Heterochromatin binding sites position information I am working on a project and I'm trying to find data on the position of genes and heterochromatin binding sites such as HP1 in Drosophila melanogaster. Is this information available for the DGRP lines? Would I be able to measure the distance between a gene and its nearest binding site from such data?

Have a look at these ChIP-seq data for HP1 in Drosophila: 1, 2 and 3. From ChIP-seq data you can find the distance between the TFBS peaks and the TSS of the gene.

You can also look for nucleosome positioning and DNAse hypersensitvity regions; for the former, I am sure that data is available for Drosophila.


How do birds deal with their eyes drying out at high speeds? My eyes tear up when cycling at 15 mph, which is nothing compared to bird airspeeds.

Do birds continuously produce lots of tears and blink a lot, or do the eyes self-moisturize from the inside without need of blinking, or are their eye surfaces just dry most of the time and they don't mind?

Birds have a body part known as the nicitating membrane otherwise known as the "third eyelid". This part has become vestigial in humans, where it remains as the plica semilunaris.

This image of a masked lapwing clearly shows its nicitating membrane in action, where it covers the eye in a horizontal motion. This is analogous to blinking in humans, and the membrane moisturises the eye and removes debris while the bird is in flight.

This paper explains in detail how the peregrine falcon (the world's fastest bird) clears and moisturises its eyes when diving at speeds of over 300km/h.


Is there a significant difference in sedentary calorie-burn between a thinker and non-thinker? I've read that, on average, a sedentary female burns between 1,600 - 2,000 calories and a sedentary male burns between 2,000 and 2,500 calories. I've also read that the brain itself burns quite a few of these.

Let's say two people are exactly the same, and have the exact same (sedentary) lifestyle—except one of them often does intense mathematics. Is there a significant difference in calorie burn?

If so, how much is it?

Is there a significant difference in calorie burn?

No.

The brain, while only making up 2% of our body weight, accounts for ~20% of our energy use at rest. That's because the brain, being critical for survival, is a very high-maintenance organ. At rest, the membrane potentials of all neurons - firing or at "rest" - need to be controlled/maintained.

Of all the energy used by the brain, about 25% of it is needed for signal-independent function (protein synthesis, phospholipid turnover, etc.) Furthermore, there are two types of cells in the brain: neurons and glial cells. The glial cells (about 30%) use from 17 to 40% of the energy depending on whose estimates you use. The rest is needed (by neurons) for signal-related processes - maintaining/restoring cell membrane potential, etc. - only a fraction of which is used for thinking.

The brain never rests - it is highly active even in sleep, with both excitatory and inhibitory activities needing energy. Higher mental functions (e.g. doing math problems) only shifts the areas of highest activity a little bit compared to all the activity that occurs without our awareness of it.

Finally, if we could measure glucose consumption of the entire brain while daydreaming vs. doing math, we might be able to answer that question, but the truth is, brain activity doesn't occur in isolation. Someone doing challenging math problems is using more energy in other areas of the body as well; respiration rate, heart rate, muscle tension, etc. varies with the stress of the challenge, so glucose levels alone can't be relied upon (in fact, stress would increase our body's production of glucose) to indicate energy expenditure.

The end result is that in isolation, rigorous mental activity (which can be maintained only for a relatively short duration without fatigue, so it occurs in bursts) expends very little of the total energy the brain uses.

  A common view equates concentrated mental effort with mental work, and it is fashionable to attribute a high demand for mental effort to the process of problem solving in mathematics. Nevertheless, there appears to be no increased energy utilization by the brain during such processes. From resting levels, total cerebral blood flow and oxygen consumption remain unchanged during the exertion of the mental effort required to solve complex arithmetical problems.

Cerebral Metabolic Rate in Various Physiological States
Does Thinking Really Hard Burn More Calories?


Why do mosquitoes hover over our heads? So I play soccer in evening at a nearby park. I noticed many times that after the game and even during it many mosquitoes hover over some of us. They sort of form a structure like a tornado.
The more the one is sweaty, the more the mosquitoes.
What can  be the possible reason?

In many mosquito species (and other diptera) males make swarm to attract the females. The vast majority of individuals in swarms are therefore males (but there are always a number of females in them as well).

These swarms are a type of lek mating which is also very common in midges (thanks to @arboviral for this info). Are you sure those you see are mosquitoes and not midges?

In order to produce these swarms, they typically hover a recognizable element in nature to swarm around, such as a small tree, a bush, a big stone, etc... On a soccer field, players are a distinct element to swarm over!

Of course, females are attracted to $CO_2$, warm bodies and odour of sweat but this is IMHO likely not an important factor causing the swarms you see. See @Kiny's answer on the subject.

References:

Takken et al. 2006
Yuval et al. 1994

  Also, why is this in the evening?

Mosquitoes typically start mating at the beginning of the evening and then forage during the night. However, this varies quite a bit from species to species. Aedes egypti for example, forage day and night while species of the genus Culex forage only for a few hours after the sun has set.

Such variation in the timing of mating behaviour can lead to (pre-zygotic) reproductive isolation between lineages. Potential reasons for being active at specific times and not others include temperature management, easier to parasite for females during the night (only females bite), timing with flowers (as both males and females feed on nectar). I would not be able to argue for why a specific species shifted its circadian rhythm in a specific way though.


What selective factors drove the evolution of lactose in lactation? As far as I can determine, lactose, and the monosaccharide galactose have few biological uses outside of mammalian lactation.  It not only required enzymes for its production, but enzymes in offspring for its digestion, suggesting that it serves some specific purpose.  Yet intuitively, it seems like it would have been significantly easier to just concentrate glucose from the blood or generate a disaccharide readily found in the diet like sucrose, for which digestive enzymes already existed.

