles and plasma. You are provided with the following four types of test tubes. Which one of them will you not use for the purpose?

Test tube containing calcium bicarbonate
Chilled test tube
Test tube containing heparin
Test tube containing sodium oxalate

In thinking through the question, I reasoned that since we are collecting blood from a patient for biochemical assay or hematocrit, we would want it to be in an anticoagulated stage. Sodium oxalate and heparin are both anticoagulants and therefore should serve my purpose well. I don't think a chilled test tube would have any effect directly, except the fact that low temperatures delay clotting. So, I had chosen the test tube containing calcium bicarbonate to be unsuitable, as $\ce{Ca++}$ is one of the factors required for clotting and hence would accelerate the clotting procedure.
The textbook disagrees with me, and gives (3) as the answer.
Is this an error in the textbook key, or a flaw in my reasoning? Which should be the correct answer, and why?

Your reasoning is sound and correct. The answer key is wrong.

An unclotted blood sample needs something to prevent clotting. Extracellular calcium is required for both the coagulation cascade and platelet activation. It even has its own name in this context, Factor IV. This why EDTA, a calcium chelator, is used in some blood collection tubes to delay clotting.

So, as you say, the most correct answer would be (1): Test tube containing calcium bicarbonate. That is the opposite of the kind of tube you should use for this type of sample.

The answer given by the key, (3): Test tube containing heparin, is incorrect. Heparin tubes are a good choice for plasma and whole blood analysis, as you indicated. Heparin is a good anticoagulant, both in vitro and in vivo.

See this nicely laid out list from UCI medical school for an example of specimen requirements for specific tubes.


Do Yersinia genus spp have anything movement factors? It can spread in blood (Type III secretion system -> apoptosis).
I am interested if there is any others ways to move.

Do Yersinia spp have anything virulence factors to move?

Yersinia enterocolitica does express flagella at a temperature around 25°C, but not at 37°C. Kapatral et al.
Besides that it can rely on peristaltic movement in the intestines.

Yersinia pestis is as far as I know nonmotile in the host, but motile if isolated Medical Microbiology.

As there are some other Yersinia species, including Y. pseudotuberculosis of course, I think you cannot totally generalize the answer for Yersinia spp., but searching for the Yersinia of interest with "flagella", "motility", "movement" or similar keywords on Pubmed might help.


Why does K+ move out of the cell? I was reading this page: Equilibrium Potentials when I found the following example at the end of the page: "If the K+ equilibrium potential is –90 mV and the membrane potential is –70 mV, in what direction will K+ move through open K+ channels?".

The site gives the answer, and it turns out that K+ moves out of the cell. I'm not entirely sure if I understand why this is the case.

(1) Because the equilibrium potential for K+ is –90mV, this means that the intracellular region must be negatively charged, at –90mV, to have zero net flux of K+ across the membrane. Therefore K+ would leave the cell, making the interior more negative from –70mV to –90mV.

(2) But the resting membrane potential is still –70mV. Will this membrane potential be established by other ions? If not the case, K+ will be pulled inside the cell again, then we wouldn't be able to tell that K+ goes out.

(3) I find the starting conditions somewhat confusing. "K+" goes out means that there needs to be a potential difference. Is the question assuming we have, as starting conditions, the same concentration of K+ at both sides? Otherwise it is not clear why K+ should stop leaving the cell at any moment (even when it is at the state of equilibrium).

(4) Can we conclude, as a general rule, that if MRP is the membrane resting potential and EP is the X+ equilibrium potential, then X+ leaves the cell if EPMRP. Would the roles be reversed for X–?

The other answer is a bit misleading.

  "Another cause is the the intracellular K+ concentration"

No, this is exactly the same cause, the differing concentrations is what causes the equilibrium potential. You can think of the equilibrium potential for one ion as "how much voltage does there need to be to prevent this ion from flowing down its concentration gradient." The Nernst equation gives you the equilibrium potential for any one ion. The equilibrium potential is also known as the "reversal potential" because if the voltage exceeds the equilibrium potential, ions will flow the opposite way, against their concentration gradient.

  Don't get confused by the resting potential, because it is only a potential that the cell arranges for itself to maintain a stable environment. This cost a lot of energy and attention in form of protein synthesis to keep this potential. This mechanism is achieved by the Na+-K+ ion-pump

The resting potential is not to "maintain a stable environment" or anything like that. The resting potential is the net potential that a cell reaches due to all of the conductances of various ions and the flowing current of each ion governed by its own equilibrium potential.

  This mechanism is achieved by the Na+-K+ ion-pump, which exchanges those two ions

This is partly true, but again, misleading. The Na+/K+ pump establishes the relative concentration of ions, which only leads to a certain resting potential because the conductances of different ions vary at rest. Because the conductance of K+ is higher at rest than the conductance of Na+, the resting potential is closer to the equilibrium potential for K+. If the Na+/K+ pump was functioning exactly as it does, pumping Na+ out and K+ in, but the membrane was more permeable to Na+, then the resting potential would be positive rather than negative. All that matters for resting potential is relative ion concentrations and conductivity. The Goldman equation is the way to calculate this resting potential.

What is happening to K+ when a cell has a resting potential of -70mV but a K+ equilibrium of -90mV?

Because you need -90mV to 'hold in' the potassium against it's concentration gradient, at -70mV K+ will flow out of the cell. However, by definition, resting potential is the potential at which the net current will be zero. That means that, yes, other ions have to be involved. This is where the Goldman equation is very useful.

Although K+ may be the ion with the highest membrane conductance, there will also always be some leak of Na+ and Cl- ions (usually others ions are ignored because these three are the major players; other ions can be important in some situations). Therefore, if -70mV is rest, there must be at least as many Na+ ions flowing in or Cl- ions flowing out as there are K+ ions flowing out.

You can calculate these currents if you know the conductance of each ion and the equilibrium potential for each ion using Ohm's Law: I = V/R, where R is 1/conductance and V is the difference between the current voltage and the equilibrium potential. Try it out with the Goldman equation! If you use the voltage the Goldman equation gives you (the resting potential) you will find that the net current is zero!

Okay, so far we've answered your questions (1) and (2). Now (3): you state "Otherwise it is not clear why K+ should stop leaving the cell at any moment". It is important to note that equilibrium potential doesn't mean no ions are moving: it means the voltage isn't changing. If you just left the cell at -70mV and waited some time, eventually the concentrations of the different ions would change. This is where the Na+/K+ pump comes in: this ATPase is constantly pumping some K+ out and Na+ in to counteract the leak that occurs at resting potential. Cl- ions move, too, but mostly passively. It's also important to note that very few ions have to move for the potential to change on the order of millivolts. -70mV might sound like a lot, but electrical forces are very powerful, so very few ions relative to all the ions available have to move.

I don't quite understand what you are asking with (4) but if you can edit the question I will try my best to answer that as well. It's possible I already answered your question by talking about what "equilibrium potential" means for one ion. For a Cl- ion, if the equilibrium potential for Cl- is -65mV, then Cl- will flow into the cell when the membrane voltage is -60mV (tending to make the cell closer to -65mV), and it will flow out of the cell when the membrane voltage is -70mV (still tending to make the cell closer to -65mV).


Is there biological evidence for self-awareness in animals? I am conducting an investigation into the topic of the intelligence of
animals, in particular farm animals. I would be interested to hear a scientific and biologic perspective as to what is perceived to be self-awareness, whether it be in a human or
not. Specifically, I am interested in the high-level self-awareness that we as humans experience and that is only now, beginning to be theorised as possible in other mammals (e.g. Dolphins).

The question is framed in a robotic context, where a being (natural or artificial) is defined to be self-aware if it can approximate enough human behaviour and thought, that it becomes indistinguishable from a human. This term we could label sentience, but this is a subjective term, and so I will avoid using it for the purpose of this question. I will define a being as self-aware in the robot context, as a being capable of both conscious reflection of itself and of its own conciousness.

One of the problems I have found in my investigation, is a serious
misunderstanding about the nature of self-awareness, amongst
the general public.

It seems that many people incorrectly assume that self-awareness is a product of
a being having a soul. This is rather unfortunate for animals as orthodox
Christianity teaches that animals do not have souls, and therefore are
incapable of attaining self-awareness.

My investigation aims to bring to mainstream public attention, a new
definition of self-awareness, and to end the centuries-old misconception
that we are the only intelligent, self-aware creatures on the planet.

Yes, there is a lot of evidence for self-awareness in animals. The gold standard test for self-awareness is the mirror self-recognition test (MSR)--we can tell from the behavior of an animal exposed to a mirror whether or not it can tell itself apart from other animals of the same species:

  Animals that possess MSR typically progress through four stages of behavior when facing a mirror: (i) social responses, (ii) physical inspection (e.g., looking behind the mirror), (iii) repetitive mirror-testing behavior, and (iv) realization of seeing themselves. (Plotnik et al. 2006)

That quote was taken from the abstract of a paper showing self-recognition in a single African elephant, but there is evidence for self-awareness in magpies (Prior et al. 2008), dolphins (Harley 2013), chimpanzees (Povinelli et al. 2006) and orangutans (Suarez and Gallup 1981). Many of these studies use the Gallup mark test (Wikipedia):

  Gallup anaesthetised the chimpanzees and then painted a red alcohol-soluble dye on the eyebrow ridge and on the top half of the opposite ear. When the dye dried, it had virtually no olfactory or tactile cues. Gallup then returned the chimpanzees to the cage (with the mirror removed) and allowed them to regain full consciousness. He then recorded the frequency which the chimpanzees spontaneously touched the marked areas of skin. After 30 minutes, the mirror was re-introduced into the room and the frequency of touching the marked areas again determined. The frequency of touching increased to 4-10 with the mirror present compared to only 1 when the mirror had been removed. The chimpanzees sometimes inspected their fingers visually or olfactorily after touching the marks.

Basically, an animal which has seen and recognized itself in a mirror recognizes the mark as being new, so it touches its own body on the marked area, which shows that the animal recognizes the image in the mirror as itself.


Identification: Creepy 'nope' While walking back from our routine evening stroll through the hills, we stumbled upon some insect(?). It was the size of an index finger, and it appeared to have some sort of wings. While I tried to take pictures of it, it started turning towards me with it 'claws'.

Additional info:

Origin: Romania, in the hills
Date/time: 17 August 2017, 19:15, sunset
Warm sunny day, just started to cool down, 19 degrees celcius

My wife doesn't want to go outside anymore unless she knows what it is, and she won't allow me to go and pet it.

That's some kind of mole cricket (Gryllotalpidae).

According to this website there's only three species found so far in Romania:

Gryllotalpa gryllotalpa
Gryllotalpa stepposa
Gryllotalpa unispina

It's most likely you've encountered a specimen of the first species as it's the most common and widespread one in Europe, Gryllotalpa gryllotalpa:


How did the horned lizard evolve? It's a lizard that has the ability to burst blood vessels in it's eyes and shoot blood as self defense.

How can this behavior be explained evolutionary? Wouldn't it mean that there had to be some intermediate evolutionary step where the lizard could bleed from it's eyes only slightly? How did that not cause it's extinction?

To generalize more, how does a specific trait evolve when it seems the intermediate traits are detrimental to survival?

The behavior can be explained evolutionarily just like any other trait. It came about either through adaptation, neutral evolution, or as a by-product of another adaptation.

An intermediate step, like the one you suggested, is not required. But if it did occur, there's no reason to believe that such a trait would cause extinction. Bloody eyes, whether they squirt or not, could be beneficial in some species. We know that blood-squirting eyes appears to be a defensive trait. Take away the ability to squirt and the blood could provide defense in some other unexpected way, or it may have had nothing to do with defense at all. Maybe the blood was just a lubricant before, or maybe the blood somehow enhanced vision during a stressful event. Or maybe it was just there and didn't do anything; nothing good, but nothing bad.

There's nothing special about this lizard. It does have a unique trait, but there's something novel in every species.


Empirical evidence for species selection Do we have any empirical evidence in favor of species (or lineage) selection? Do we know some cases that can only be explained (or seem to be only explained) by lineage selection? What are today the best study cases in favor of lineage selection?

If not, how could we find any evidence for lineage selection?

Note: I call lineage selection a differential in speciation and/or extinction rate that drive the proportion of lineage (species for example) displaying a given trait (emergent traits or not) to increase or decrease over time.

A commonly used empirical example of species selection (a.k.a clade selection, lineage selection) is pelagic larvae in sessile ocean species. See Maliska et al (2013) for a recent paper discussing this in Tunicata and Jablonski & Hunt (2006) for larval modes in gastropods. The idea is to some extent really intuitive - pelagic larvae means higher dispersal rates, so the species will be exposted to and can colonize new environments. This can lead to speciation through adaptive radiation. Larger ranges also means lower extinction rates (e.g. through less population synchrony). If the trait is fixed within a lineage, this lineage as a whole will, as compared to an sister lineage lacking the trait, contain more species (i.e. species selection).