What drove the evolution of lactose in mammalian lactation?

As it happens someone has just published a theory about this. To save you following the link, I reproduce the abstract below.

I must admit that I had never realised that lactose is synthesised within the organelles of the secretory pathway (β4-galactosyltransferase is a Golgi enzyme and α-lactalbumin is, of course, a whey protein, so is in transit through the pathway). This may go part of the way to answering your question: by having a disaccharide that is made within the Golgi, the cells of the mammary gland will effectively partition their glucose metabolism between the cytoplasm and that destined for secretion as lactose (transported into the Golgi lumen).

  Mammalian milk or colostrum contains up to 10% of carbohydrate, of which free lactose usually constitutes more than 80%. Lactose is synthesized within lactating mammary glands from uridine diphosphate galactose (UDP-Gal) and glucose by a transgalactosylation catalysed by a complex of β4-galactosyltransferase and α-lactalbumin (α-LA). α-LA is believed to have evolved from C-type lysozyme. Mammalian milk or colostrum usually contains a variety of oligosaccharides in addition to free lactose. Each oligosaccharide has a lactose unit at its reducing end; this unit acts as a precursor that is essential for its biosynthesis. It is generally believed that milk oligosaccharides act as prebiotics and also as receptor analogues that act as anti-infection factors. We propose the following hypothesis. The proto-lacteal secretions of the primitive mammary glands of the common ancestor of mammals contained fat and protein including lysozyme, but no lactose or oligosaccharides because of the absence of α-LA. When α-LA first appeared as a result of its evolution from lysozyme, its content within the lactating mammary glands was low and lactose was therefore synthesized at a slow rate. Because of the presence of glycosyltransferases, almost all of the nascent lactose was utilized for the biosynthesis of oligosaccharides. The predominant saccharides in the proto-lacteal secretions or primitive milk produced by this common ancestor were therefore oligosaccharides rather than free lactose. Subsequent to this initial period, the oligosaccharides began to serve as anti-infection factors. They were then recruited as a significant energy source for the neonate, which was achieved by an increase in the synthesis of α-LA. This produced a concomitant increase in the concentration of lactose in the milk, and lactose therefore became an important energy source for most eutherians, whereas oligosaccharides continued to serve mainly as anti-microbial agents. Lactose, in addition, began to act as an osmoregulatory molecule, controlling the milk volume. Studies on the chemical structures of the milk oligosaccharides of a variety of mammalian species suggest that human milk or colostrum is unique in that oligosaccharides containing lacto-N-biose I (LNB) (Gal(β1 → 3)GlcNAc, type I) predominate over those containing N-acetyllactosamine (Gal(β1 → 4)GlcNAc, type II), whereas in other species only type II oligosaccharides are found or else they predominate over type I oligosaccharides. It can be hypothesized that this feature may have a selective advantage in that it may promote the growth of beneficial colonic bacteria, Bifidobacteria, in the human infant colon.


I'm trying to identify this salamander-looking creature I found in my house today in Coos Bay, Oregon. It is about 2" long. What is it? This is about 2" long. It is white on its underside and looks like a small salamander, except for it being white underneath. It is about 1/8th inch wide.

That is definitely a lizard, not a salamander. Salamanders don't have scales. It is a Northern Alligator lizard, Elgaria coerulea, in the family Anguidae.
https://www.inaturalist.org/check_lists/9307-Reptiles-of-Oregon
https://en.wikipedia.org/wiki/Northern_alligator_lizard


Camouflage grasshopper identification I came across the following grasshopper this afternoon while walking to my car. It was initially resting amongst some fallen tree leaves, but as I got closer to my car I must have startled it, as it then ran to the tree, and is also how I noticed it.

It was calm enough for me to temporarily hold it in a cut-in-half water bottle, and I was able to take a few more pictures, and record a brief video. Afterwards, I released the grasshopper back into the grass and it promptly flew away. :)

When searching for its species, I was only able to find a dessert grasshopper, Trimerotropis pallidipennis, but I live in KY, and not out west, so I don't think that's it.

Can someone ID this for me please?

Location: Central KY, USA.

You've found a Dissosteira carolina or carolina locust.
I'm not completely sure, but I think this is a male.
They are quite common in North America.

idtools.org/id/grasshoppers/factsheet Dissosteira carolina
uwyo.edu: Dissosteira carolina


What's the relation between Kinase, Phosphatase and ATPase, GTPase (GTP/ATP)? I'm wondering what's the relationship between Kinase, Phosphatase, ATPase (ATP) and GTPase (GTP).

For example, when reading online the impression is created that ATPase is a type of Kinase (?). But I can't find any explicit information about it.

Enzyme names usually refer to the substrate of the enzyme, i.e. the molecule or chemical group that the enzyme targets and then removes or modifies.

Kinases are enzymes that add phosphate groups, usually to other proteins. One of the older enzyme classes that have a more "creative" name. Phosphatases remove phosphate groups.

In signalling pathways, kinases often transduce signals and phosphatases shut them down when their job is finished.

ATPases and GTPases target ATP and GTP respectively and catalyse the removal of one phosphate group by hydrolysis, the product being ADP or GDP. This makes them a type of phosphatase.

Many proteins are ATP/GTPases but have different names because there's a more significant function to name them after. Usually the ATP/GTPase function serves to deliver energy for the main function. Your impression might be caused by an enzyme which is both a kinase and an ATPase because it transfers phosphate groups from ATP to a target protein.

Enzymes that target ADP/GDP and add another phosphate group are called ATP/GTP synthases (rather than kinases).


What does DNA taste like? I've seen plenty of speculation online, but does anyone know of a scientific study or have a definitive argument?