However, you can also argue that pelagic larvae will lead to higher gene flow between populations, which could inhibit speciation. Therefore, the effect of pelagic larvae, and how these mechanisms are weighted in practice, is really an empirical question (see Duda & Palumbi, 1999 and Jablonski & Hunt, 2006 for discussions on this issue).

Jablonski (2008) provides a nice general review of species selection (concept, mechanisms, theoretical models and data), and Okasha (2006) (chap. 7) is good for a theoretical/philosophical treatment of levels of selection. Also remember that traits are selected for at the individual level, but can (especially if fixed) still act on a lineage level.


Is there any math formula that can be used to describe shape of leaves? There can be great variation in shape of leaves. Neverthless they are fairly simple shapes. How far are we in describing the shape of leaves in a mathematically rigorous way? Do we have a general formula that can be used to describe all shapes of leaves (or, at least, a reasonably large subset)?

There are algorithms which can be used to describe leaves, if that is what you mean.

The following description takes into account that leaf shape is not solely a function of genetics, but is also effected by environment. It also models how different growth rates within the cells have consequences. Mutant, cloning cells are also factored into the description.

The mathematical model has interesting allometric implications.

Here is a very readable paper (PDF),which endeavours to describe differences using mathematics and for which for which we can thank Cornell University Library for hosting the paper and Lawrence Livermore National Laboratory.


What decides between the synthesis of eumelanin and pheomelanin on a biochemical level? MC1R is a very well known gene where a loss-of-function mutation will cause the synthesis of pale/redish pheomelanin instead of black/brown eumelanin. MC1R is only a receptor which doesn't directly participate in the synthesis. it affects the expression and transcription of several important enzymes for melanin synthesis (Tyrosinase, TYRP1, TYRP2).

In one study (Ito, 2003) they proposed that increased tyrosinase activity and decreased cysteine levels would promote the snythesis of pheomelanin. Since MC1R controls the expression and transcription of tyrosinase I think it makes that mainly the increased tyrosinase activity is responsible for the decision between eumelanin and pheomelanin.

The question is whether this is correct or false or if we just don't know yet.

Let's have a look at the pathway first (this figure is figure 2 from reference 1), which shows the basic pathway of pigment biosynthesis:

The first important step, the oxidation of the amino acid tyrosine to Dopaquinone (DOPA) by the tyrosinase is the same for both pathways (eumelanin and pheomelanin production) and rate limiting.

The important step is the next one: Either the formation of Cyclodopa (for eumelanin) or Cysteinyldopa (for pheomelanin). As long as the concentration of cysteine in the melanocyte is above 13µM (see reference 1) the formation of pheomelanine is favored and biochemically much faster than the cyclisation of DOPA.

If there are high levels of tyrosine and normal to low levels of cysteine, the cysteine will be depleted at some point and only eumelanin is made.

The opposite will happen if either a lot of cysteine or little tyrosine is available. It will also happen, when the available tyrosine cannot be oxidized into DOPA when there is little or reduced Tyrosinase activity.

And this is actually what happens in the case of the MC1R mutation. MC1R is a receptor on the pigment producing cells which regulates the production of pigment upon external signals (as UV radiation to the skin) (see reference 2 for more details). When mutated is is not or much less functional leading to much less (or no) signals to the downstream gene (MITF) which regulate the enzymes for the pigment production.

Low signals lead to low tyrosinase production which then can only produce little DOPA. Since the cysteine stocks of the cells will not be depleted then, only pheomelanin is produced causing people with MC1R mutations to be red haired and having light skin and freckles.

References:

Chemistry of mixed melanogenesis--pivotal roles of dopaquinone.
MC1R, Eumelanin and Pheomelanin: their role in determining the
susceptibility to skin cancer


Arthropod identification request (a spider with no legs?) My mother sent me a picture of a creature she encountered and couldn't identify. It looks kind of a like a spider - a mostly black body, about 1cm in size, with white specks - except without any visible legs. Apparently it was hanging from a thread, descending to the ground, and still moving.
I don't know a lot about arthropods, and, perhaps unsurprisingly, searching for "spider without legs" gives no useful results, so I'm at a loss.
This is in Northern Germany, mid-March. (The background is a cork floor.)

Any info on what this could be - and whether it's dangerous or not - would definitely help put her at ease.

This appears to be the underside of a walnut orbweaver:

These orbweaver spiders are not medically significant.
Spiders often lose their legs in wasp attacks. Some spider wasps will remove the legs and then try to bring the spider to its nest for larvae to feed on. Sometimes they drop their spider victims accidentally.
Some will simply deposit eggs into the spider and leave it there, letting the larvae grow inside the spider and feeding on it from the inside.. these ones don't usually remove the legs - they usually just paralyze the spider.
Spiders can lose their legs through various attacks, but they can also lose their legs in molting accidents... particularly if they are in the middle of a molt and then are aggressively interrupted.


Are recessive, deleterious alleles less common on the X chromosome than the autosomes in humans? As there is a potential for them to be more readily purged in hemizygous males (and in cell lineages in females with the deleterious-allele-bearing chromosome activated), I would expect the frequency of deleterious alleles to be lower on this chromosome than in autosomes. Is this information known?

"Monosomy for the X chromosome in humans creates a genetic Achilles' heel for nature to deal with."

The article I quoted1 tackles this issue.  It's from the turn of the century, though, so quite old in sequencing/genetic terms, but the science is still sound as far as I can tell.  Here's the money quote:

  Hence, the X chromosome appears to have a lower gene density and should yield fewer deleterious mutations per megabase of DNA.

In short, yes, you're correct.  There appears to be less overall information on the X-chromosome, deleterious or not, and selection is faster; the X chromosome is just flat-out less diverse.  This article goes into quite a bit more but says essentially the same thing: "On one hand, the greater effectiveness of selection on males due to the hemizygous expression of the X, which may be further reinforced by sexual selection, is expected to lower the mutation load for females at shared loci."  Here is a more recent article stating the same: "This finding [X-chromosomes with lower linkage disequalibrium] is consistent with more rapid selection against deleterious mutations when the X is monosomic in males, and to a lesser extent, under random inactivation (Lyonization) in females."

Finally, here is a piece written a few years back by a colleague of mine that goes into depth on the subject.  The second half deals with population differences (also fascinating), but the first part has a lot of good detail on what you want.


Are Asian people genetically predisposed to be shorter than Europeans? People in different countries have different average heights. For example, Wikipedia's article on human height states that Australian men have an average height of 177.8 cm, and Australian women 163.8 cm, whereas Japanese men have an average height of 170.7 cm, and Japanese women 158 cm.

Are these differences in height due to environmental differences between people in different countries, or does genetic differences play a role?

In particular, are Asian people (people from Far East countries like Japan) genetically predisposed to be on average shorter than people who are of European descent?

Note: This is too long for a comment, so I will post it as an answer, even though it is merely an example and not a full answer to your question.

An example of the environmental influence on human body height can be found in the statistics assembled by the Swedish conscription service from 1840s to 2010 (when general conscription ended). During this time the average height of Swedish men (aged between 18-21) increased from 167.4 cm (in 1841-45) to 180.2 (in 2004), an increase of 12.8 cm or 7.6% (Werner 2008, unfortunately in Swedish, but tables 2 and 3 should be understandable). Here is a graph of the data found in the paper:

During this time Sweden has gone from what would have been a bottom-20 position in the wikipedia list of average human heights (close to contemporary India or Mexico) to a top-10 position. This is clearly not due to changes in the genetics of the population, but to changes in the environment (probably mainly due to nutrition). I know that many countries have gone through a similar development, and this is usually refered to as a secular change or trend in body height and weight (see e.g. Roche, 1979 and Loesch et al., 2000 for further examples).

Nothing of this naturally contradicts that genetics is a powerful determinant of human height. However, it shows that the average height in two countries cannot be compared in a meaningful way (at least if you want to infer genetic differences) without knowing something about the nutrition status and the average living conditions in both countries. The situation is rather that genetics is setting the limits of potential height, but that environmental factors will determine the actual outcome. This is also discussed in the paper above, but there are certainly better references to be found in English. In the reference list (#9, #10) you can also find examples of how there are also well-known genetic determinants of e.g. short stature in some human populations (in this case decreased insulin-like growth factor I receptor expression and function in African Pygmys, see ref #10)


What characteristics of the protein folding process ensure that the energy landscape is a funnel? The folding funnel hypothesis states that the energy landscape that proteins observe when they fold is funnel shaped with a single global optima. This ensures that no matter what sequence of folds the protein follows, it should eventually end up in the same folded configuration thanks to the laws of thermodynamics.

For example, see this illustration of the energy landscape from Dill & MacCallum (2012) "The Protein-Folding Problem, 50 Years On" Science 338 (6110) pp 1042-1046:

Clearly, the folding works because the energy landscape is funnel shaped. Any other configuration, e.g. a landscape with multiple significant local optima or a flat landscape, would result in a protein folding in all kinds of different ways.

What are the characteristics of the overall system that ensure that the energy landscape is funnel shaped, and that nearly any protein in an unfolded state will reach the global optima? (e.g.: is it because the proteins themselves have certain statistical properties? or it is something to do with how the types of "moves" the protein makes on the energy landscape?)

Naturally occurring proteins are evolved such that this is the case

Natural proteins only occupy a very small amount of sequence space. For a 200 aa protein, there are $20^{200} \approx 10^{260}$ possible sequences. There are nowhere near that many naturally occurring protein sequences, even if you take into account all the different alleles in the different organisms in the world.

What happens when you synthesize and express a random (non-natural) protein sequence? You get junk. It doesn't fold or it aggregates or something else happens. You don't get a stably folded protein. Heck, you don't even need to have a fully unnatural protein. You can take a naturally occurring protein and make a few mutations in it, and end up with non-folded junk.

Evolution has a very strong selective pressure to make sure proteins can fold properly and beat Levinthal's paradox. If a protein can't fold, it can't perform any function in the cell, and thus there's no selective pressure to maintain expression. (The promoters get trashed, and the DNA gets mutated away to "junk" DNA.) Only if the protein is stably folded is selective pressure maintained. So you get the one-in-a-million sequences which does have a decent folding funnel.

So it's not that there isn't protein sequences out there with a flat energy landscape, or an energy landscape with lots of local minima. It's just that whenever such a protein forms, it can't fold. And if it can't fold, it's freed from evolutionary pressure and disappears from the gene pool - either because the organism that holds it can't survive without it, or because random mutations wipe it out with random noise. It's survivorship bias -- you see proteins with a reasonably well-formed folding funnel because they're the only ones you would see.

(There are proteins out there with less-than-robust folding funnels, or with alternative energy states. A brief search of the literature will turn up a number of examples where protein folding requires cofactors or chaperones. Or where a protein has two different folded states, depending on environmental condition. Or where the most commonly folded state is only a meta-stable state, and there's a more stable conformation which the protein will convert to, if given a chanvce - amyloid fibrils being the most common example. These are refinements on the general principle. You don't need a rock solid folding funnel, you just need one "good enough" for the organisms' purpose.)

You can see some of this in the "de novo" protein designs that come out of labs like David Baker's. They're able to take a protein topology and use a computer to design a sequence "from scratch" which folds to that topology. But far from all of the sequences which their computer program spits out actually will fold. Only a small fraction of such designs will actually fold into a compact protein.

But one of the things that they've found which improves their success rate is to check the designs by "forward folding". That is, the computer spits out a design which it predicts will be a low-energy sequence for that structure. But just having a sequence which is predicted to be "low energy" isn't enough. As an additional step they run the sequence through a folding simulation to see if the sequence they designed also has a clear preference for the designed state. Roughly speaking, checking if there is a clear "folding funnel" which will drive the protein toward the desired folded state. By doing this subsequent computational check, they're able to greatly increase their success rate when the proteins are actually expressed.


How is a bacterial strain defined? When a species of bacteria is referred to by its strain, are they a clone of single founder or is a certain amount variation allowed?

In theory they're clones, but depending on the age of the strain(some strains are surprisingly old: ~40 years) there's variation inside strains.

The reverse is also true. Bacteria from a single species are isolated twice and named different things by different labs and the mistake can take years to even find, much less correct.


Do colour blind people see white? I know that white colour is perceived on excitation of red, blue and green cones simultaneously.

It is also said that a colour blind person doesn't see a particular colour and just perceives it as a shade of grey.

If their (for example all red) cones are affected, then how do they perceive white colour?

Clarification: Will a person with defect in red cones perceive white colour when green and blue colour only fall on his retina?

So, basically he will detect RBG and BG both as white.

If not then how will he be able to differentiate?

No not white or grey generally, it's a mix of other colors, they often have low resolution of a particular color.