I'm thinking probably not sweet, because the deoxyribose sugar is bound in the structure of the helix. Salty, due to group I counterions? Bitter due to the alkaline phosphate groups? I'm guessing not sour, because despite the name nucleic acids are in their conjugate base form at physiological pH. I've read some nucleotides can activate the umami/savory taste, would this be significant?

I am aware essentially everything we eat contains DNA, but I'm interested in the taste of DNA itself, pure/isolated if necessary you like.

Youtube chemist NileRed chemically extracted DNA from strawberries in this video, he also tastes it if I remember correctly: https://www.youtube.com/watch?v=araeHtN_3Lk

TL;DW: He gets the DNA from the strawberries and says it has a slimy texture as it isn't soluble, and it tastes salty more than anything. Note though that this could be from leftover reactants from the reaction, so take this with a grain of salt.


How to reduce/eliminate cell clumping in suspension CHO cells, without using an anti clumping agent? what is the best way to eliminate clumping suspension cells used for transfection. Anti clumping agents interfere transfection and hence can't be used. Though maintaining the cell density low helps, but doesn't help in the long run.

After looking around for a bit, I came across a few potential solutions however they are not a definitive answer to your question and requires testing under your experimental conditions to see which works best.

This page contained one excellent suggestion and that is to select for cells that do not clump during the passage, by pooling the cells in 15ml of media in a tube and letting the clumped cells to settle down by gravity for 5 minutes and afterwards taking the top 1ml and passaging it and after 20 passages using the exact same technique, you should be able to get single cell suspension. The main caveat is the heavy selection for non-clumped cells, which might harbour certain properties that might be undesirable for the procedure you are interested in so it might be nice to do some RNA expression profiling to observe the differences and perhaps even publish it! Amongst the suggestions on this page included using different concentrations of Mn2+, Mg2+, and Ca2+ in your (custom?) media since cell adhesion is regulated by integrins, cadherins, and selections and in general, Mn2+ increases ligand affinity, Mg2+ promotes adhesion to cells, and Ca2+ decreases cell adhesion as referened here. You can also try heparin, as tested by this paper on CHO cells and it impotent to note that in the study, heparin did not reducing cell growth, antibody secretion, and antigen-binding activity although I'm unsure as to whether heparin would be classified as an anti-clumping agent and whether it interferes with the ability of the cells to get transfected but that can be simple tested by a GFP transfection and looking at the transfection efficiency of the heparin treated and control cells treated with whatever heparin is dissolved in.


Would expression of GroEL and GroES in erythrocytes be a potentially effective therapy for sickle cell disease? Would expression of GroEL and GroES in erythrocytes be a potentially effective therapeutic strategy for sickle cell disease? Why or why not?

GroEL and GroES are multiprotein chaperonin complexes: Not so easy to ectopically express
Erythrocytes do not have nucleus: you cannot stably express anything in mature erythrocytes.
If your aim is to do a stable gene expression (which would require genomic integration), the better way is to do a gene therapy: culture haematopoetic stem cells, Correct the mutation by homologous recombination. Put the cells back into the bone marrow.


In a Sanger sequencing, what would be happen if different DNA sequence binds to same primer? And how this situation avoided if problematic? Sanger's PCR chain-termination sequencing, by its theory, is a simple method to sequence DNA from organisms. But what will happen if there are 2 allelic DNA with same primer binding site, but variations in some-other part?

My question is; 1. Is such overlap practically happens? 2. If it happens, then what problem it creates? (or does it create any problem at all); and 3. if it is problematic, then what techniques used to avoid or reduce such noise?

Yes, this can happen if you are not checking your primers against the reference sequences.
Your PCR is done from two different pieces of DNA leading to two sets of chain-terminated fluorescence marked DNA. This leads to superimposed sequences, which looks like this and where you cannot differentiate, which sequence belongs to which strain (image taken from here):

It is problematic, the solution is to design new primers (which are located slightly outside the old target sequence) which only bind to one specific sequence. You cannot purify only one product, as you cannot discriminate between the two.


DNA methylation and genome size Is there any relationship between DNA methylation as a level of stability to epigenetic states and genome size? For example, it is claimed that DNA methylation is not required for epigenetic stability in Drosophila melanogaster and yeast, both genomes much smaller than mammalian or plant genomes. Could it be that DNA methylation is needed to help activate/repress certain genomic regions on top of other epigenomic marks when the genome is so vast that there is a need for an extra level of marking? Is there any evidence along those lines?

Is there any relationship between DNA methylation as a level of
  stability to epigenetic states and genome size?

I would say yes, because methylation is used to disable genes in differentiated cells. Disabled genes in differentiated cells generally need to stay disabled to maintain normal behavior for the cell type. Larger genomes usually encode more different types of cells.

  it is claimed that DNA methylation is not required for epigenetic
  stability in Drosophila melanogaster and yeast, both genomes much
  smaller than mammalian or plant genomes.

According to my book (S377 molecular and cell biology, book 2, p140) Drosphila don't need methylation because they perform transcriptional regulation by persistent chromatin remodelling instead. Yeast being single celled would have less need for this type of control.

  Could it be that DNA methylation is needed to help activate/repress certain genomic regions on top of other epigenomic marks when the genome is so vast that there is a need for an extra level of marking?

It is used as a repressor because it inhibits  hydrogen bonding of transcription factors and the like. I have not heard of it functioning as an activator.

There are also other uses for methylation, for example  newly synthesized DNA is hemimethylated - where the parent strand is methylated and the child one not. From this it can be determined which is the parent strand during DNA repair.