Here's a page where you can mouse over a color wheel and see a version in color blind mode:
http://www.archimedes-lab.org/colorblindnesstest.html

The first type of cone is primarily sensitive to short wavelengths (blue), another to medium wavelengths (green) and one to long wavelengths (yellow). The yellow cone is usually referred to as the red cone. While its sensitivity peak lies in the yellow wavelength band, it is also quite sensitive to red. A single cone cannot detect color, as it provides only a scalar number indicating the total light energy it absorbs. For example, the red cone by itself cannot distinguish red from yellow, green or orange. Red is detected by a combination of high activation of the red cone, low activation of the green cone and no activation of the blue cone. This page has a very comprehensive graphs and a first hand account of Tritanomaly

Evolutionary gene mechanisms have a particular knack of varying vitally important organs and functions, arm length, walking gait, hair type, color, and colorblindness is perhaps an expression of high variance to a survival critical and modular organ which animals have a high variance in depending on their habitat and survival requirements.


Polar renal scarring in pyelonephritis? Why does infection and scarring occurs at poles in Vesicoureteric reflux but not in Obstructive pyelonephritis?

It is said in Robbins that, it is due to polar papillae being flattened or concave unlike convex lateral papillae, but why is it not the case in obstructive pyelonephritis?

Also why polar papillae are not convex?

It's more an issue of the extent of reflux than anything else. If you look at the data on scarring, you'll see that grade III and IV VUR present with lateral scarring as well. So, any pyelonephritis that is associated with gross dilation of the ureter and collecting system will give diffuse scarring. Mild dilation, you'll get scarring where the reverse flow goes first. I can't answer the question about why the reverse flow goes to the poles first. The authors of the paper I linked have their own speculation. Robbins has another. Neither have evidence on the mechanism.


What does phasing mean? What does phasing mean in genetics/informatics? I've heard that a phased file is a file that has genes separated by chromosome, but can someone give a concrete definition of what phasing actually means?

This refers to haplotype phase (aka gametic phase). This essentially means knowing which allele belongs to which copy of the chromosome, or alternatively, which alleles appear together on the same chromosome.

In short-read sequencing, for example, it is difficult to resolve the haplotype of two heterozygous SNPs if they have not been covered by the same read. If you observe A/a and B/b, you do not know whether you have AB + ab or aB + Ab. So you would say you do not know the phasing.

See the Wikipedia links for more information.


Why does scar tissue change color? I was wondering why, when you are cold, scar tissue turns bluish or purple while original skin stays the same color.

The only thing I can think of, is that maybe scar tissue gets less circulation than regular skin, so when it gets cold it restricts circulation.

The main mechanism behind the scar changing its color is the dilation of blood vessels within the scar tissue. The dilated vessels lead to the congestion of blood flow. The red blood cells moving more slowly leave more oxygen due to its diffusion to the tissue and the hemoglobin -- the oxygen holding protein -- changes its color from scarlet (bound to oxygen) to cyan (released/bound to CO2). Since scars are not covered by skin, the blood vessels are clearly visible here and you see this characteristic color.

The triggering mechanism here is cold that increases the energy barrier for many biochemical reactions, first of all those required for smooth muscle contraction.

Cold-induced vessel dilation (that can be seen, for example, on cheeks and extremities) with mild circulatory disturbances ultimately undergoes into so-called cold vessel paralysis when smooth muscles of blood vessel walls completely loose their ability to contract and are maximally dilated. The cyan color of the scar is usually seen at the very last stage, that can occur unexpectedly quickly because scars do not have any warmth insulation layer compared to the regions covered by skin.


How can a polar molecule pass through polar channels of proteins in the cell membrane? To transport a polar molecule through the nonpolar cell membrane, a protein with a polar channel is needed to allow it to diffuse. However, if the molecule is polar and the channel is polar, wouldn't the molecule just be attracted to the polar amino acids and "stick" on the inside of it?

I may be thinking of this totally incorrectly, so please bear with my ignorance!

Thanks in advance :)

The molecule won't "stick" to the polar amino-acids for at least three reasons :

The amino-acids might not all be on the same plan, so their is always a force pulling the molecules transiting trough the channel in one direction (in or out the cell)
When  a flux is established, the repulsion forces between the molecules will force them to go in a direction, meaning that a coming molecule will basically push the ones already engaged in the channel.
For an ion or a protein, the water molecules constituting the hydratation shell of the molecule can't always follow it into the channel, so the water molecules present at the end of the channel (entry and end being relative to the direction of the flux) will more or less pull it outside the channel, as it is thermodynamically more stable to have a shell.  The fact that water molecules are able or not to follow the molecule depends on the size of the channel.

It's worth noting that water is itself a polar molecule, and that it can selectively cross the membrane thanks to channels called aquaporins.


How many mega pixels does the eye have? What is the number of mega pixels available in the human eye? It seems that newer camera models continuously keep increasing their pixel count. However, they never seem to be capable of reproducing what the eyes can see.

Short answer
The total number of photoreceptors ('pixels') in the human retina is 63 million. Approximately 3 million of them transmit focused, color-coded information.

Background
In essence, each photoreceptor on the retina acts as a photosensitive sensor. We have rods and cones in our retinae. Rods confer gray scale vision, while cones are responsible for color vision.

The raw average tally of rods in the human retina is 60 million, and cones count a little over 3 million (Jonas et al, 1992). Hence, we could conclude we have 63 megapixels per eye available.

However, this does not mean that 63 million pixels are sent off to the brain. Instead, just as with a JPG image, it's instantly reduced in size even before the information leaves the retina.

Most importantly, rods are specialized for scotopic (night) vision and 10 to 30 rods connect to a single bipolar cell (Kolb, 2011). Hence, this feat only reduces the number of 'rod pixels' to about 3 million. Cones generally synapse onto a single bipolar. Hence, 6 megapixels leave the retina approximately.

The retinal image is generally focused onto the fovea, which is the central 18o of the total ~160o that is covered by a retina (Fig. 1). The remainder of the retina may receive a blurred image projection.

Fig. 1. Image focussing through accommodation on the retina. Source: Health Problem and Solutions

The fovea is densely packed with cones and contains nearly all of them (fig. 2).

Fig. 2. Distribution of rods and cones in human. Source: (Kolb, 2011)

Hence, the focused part of the image may be encoded by as little as 3 million cones. Since rods don't provide color information, it can be concluded that focused, color-coded information is conveyed by 3 million photoreceptors per retina.

Ultimately, however, it is important to note that the brain fills in missing gaps. For example, the optic disc, i.e. the point where the optic nerve leaves the eye, measures about 1.5 mm in diameter (Kolb, 2011). Given that the total diameter of the retina is about 30-40 mm this is quite a big blind spot. The brain simply fills in that gap by estimating what supposed to be there. In fact, many people with degenerative diseases of the retina don't even notice their deficits until they start bumping into objects that they did not notice. However, they do not see black holes, but instead their brain has been filling in the gaps with the information available in the remaining image, just like it does with the optic disc in normally-seeing people.

References
- Jonas et al, Graefes Arch Clin Exp Ophthalmol (1992); 230(6):505-10
- Kolb, Webvision, The Organization of the Retina and Visual System, Simple Anatomy of the Retina (2011)
- Kolb, Webvision, The Organization of the Retina and Visual System,
Circuitry for Rod Signals Through The Retina (2011)


In which direction plants' root grow in weightlessness? As far as I know, roots of plants grow to the direction of Earth's gravity - this is called gravitropism.

But what happens if plants are in space? Are they able to perceive gravity in state of weightlessness? Either way, where do they grow their roots in those circumstances?

Note: this question may fit better either to Space.SE or to Astronomy.SE, but I was not sure about it.

Astronomers on the International space station have done exactly that and grown Arabidopsis Thaliana in space. You can read the whole article here.
Plant roots apparently grow away from the seed exactly like on earth seeking out nutrients.


By what mechanism do our nerves lengthen as people get taller? How do nerves get longer as kids grow taller?  I searched for an answer but I can only find information on the formation of nerves in embryos.

They grow

Nerve axons can grow rather quickly as long as the body of the cell is intact, quickly as in the mm/day range. This is also the basis of how nerves can regenerate.


Is warmth/temperature sensed linearly or on a different scale? I understand that the atmospheric temperature is sensed relative to external body temperature. However, is the sensation of warmth registered linearly, or is it on a logarithmic scale, similar to sound that works on the Decibel scale? Or is it on another scale entirely?

The human sensation of warmth is not the measurement of static temperature.  Humans detect the rate at which heat is leaving (or entering) their body.  For instance, if you are sitting in your 0 degree car in the morning, your hand in the open air will feels warmer than your hand touching the steering wheel, despite them both being at 0 degrees.
The reason is that heat conduction from your hand to the steering wheel is much faster than convective heat transfer from the air.  So you feel "colder" touching the steering wheel, but it's really that you're losing heat faster.
Scholarpedia's article on temperature receptors:
http://www.scholarpedia.org/article/Thermal_touch#Temperature_receptors

...Cold receptors respond to decreases in skin temperature over a range
of 5-43 °C...
...In contrast, warm receptors signal that skin temperature has
increased...


In terms of differentiation, how many generations of asexual reproduction, will usually be equal to 1 of sexual? As far as I understand, in sexual reproduction, there is a mix of 50/50 genes from parents. In how many generations of asexual reproduction, will offspring reach differentiation level that of sexual one ?

Welcome to Biology.SE!
Clarification of the question
It is unclear what you mean by differentiation? I will assume that the question is

For what value of $n$. is the number of pairwise differences between any two siblings under sexual reproduction is equal to the number of pairwise differences between any two $n^{th}$ cousins under asexual reproduction?

Answer
The answer to this question mainly depend on (1) the mutation rate and (2) the amount of genetic variation present in the sexual population (which itself is a function of the mutation rate).
Assuming a panmictic population of constant size $N$, assuming equal sex-ratio and non-overlapping generation (and a few other assumptions), we can make some estimations. Let's assume that the sexual and asexual populations that we are comparing have the same mutation rate $\mu$.
Sexual population
Using coalescent theory, one can show that the expected number of pairwise difference between any two individual in a sexual population is $4 N \mu$. It would be off-topic to explain why this is true. I let you open a population genetics book and/or open a different post.
Asexual population
Assuming an infinite site model (just like coalescent theory does), the number of pairwise differences between $n^{th}$ cousins is $2 n \mu$.
Comparison
Let's set the equation
$$2 n \mu = 4 N \mu$$
and solve for $n$, we get
$$n = 2 N$$
In words, $2N$ cousins in asexual populations have the same number of pairwise differences (on average) than two sibling in a sexual population of size $N$.
Remarks
Please note that the conclusion is drawn from important (but common) assumptions. Note also that drawing conclusions from the above calculation such as "sex helps retain genetic diversity" would be wrong, as we are comparing sibling to $n^{th}$ cousins and not randomly chosen individuals in the population.


What regulates production of first transcription factors during development? In my biochemistry class, we learned that transcription factors regulate the transcription of genes. However, transcription factors are also coded by genes, so what activates the transcription of genes that code for the first transcription factors during development?

The first transcription factors for the first transcription after fertilization are already present in the ovum (egg) before it is fertilized.

Generally, all the machinery needed for transcription, translation, and the rest of the many necessary cellular functions are already present in a cell before it divides and develops.  This chain of dependency goes back eons of time to the origin of cells and the very origin of life.


Are there any known mutual symbiotic relationships that has more than two agents? We are all familiar with the examples of symbiotic relationships in nature consisting of two agents, like lichen or the co-evolvement between certain birds and flowering plants.

Do we know of any mutually symbiotic relationships that has three of a even higher number of agents?

Edit: To make a implicit distinction clear, let's specify that the agents in question have distinctive and fully interdependent roles in the symbiosis. In contrast to a scenario where a range of bird species might co-evolve for a single specific flower and have the same role as pollinators in the symbiosis.

This image represents my current models in thinking about this:

The type I'm searching for here is mainly the "3-agent symbiosis", but the bidirectional one is of interest as well.

I think what you are asking for is "Multiple Mutualism". Normally,

Most of the known cases of multiple mutualism involve relationships in
which two of the partners are at the same organizational level—usually
two bacteria that might be interacting directly—but are both essential
for the survival of the host
— Entente cordiale: Multiple symbiosis illustrates the intricate interconnectivity of nature -Philip Hunter

For example, the glassy-winged sharpshooter (Homalodisca coagulata) primarily feeds on xylem-fluid which is low on organic nutrients…so it depends on 2 bacteria, Baumannia cicadellinicola and Sulcia muelleri. The sharpshooter provides these with raw carbon skeletons present in the xylem fluid, and those bacteria in return synthesizes vitamins, essential amino acids, etc. For more detailed study, see Wu et al, 2006.
However, there are also examples of three-way mutualistic symbioses in which all the partners are at different organizational levels. One known case involving a virus, a bacterium and an insect, see Moran NA, Degnan PH, Santos SR, Dunbar HE, Ochman H (2005) The players in a mutualistic symbiosis: insects, bacteria, viruses, and virulence genes. Proc Natl Acad Sci USA 102: 16919–16926
Anyway, the essence as stated by Andreas Brune, Professor of Biogeochemistry at the Max Planck Institute for Terrestrial Microbiology in Marburg, Germany:

Multiple symbiosis is probably more widespread than we think, especially in view of the symbiotic systems involving different organizational levels, for example between bacterium, nematode and insect, or bacterium, protozoan and insect.