Photosynthesis immature fruits Do immature fruits perform photosynthesis? Yes they have chlorophyll bodies. But do they have stomata through which they can absorb carbondioxide like the green leaves? Sincerely Ulrik

Yes.  Both fruits and seeds often possess stomata as well as chloroplasts, which have been shown to be quite important in many cases for seed and fruit development.  It makes sense when you think about it.  If these vital components of the plant can make some of their own energy, rather than relying entirely on sugar reserves produced elsewhere (especially given how much sugar your average fruit has to produce), this would be a vastly more efficient system.  If you are interested in a more detailed look at fruit and seed stomata, the following paper should make for a good starting point:

https://www.jstor.org/stable/2442508?seq=1#page_scan_tab_contents

The authors of this paper conducted an in depth investigation of the structure and functions of the fruit and seed stomata present in a number of species within the Eschscholzia genus.  It's an interesting read.


A limit to birds affinity for high vantage points Birds seem to have a natural affinity for high vantage points, including power wires, the tops of trees, and the sides and tops of buildings.

However I presume the top of the Burj Khalifa is not packed with birds, flyover video of cities full of skyscrapers suggest this would not be the case.

Q: Therefore, is there a cap, if so at what height, where higher is no longer better? Perhaps the birds vantage point is reduced by going higher.

Related, but I feel different: Why do crows sit on treetops even when it is cold?

Birds find their niches based on many reasons. Their choice is based on primarily resource availability, predation risk, and competition. Keep in mind there are variations among species, most birds like to forage for food at a hight safe enough to avoid ground predation, at the same time to be able to see and find food without much competition. Therefore very high altitudes do not seem beneficial for food resources and its a cost in energy, thus reasonable altitudes are preferred. But again many variations depending on species and location.


Can jellyfish swim backwards? Jellyfish use jet propulsion to move forward, according to http://earthsky.org/earth/how-do-jellyfish-swim. Otherwise, they drift with the ocean currents.

Does this mean that, without the presence of water currents, jellyfish cannot swim backwards?

(This question was inspired by watching countless SpongeBob episodes and seeing the efficiency in which SB catches jellyfish).

Jellyfish move by a form of jet propulsion and it moves in the direction that the head is facing. If it needs to change direction, it just needs to pivot and propel itself in the direction that it needs to move. Comb jellies (which are not really jellyfish) have cilia that beat continuously in the water for it to move forward. So water currents are not necessary. Here is an article with videos on how jellyfish move.


Is a corpse more flexible than a living person? I read that the majority of humans have the muscular-skeletal potential to perform the splits that you see many gymnasts perform.  The reason a living person with no flexibility training can not achieve the splits is because the person's central nervous system (CNS) automatically constricts the muscle fibers of the legs when the legs move beyond the person's normal range of motion.  I read that this automatic CNS response is called the stretch reflex, and it is the CNS's way to protect the body from performing potentially dangerous movements.
So my question is: does this mean a body with a non-functioning CNS is very flexible?  For example, if I could not perform splits while I was alive, could someone position my corpse into the splits before the event of rigor mortis?

According to the science in this article: healthunify.com/why-cant-everybody-cant-do-a-split/, not really. Flexibility such as splits are only possible by lengthening the skeletal muscle fibers (in the case of splits, this includes the hamstring and iliopsoas). Which means that splits aren't solely dependent on how your CNS functions.
Furthermore, with death eventually comes rigor mortis where due to the body's chemical changes after death (lack of ATP production etc... https://biologydictionary.net/rigor-mortis/), the body becomes rigid which makes it even more difficult for a dead person to do splits than a live one without seriously damaging the dead person's body/muscles.


Why do human vaccines affect different animals differently? Doubtless the simple answer is that these animals differ, and that the amino acids of their ACE2 receptors differ. Are there other reasons?

  Chan, working with his HKU colleague, microbiologist Kwok-Yung Yuen, and others, pinpointed the problem by doing a cross-species comparison of the segment of ACE2 to which SARS-CoV-2 first attaches. In the mouse, 11 of 29 amino acids of this critical domain differed from the human version. (Rats had 13 differences, but hamsters only had four.)

I quote p 738 of Y. W. Kam et al. Vaccine 25, 729–740; 2007.

        Vaccine-mediated protection against SARS-CoV infection
  in mice has been demonstrated using different vaccine
  approaches [19,20,65]. However, mice do not replicate
  SARS-CoV to high titers and do not showpronounced pathology
  in lungs [15]. On the contrary, ferrets [28], cynomolgus
  macaques [29] and hamsters [30] have been shown to support
  high titer replication of SARS-CoV in the respiratory tract
  associated with pneumonitis. In order to assess the respective
  role of neutralization or ADE in vivo we performed SARSCoVchallenge
  experiments in hamsters vaccinated with three
  doses of 2, 10 or 50 g of protein in alum adjuvant. All vaccinated
  groups showed a significant decrease of viral load at
  3 days post challenge by at least four orders of magnitude
  without signs of enhanced lung pathology. The rare foci of
  hepatocyte necrosis that we observed in these hamsters did
  not correlate with pre-challenge neutralizing antibody titers,
  liver enzyme levels (pre- or post-challenge), or immunohistochemical
  detection of SARS-CoV antigen suggesting that
  hepatic cellular necrosis is unrelated to SARS-CoV immunization
  or infection in Syrian golden hamsters. This contrasts
  with a report of hepatitis 28 days following challenge with
  SARS-CoV in ferrets vaccinated with a poorly immunogenic
  recombinantMVAvaccine expressing SARS-CoV spike protein
  [24].

Why will it take so long to develop a COVID-19 vaccine? - The Globe and Mail

  Another study revealed that some investigational SARS vaccines produced negative side effects in some types of animals (such as ferrets) but not in others (such as mice). For that reason, many researchers are convinced that a vaccine should be tested in two different types of animals, Kozak says.

One big reason for the difference is how close the vaccine's epitopes match the natural epitopes in the animals. When they are similar an attempted immune response to the vaccine will either tend to give an autoimmune response; or no response as the relevant immune cells were destroyed during maturation (to prevent autoimmune diseases).

The reports of autoimmune disease from SARS-Cov-2 (kawasaki disease) would seem to reduce the targets for a successful vaccine.

Sorry no refs on this.


How to create a collection of anonymous sequences for teaching and testing? I am looking for a large collection (>1000) of sequence files (eg. FASTA) from any real organism or a tool to create such a collection.

The sequence files would be used for teaching and for testing automation methods.

Students would be assigned one unique sequence file and asked to look at it (eg. using gORF) and to identify it (using BLASTn).

The sequence file would thus need to contain only the sequence data (no meta data about species or gene).

I would need an associated answer sheet.

There are a couple key words in this question - anonymous and teaching. Yes, NCBI is a source for sequence data, but it is not anonymous (it is annotated, which means a student could also find it and copy/paste that annotation without doing the actual analysis). Notice, I am not assuming that the request is for human data. Now, if anonymous human data are needed, most available sequence data are anonymous but there remains that annotation issue: If it is annotated already, what will they learn?

A good alternate source for some human genome data would be from Complete Genomics. They have released anonymized (de-identified) data for at least 69 subjects. The question asks about 1000 sequences, but how large? This is an important consideration. Other details are also lacking in the question.

Another source may be the 1000 Genomes data, also human. If you're interested in plants, there are sequence data out there from ~98 different Arabidopsis thaliana accessions/cultivars/strains.


Specific examples of signalling pathway using logical 'OR' and 'AND'? I have read here that
"signals from two different pathways may be needed to activate a response, which is like a logical "AND." Alternatively, either of two pathways may trigger the same response, which is like a logical "OR."
But no example is mentioned. I want to know some specific examples in which cell signalling uses logical OR and Logical AND. Any references will be appreciated.

There are thousands of examples, here I list just a few.

1) Macrophage activation. This is a complex case with many proteins acting as AND/OR. The following paper depicts a nice scheme that helps to understand the circuit.

https://bmcsystbiol.biomedcentral.com/articles/10.1186/1752-0509-2-36

2) The Lac operon that follows the logic:

if low_glucose AND lactose:
    express(lac_genes)

if (high_glucose OR low_glucose) AND no_lacotse:
    inhibit(lac_genes)

if high_glucose AND lacotse:
    express_at_low_level(lac_genes)

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

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

3) Phosphorylation and ubiquitination pathways. For example,

  ... proteins primed through phosphorylation by one protein
  kinase are often phosphorylated processively on the N-terminal side of
  the priming phosphate by GSK3 at a series of Ser/Thr spaced by three
  residues, with the cluster of phosphates regulating protein activity
  (e.g., glycogen synthase, β-catenin). If the two sites are
  phosphorylated by different protein kinases, then this can in
  principle provide a logical AND gate in a downstream response.

http://www.sciencedirect.com/science/article/pii/S1097276507007988

4) Neurotransmitter signaling pathways.
Figure 2 of the following paper

http://www.sciencedirect.com/science/article/pii/S0022519306003675

describes the boolean logic underlining the signaling pathway

  Tyrosine hydroxylase activates itself in this model.
  There is an “AND NOT” gate between
  tyrosine hydroxylase and COMT to activate dopamine as
  tyrosine hydroxylase and not COMT activates dopamine...

  ...adenylate cyclase is activated by dopamine
  receptor 1 and not by dopamine receptor 2, which has been
  represented by the “AND NOT” gate between the input nodes.

  ...

  DARPP32, is activated by protein kinase A, and
  not by calcineurin, therefore protein kinase A “AND NOT”
  calcineurin activates DARPP32.

  DARPP32 inhibits protein phosphatase1, which is
  represented by the “NOT” gate from DARPP32 for protein
  phosphatase1.
  ...
  The activation of glutamate receptor, needs the presence of both
  protein kinase A and the ligand, glutamate therefore, a
  “AND” gate between protein kinase A and glutamate, “AND NOT”
  protein phosphatase 1. ...

Here the link to a database of natural and artificial biological logic gates and here the article presenting the database

To conclude, I would like to highlight this work on the engineering of a biological transistor.


Why are trichromat cone cells unable to sense ultraviolet and infrared radiation? I understand that cone cells vary in the color they sense, is this because of wavelength, frequency, something else, or a combination of the previous? I also understand that tetrachromats can see an extended spectrum of color because they have four as opposed to three (for trichromats) color channels, hence, I believe, an extended variation of cone cells.

The range of color perception in humans is primarily limited by the sensitivity of cone cells (specifically, the opsin proteins in cone cells) to various frequencies of light.  This sensitivity drops off at 700 nm on one side and 380 nm on the other, which is where infrared and ultraviolet begin, respectively.

Even with hypothetical infrared or ultraviolet cones, we wouldn't necessarily be able to perceive color much further beyond our current range anyway.  The various parts of the eye (cornea, lens, and the liquid inside) block both ultraviolet (starting around 400 nm) and infrared (starting maybe at 1400 nm) beyond certain wavelenghts.

http://en.wikipedia.org/wiki/Color_vision

Tetrachromaticity, at least in humans, does NOT confer an extended spectrum of color perception.  Tetrachromaticity results from a mutation on one of the light sensing proteins, changing its peak sensitivity by a few nanometers. So a tetrachromat can't see beyond the normal color spectrum, but they can probably distinguish shades of green and blue more precisely than trichromats. This has been an area of active scientific research recently; I think most scientists didn't think they existed.  Now studies suggest they're 2-50% of the population.  Humans with 5+ cone types are also hypothesized, and with the ubiquity of genome sequencing I imagine we'll be learning a lot more about that soon.