Why is freezing bacteria not a problem? I have a follow up question to this question: Does freezing microorganisms such as probiotics kill them?

If freezing bacteria kills some of them, then you are effectively putting selective pressure on bacteria when you freeze them (the bacteria more resistant to low temperatures survive, bacteria less resistant die). Why then is it a good idea to freeze bacteria?

The ice crystals that form tear and shear the bacterial cells, unless you add a cryoprotectant (for example, glycerol) to the cells beforehand.

Remember, when water freezes its volume increases.  This is why a closed soft drink can that you put into your freezer to chill faster, will burst if you leave it in until the contents are frozen.

Exactly the same thing happens to cells (animal cells, plant cells, yeast cells, etc.) if they are frozen without a cryoprotectant.


What is the purpose of ultrahydrophobicity in lotus flower leaves? I read about the lotus effect on wikipedia, but I haven't found an explanation as to why droplets collecting dirt on the surface of a leaf is helpful to the flower's survival.

Lotus benefits from hydrophobicity for that it decreases the likeliness of being infected by pathogens (found in "dirt") and increase the ability to perform photosynthesis.

According to a study by Darmanin and Guittard, the plants (not only lotus) with ultraphobicity benefits from these structure for :

  self cleaning

and

  these structures are able to stabilize the presence of air underwater and be submerged for several weeks

Let's talk a little about the second part : having a good access to gas is vital for plants to do photosynthesis. In an environment which is very wet (like the one the lotus lives in), it is better to be dry to maximise air/plant surface area.

Now, about the self cleaning.
First, lotus lives in backwater or muddy environment
In this study by W. Barthlott and C. Neinhuis, it is said that big particles can occlude stomas, the small "holes" that allows the plant to breath.
Wet environment is ideal for bacterial/fungal growth and different kind of disease. Unclean water could also block light and make photosynthesis less efficient.

  Again, wettability
  is important for the adhesion of microorganisms to
  leaf surfaces. In addition, on waterrepellent
  surfaces, spores and conidia are deprived of the water necessary for germination. Therefore, the epicuticular
  wax crystalloids and their physical properties
  may be regarded as the first line of defense against
  pathogens.


Why do skin and nail go blue in cyanosis? I have learned that Cyanosis presents with blue skin and nails. What is the reason for the blue coloration of the skin and nails? Why wont the skin and nails turn another color in the visible spectrum such as green for instance? How is this disease diagnosed?

The skin appears blue due to the diffraction of light through the skin. Blood is either bright red (sufficiently oxygenated) or dark red. "The blue appearance of surface veins is caused mostly by the scattering of blue light away from the outside of venous tissue if the vein is at 0.5 mm deep or more. Veins and arteries appear similar when skin is removed and are seen directly" 1. The color of blood is due to the difference in color between deoxyhemoglobin and oxyhemoglobin.

Let's consider the "blue fugates" of Kentucky. The ancestors of this family have different shades of blue skin tones. Dr. Madison Cawein discovered that the family had a high concentration of FE$^{3+}$ brown methemoglobin. This form is useless to the body so the enzyme diaphorase reduces the methemoglobin to FE$^{2+}$ (hemoglobin that can carry oxygen) [2].

Basically the skin color comes down to light diffraction not the blood changing from red to blue.

Cyanosis is the appearance of a blue or purple coloration of the skin or mucous membranes due to the tissues near the skin surface having low oxygen saturation [3]. Cyanosis is a clinical sign diagnosed visually. Cyanosis is an indication for blood gas testing.

References:

http://en.wikipedia.org/wiki/Venous_blood
http://courses.chem.indiana.edu/c122/documents/Experiment10_BloodandHemoglobin.pdf
http://en.wikipedia.org/wiki/Cyanosis
http://www.webmd.com/lung/arterial-blood-gases


What is the name of the plant with the down-falling light purple leaves? I've seen this flower in Scotland in August 2015:

What is the name of that flower?

To help people google it:

The plant has light purple leaves with some white spots. On those white spots are dark purple points. It is sometimes quite high (about 1.70m I guess). The bloom points downwards.

It is a Digitalis purpurea

From the wikipedia page:


What tool can I use to align multiple protein sequences to one reference sequence? I have a protein of interest which is ~300 amino acids in length. I also have around 40 short sequences (all 9 amino acids in length); these are all very different from each other. I would like to perform multiple pairwise alignments to see if these sequences match up with (or have high sequence identity similarity) any areas in the protein of interest.

Since the short 9-a.a. sequences are very heterogeneous, they will have similarities in different regions of the protein of interest. I would like to know if it is possible to perform the alignments for all 40 sequences in one step, rather than using COBALT 40 times (and checking each of the short sequences against the reference sequence individually).

Please let me know if the description of my problem is not clear enough, I would appreciate any help in identifying a way to do this.

What you want to perform is commonly called a multiple sequence alignment.  As @Wayne_Yux said, the first step is to put all of your protein sequences in a single fasta file.  You can then use one of several online tools to apply different alignment algorithms to your protein sequence set.

A popular sequence alignment algorithm is Clustal, which progressively builds a multiple sequence alignment from all of the pairwise alignments.  genome.jp hosts a web-based alignment tool that allows you to choose from Clustal and other alignment types (1).  For alignment of many small sequences to a single larger sequence, you should use the "SLOW/ACCURATE" option (2).  After you upload your fasta (3) and execute multiple alignment (4), an aln file will be generated which you can download (5).

You can then take this aln file and upload it to a different tool that allows you to visualize alignments.  Personally, I like ESPript, which gives color-coded alignments in pdf or image formats.  Because you want to compare many sequences, it will probably be necessary to change the "Alignments output layout" parameters, e.g. change "Gap between blocks" to a smaller number to fit all of your sequences in one frame.


Liver - Regeneration in Cirrhosis Liver is the most resilient of the human organ (on par with or next to skin). A very interesting experiment on liver regeneration is here. Even if two-thirds of the liver is removed, the remaining liver would regenerate to recover the full volume and function.