Other species have more diverse color perception, with ultraviolet being especially common in insects and birds. The mantis shrimp has an astounding 16 different kinds of photo receptors, plus a few specialized eyes for detecting polarized light. For a loving account of mantis shrimp, I recommend this comic. http://theoatmeal.com/comics/mantis_shrimp


How to determine whether a newly discovered dinosaur is not a young one and not an entirely different species? Every once in a while, there is an official announce that a new species has been discovered. For example, paleontologists have recently discovered a dinosaur they named Nanuqsaurus hoglundi, which really resembles Tyrannosaurus Rex, but in a smaller version. It also lived during the same era. Is there something that indicates it's a cousin of the T-Rex, and not Mr. Rex's son?

Other small dinosaurs include the Compsognathus, the Microraptor and others. Why were they classified as new species when they were discovered?

Considering evolution over a few million years, my guess is that some earlier species may have been smaller and evolved into more complex animals, bigger bodies, horns, frills, etc.

Diagnosing extinct species is even more difficult than extant taxa (see this question). Because systematists describing fossil species (usually) only have skeletons, they compare to other fossils. You are correct that diagnosing a species from only a skeleton can be tricky. What defines what you call a genus, a species, etc.? How morphologically dissimilar can two skeletons be before you call them different species? The running joke is that if you found fossils of a chihuahua skeleton and a great dane skeleton, you would certainly call them different species. But by modern biological species concepts, they are the same species. Then there are extant species that are essentially indistinguishable in terms of their skeletons, but do not interbreed, and so are probably different species.

Sometimes there is consensus, and sometimes there is not. This disagreement can lead to a description of a new species by one person being reclassified ("revised" is the term used) as another species. There are lots of examples of this among dinosaurs. Most famously, Brontosaurus was revised as actually being Apatosaurus. More recently, and relevant to your question, Nanotyrannus is thought by some to be a juvenile Tyrannosaurus rex.

So then how did Fiorillo and Tykowski, who described Nanuqsaurus hoglundi, decide that it was (1) not just a juvenile T. rex and (2) that it was a new species? Their rationale is laid out really well in their paper, primarily in the sections "Diagnosis" and "Description". You rightly picked out the two questions that paleontologists reading this paper would want to know.

Nanuqsaurus is not a juvenile:

  The dorsomedial edge of the maxilla is marked by deep pockets separated by pronounced transverse ridges. These together formed a strong peg-in-socket articulation between the dorsal margin of the maxilla and the ventrolateral edge of the nasal. The same kind of deeply interlocking naso-maxillary contact is a well-documented character that is also present only in developmentally mature individuals of the derived tyrannosaurines Daspletosaurus torosus, Tarbosaurus bataar, and Tyrannosaurus rex 2, [6], [20], [21], [22]. The nasal-maxilla contact is either smoothly grooved or bears only weak scalloping in immature individuals and more basal tyrannosauroids 2, [6]. The presence of this feature in DMNH 21461 is evidence that the material also represents a developmentally mature individual.

What they are saying here is that maxilla (part of the front of the upper jaw) in Nanuqsaurus has a very characteristic relationship to the nasal bone in which they form a peg-and-socket joint. This relationship is found in tyrannosaurine dinosaurs like Tyrannosaurus, Daspletosaurus, and Tarbosaurus. But more importantly, it is only found in adult tyrannosaurines. So they conclude that Nanuqsaurus is an adult.

Nanuqsaurus is a distinct species from Tyrannosaurus and other tyrannosaurines

  In all three hypotheses of phylogeny, Nanuqsaurus hoglundi was found to be a derived tyrannosaurine, the sister taxon to the Tarbosaurus + Tyrannosaurus clade (Figure 6). This node was supported by a single unambiguous character, the presence of a dorsoventrally tall, paired sagittal crest on the frontal. The age of Nanuqsaurus hoglundi (70-69Ma) is consistent with its place in the recovered hypothesis of tyrannosauroid phylogeny, positioned in time between the more basal Daspletosaurus torosus (Middle to Late Campanian) and the more derived Tyrannosaurus rex (latest Maastrichtian) among other North American tyrannosaurines.

The authors ran a phylogenetic analysis of characters coded for Nanuqsaurus and about 20 other taxa. Nanuqsaurus has enough shared characteristics to put to solidly among tyrannosaurine (near Tyrannosaurus, Daspletosaurus, and Tarbosaurus). But, importantly, it has a characteristic that none of these others have: "the presence of a dorsoventrally tall, paired sagittal crest on the frontal."

Based on its being an adult and having a character that is not found anywhere else among tyrannosaurines, Fiorillo and Tykowski name a new species. I'm simplifying what they did, but that's the general idea. To their credit, they acknowledge that there is not a lot distinguishing the new species and discuss in much more detail their rationale and the implications of their results.


By what mechanism can two chromosomes fuse? What condition(s) would likely exist which could cause 2 chromosomes in the newly fertilized egg of a placental mammal to fuse? Assume this is more likely than having the same chromosome pair fuse in an individual egg, as well as an individual sperm.

Chromosome fusions (as well as fissions and other changes) usually take place during cell division or pairing, therefore, it's very unlikely that two chromosomes will fuse in an already fertilized egg. If they do such, this egg would probably be aborted.

One factor that may lead to chromosome fusion is loss of thelomeric sequences (telomere = chromosome extremity) (O'Sullivan and Karsleder, 2010) - but probably not in an fertilized egg.


How does different sensory stimuli differ in nerve signal? Every day, we experience different types of sensory stimulus,  like heat, pain, cold, etc. However, in each case, the transmission of the stimulus to the brain through the neurones is carried on in the same way: through propagated depolarisation and repolarisation in axons, while through the release of acetylcholine at the synapses.

So, how does the different sensory stimulus differ if they are transmitted the same way? (I mean to say that how does the nerve signals differ for two different kinds of stimulus?)

Let's put the question simply:

How do two nerve signals originated from two different stimuli differ? If they do not differ, then how does the brain differentiate between different nerve signals if they are all alike? How does it understand what nerve signal carries what message?

I think the short answer to your question is that the contents of different types of sensory stimulation are communicated to different populations of cells in the brain (note this transmission is mostly glutamatergic, not cholinergic). From there, the remaining associations and experiences derive from connectivity with other networks of brain neurons that result in different types of experience, based on the networks that those networks form and learned associations over development and a lifetime.

Computer analogies aren't always appropriate to understanding things about the brain, but maybe it could work out a bit here. How does a computer distinguish between input on your keyboard vs your mouse? On many modern computers, it is common for both to be connected with USB. The computer has some software that distinguishes between the different inputs - the brain has hardware that does the same.

Later on in the brain, or at a different stage in a computer program, those inputs can be mapped to functions that underlie experiences or functional outputs. Movement of the mouse can be converted to the movement of a screen cursor ("motor output"). Proprioception (the sensation of the relative position of the body from receptors in the muscles, tendons, and joints) can be combined with motor plans to create an error signal to move a particular muscle to match the intended movement.

Explaining any further than this probably requires entire textbooks of material, so I will leave it there.


How is it possible for monosomies to occur? I was taught in biology class that a cell dies if it doesn't have at least one copy of a chromosome "type". If this is the case, that means that:

Zygotes without a copy of a specific chromosome (for example chromosome 21) die.
But this would also mean:
Gametes without a copy of a specific chromosome would also die.

If this is the case, how is it possible for monosomies to occur? Wouldn't there have to be at least one haploid cell with (n-1) chromosomes when fertilization occurs?

Gametes cannot be compared to regular (id est, somatic) cells for two main reasons:

Their lifetime and...
Their gene expression.

In human beings, gametes have a very short lifetime. Supposing the nondisjunction happened at meiosis I (which is the worst case scenario), a "nulissomic female gamete"1 has to be alive for some days, from the end of the dictyotene to the fertilisation. The male gamete would have to stay alive for a little more time, some weeks, from the spermatogonium stage to the end of meiosis. Those are not big time spans.

But the most important reason is that gametes are basically a structure to "deliver" genes. They normally don't express the genes they have, at least not as a somatic cell would do. Sperm cells, for instance, have densely packed chromosomes and gene expression, if any, is little and poorly understood.

Thus, the problem in your reasoning lies in assumption #2:

  Gametes without a copy of a specific chromosome would also die.

Gametes lacking a given chromosome can and do exist, and they form aneuploid zygotes.

Note 1: the name "gamete" here is a wrong choice, since a primary oocyte is not a gamete, as it is the name "nullisomic", which doesn't apply to haploid cells.


What happens to Bacteria at a low pH? I am conducting an experiment on how different pH levels effect the growth of E.coli. After researching, it is predicted that the most acidic pH level (pH 2) will be most effective at killing (or at least slowing down the growth) of bacteria. But my question is what does pH actually do to the bacteria cell and the biology behind it. How does the pH actually affect the E. coli cell itself? Thanks for your time.

pH affects the structure of all macromolecules that compose bacteria, and indeed all cells.

Here's a shortlist of examples:

Lipids

Lipids are hydrolyzed by extreme pH levels. They undergo chemical reactions and fall apart into constituent molecules, which may be toxic. The membrane is made of lipids; if it is disrupted, the cell ceases to exist.

Nucleic acids

At low pH, RNA and DNA hydrolyze - bonds are broken between individual bases (phosphodiester bonds) and nitrogen bases break off from the (deoxy)ribose groups. Structures and hydrogen bonding (necessary for DNA replication or transcription of genes) are impaired.

In alkaline conditions, DNA typically denatures but remains intact. Structures and hybrogen bonding are still strongly impaired though.

Protein

Low or high pH environments affect ionization of amino-acid functional group ionization. This affects hydrogen bonding in such a way as to denature the molecule, because it adopts very different conformations. This of course renders the protein or enzyme non-functional, and may cause it to aggregate or become cytotoxic. If any one of the hundreds of essential enzymes fails to function correctly, a bacterium will die.

Potentials across membranes

Changes in pH have drastic effects on proton concentrations both in and outside the bacterium. Respiration depends on a concentration gradient of protons. Low or high pH will make it difficult for cells to establish a potential (different in concentration across a membrane). This gradient must be upkept for a bacterium like E.coli to generate energy, and it's difficult if protons are being neutralized or are in sheer excess!

Any one of these is enough to have a bactericidal or bacteriostatic effect! This is also why cells that do live in slightly alkaline or acidic environments have to specialize, and they have narrow windows of pH that they can survive under, because they have to compensate so much to counteract the protonation or lack-thereof in their environments.


Can anyone help me identify this plant? I have a Chamaerops humilis in my apartment and in there is these small plants growing. I live in Denmark, Europe and my palm tree has only been inside my apartment since i got it.

Can anyone identify this plant?

Click on photos for full size

It's a bit early yet, but it looks very much like a weed known in my area as "cleavers" or "clingweed" (Galium aparine) because of it's tiny stiff hairs which make it catch and cling to clothing. The picture below is for a fully mature plant, which is stiffer and stickier than when they first sprout. Note the whorl arrangement of (usually six) leaves, with each leaf having a "point" protruding from the tip, the distrubution of hooked hairs along stem and leaf, and the initially prostrate habit (they grow along the ground initially). The mature stem will be squarish and easily crushed.