Cirrhosis of liver is a condition where excessive fibrosis occurs shattering the architecture of the liver. The blood vessels and the parenchymal cells of the liver get constricted into narrow spaces causing portal hypertension and fall in the Liver Function Test parameters (albumin level falls, clotting factors fall leading to spontaneous bleeding, bilirubin level rises causing jaundice, etc...). It can be either congenital or acquired. Cirrhosis is considered an end stage liver disease.

In the end stages of cirrhosis the only treatment option available is liver transplantation.

Question:

Why is partial hepatectomy (removal of part of liver) not a treatment option for end stage liver disease (cirrhosis of the acquired variety)?

The answer lies in the question. Liver cirrhosis constrains hepatocytes into small fibrous spaces limiting regeneration, hence the nodular pattern.
However,fibrous degeneration occurs in specific patterns. It can be located mostly around portal regions (centrolobular pattern) or diffusely through the whole lobule.

So basically, it is all good that hepatocytes can regenerate, but the limiting factor is not that. It is the structural impairment of the liver lobules and drainage system that will impair regeneration.

Moreover, most cirrhotic patients could not tolerate halving of their residual hepatic function. Not to mention the extensive surgery required. It would kill them swiftly.


How come all my family have brown eyes and I have blue eyes? My whole family tree up to my grandparents have brown eyes,

I have blue eyes, how come?

I don't know if it matters but I have not received enough oxygen at birth, doctors said it's probably the reason I'm left handed while my most of my family is right handed

The eye color follow quite well mendelian inheritance rules...
Probably your parents are heterozygote recessive for the blue color, hence the children have 25% of probability of having blue eyes.

Let's say color of the eyes has 2 alleles "BLACK" for the dark eyes and "blue" for the light eyes. Your parents are probably both BLACK-blue, BLACK-blue. They show the dark eyes because that allele is dominant over the blue one.
During recombination all the possible combination can come out:

BLACK x BLACK=25% resulting color=dark
BLACK x blue=25% resulting color=dark
blue x BLACK=25% resulting color=dark
blue x blue=25% resulting color=light

Check out the wiki page about mendelian rules of inheritance if you wanna know more!!
Of course in realty the situation is much more complicated, however you can still approximate the results to mendelian rules...

have fun!!


Identification of this bug or insect I found this bug dead in my house in Mississauga, ON, Canada.

I didn't have a ruler around so a regular toothpick was used to show the size.

I'm thinking it's a pill bug but I want to make sure.

Yes, that is a pillbug, or "roly-poly", Subphylum, Crustacea, class Malacostraca, family Armadillidiidae.  https://en.wikipedia.org/wiki/Armadillidiidae


Measuring luminescence in a fluorescence plate reader We're considering organizing some interlaboratory work on calibrating luminescence reporters (e.g., luciferase), and one of the key questions I don't know the answer to is whether most plate readers can measure luminescence or not.
From a first principles perspective, any fluorescence plate reader ought to be able to measure luminescence as well - just don't turn on the excitation light source. Thus, I would expect that a typical fluorescence reader should also be able to measure luminescence.
On the other hand, searching online, I am swamped by manufacturers eager to sell me specialized luminescence readers that emphasize their sensitivity, which leads me to think that maybe typical fluorescence plate readers can't measure luminescence.
My question, then, is this: should I expect that a typical current fluorescence plate reader will also be able to measure luminescence, or is this a much more specialized capability?

I am René Inckemann and  I am PhD student at the Max Planck Institute in Marburg, Germany. In my PhD I am using luminescence on a regular basis and I was also responsible to organize some of our Platereaders.
So therefore I can tell you that you need a Platereader which is able to measure luminescence and you can not simply take a fluorescence platereader. The hardware for measuring luminescence and fluorescence is different.
However many Platereader models in these days already come with both options for the hardware, which means that you can measure luminescence and fluorescence in the same device. You just have to check your platereader model if it is capable of measuring luminescence.So you don't need a seperate platereader just for luminescence, but you need one, which has the luminescence addon installed.
Regarding your idea for normalizing luminescence, I also have strong interest in that and we have already started working on that. Maybe we can exchange ideas at some point?


Fruit-bearing tree identification Just moved into a new house in Puerto Rico and I found this tree in the back garden. Can anyone tell me what tree this is, and whether its fruit is edible?

I think this is a Canistel (Pouteria campechiana):

The fruit are yellow when when ripe, but the form and also the leaves look very similar. The fruit are edible raw, you can find some more information here.


What other cognitive behaviors in bees, outside of navigation, are affect by neonicotinoids It is conclusive that neonicotinoids alter navigation in bees when locating food sources. http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0091364

But if so, shouldn't cognition also be affected? And if it is affected, then wouldn't the effect on the hive be even more pronounced due to inaccurate bee dances and an overall delay/inability in finding food source? Shouldn't this be conclusive in explaining neonicotinoids to be a contributor to colony collapse disorder?

It is assumed that this effect of locomotive behavior IS an effect on cognition (1-4). Navigation requires snapshot memory, learning, and attention (2-4). You asked if this effect of neonicotinoids on cognition manifests itself through other vital behaviors. The short answer, yes. Specifically neonicotinoids are shown to effect mating, queen behavior, and foraging short and long distance (5-7). It is suggestive that neonicotinoids are a contributing factor in collapsing colonies with both meta analysis and direct evidence of effects on behavior (5-8). I think you are more questioning why people have not done anything about this issue or more definitive in their action against colony collapse. That is more of a political issue. Since the pesticide does not have as many human health effects at levels that cause bee collapse, the policies to resolve this issue are not as clear. EPA has discussed making restrictions regarding use the use of neonicotinoids, but they will still be used. However, they have actually been banned in France due to these effects. Hope that answered your question!

Sources

Honey Bee Behaviors  doi:10.1016/S1364-6613(00)01601-6
Bee Navigation and Memory          doi:10.1006/anbe.1997.0574
Learning and Memory in Bees doi: 1146/annurev.ne.19.030196.002115
Behavioral Neuroscience ISBN: 978-0-87893-092-0
Bees, neonicotinoids, and Dance Behavior Effects doi: 10.1242/jeb.068718
Bees, neonicotinoids, and Foraging Behavior Effects  DOI: 10.1046/j.1365-2435.2000.00443.x
Queen and Colony Effects   DOI: 10.1126/science.1215025
Colony Collapse meta study DOI: 10.1007/s10646-010-0566-0