Though your plant's leaves are broader, there are ~650 species of Galium, and I believe yours will be either Galium aparine or Galium mollugo. But you'll be able to tell what it truly is when it flowers.


Can mutation take place in G1 and G2 phases during the cell cycle? We know that the DNA replicates during the S phase in Interphase. There it might undergo a number of mutations. We also know that the forward half strands are more susceptible to undergoing a mutation since they live most of their lives single-stranded. But can mutation take place anytime before or after the replication? It is weird that the strands "wait" to open up in the S phase and only then undergo a mutation.

Yes, it can. A mutation can potentially occur at any given moment in the cell cycle, not only in S phase, which is why revision mechanisms remain alert during the whole cycle. Such mechanisms not only make sure every important event in the cycle takes place adequately (e.g. DNA replication, chromosome segregation) but also repair any damage associated with DNA (e.g. AP sites, single strand breaks, double strand breaks, to name a few). Once DNA damage takes place, specialized sensors detect such events and activate several mechanisms. One of these will pause the progression of the cell in the cell cycle, and another will repair the DNA-associated damage, in case that it can actually be repaired [1].

[1] Karp, G. (2009). Molecular and Cellular Biology: Methods and Concepts. Wiley. New York.


Function of the spermaceti organ What is the use of the spermaceti organ of the sperm whale?

One possible theory considered is that it was used for floating and going underwater by heating/cooling the oil. However, it is a lot easier for this to be done mechanically.

Another possibility is that it is comparable to a helmet to safeguard it when it collides with another whale. However, other animals have much simpler structures to deal with this problem.

A third possibility is that it uses it to stun its prey like squid. However, research in inconclusive on whether squids can hear or not. The link below, says that it is probable that squids can only hear upto 500 Hz which is not the frequency used by whales, thus this theory is probably false as well.

https://www.treehugger.com/natural-sciences/what-can-squid-hear-and-why-does-it-matter.html

The principal function of spermaceti and the associated structures in a sperm whale head, is echolocation. The composition of spermaceti suggests that it functions as an acoustical transducer, helping to focus the powerful sound waves used for echolocation. These sound waves likely do not actually stun squids, but they do help sperm whales to find and pursue squids in deep, dark waters.

An echolocation click is formed at the tip of sperm whale's nose, where it is directed backwards, through the spermaceti, toward the sperm whales brain. It then is reflected off an air sac on the sperm whale skull, and redirected forward through a series of lenses before it moves into the water. Check out an illustration of this in the Møhl et al 2003 paper: https://pdfs.semanticscholar.org/88d4/271e9f7490c1173234a2445cf8ddf92fd51f.pdf

The complicated anatomy in a sperm whale's head seems to be directly evolved for echolocation.

Sources:
Karol, R., Litchfield, C., Caldwell, D.K. et al. Mar. Biol. (1978) 47: 115. https://doi.org/10.1007/BF00395632

Møhl, B., Wahlberg, M., Madsen, P. T., Heerfordt, A., & Lund, A. (2003). The monopulsed nature of sperm whale clicks. The Journal of the Acoustical Society of America, 114(2), 1143-1154.


What is meant with “the chest wall and lungs are coupled together”? Since the lung and chest are elastic, we can represent them with springs. Under normal conditions, they are coupled together: the “lung” springs are stretched and the “chest” springs are compressed. During a pneumothorax, the lungs and chest are independent and the springs representing them go to their relaxed positions, causing the lung to collapse and the chest wall to enlarge.

This analogy is honestly completely flying over my head. How are the lung and chest wall “coupled”? Heck, earlier in this book it’s mentioned that one of the two forces keeping the lungs from collapsing is “the surface tension between the lungs and the chest wall” (the other being the intrapulmonary pressure).

This and the said analogy make it sound like there is a physical-contact adhesion force between the lungs and the chest wall, which, from what I’ve looked into (and several other analogical figures the book has provided), seems to not be the case.

I believe this analogy of “coupling” is probably related to pressure relations, but I don’t understand how those are exactly set up either, and why during a pneumothorax they just cease as the two become “uncoupled”.

For those interested, the book is Medical Physics by John R. Cameron.

How are the lung and chest wall coupled?

You have your answer in the text:

  the surface tension between the lungs and the chest wall

And as you say, it is very much

  like there is a physical-contact adhesion force between the lungs and the chest wall

A good, medical school level anatomy textbook will walk you through this. Moore's Clinically Oriented Anatomy gives the appropriate level of detail. Lets refer to Fig 1.30 (pg 107 of the 6th edition):

Below, you can see that there is a bag of fluid (the pleura) around the lung itself, like an under inflated balloon wrapped around the lung (see the picture of the fist, representing the lung, wrapped in a balloon, representing the pleural sac). The space inside the bag of fluid is very small, very thin, in a normal lung. The size of that space is exaggerated in the figure below in order to show the layers more clearly. In fact, in medical images of a healthy chest, it doesn't even appear as a space. The thin layer of fluid provides surface tension, keeping the two pleural walls close together. Since the chest and lungs are physically attached to the pleural walls on either side, that surface tension pulls the elastic lung outward (expanding it), and the chest wall inward (collapsing it, slightly). If the pleura is punctured, blood or air can enter, surface tension can no longer keep the two pleural walls next to each other, the chest wall returns to its preferred state (slightly more expanded than it would otherwise be), and the lung returns to its preferred state (substantially more collapsed than it would otherwise be).


Can a ladybug be determined just by its number of points? I saw a ladybug on my balcony one day and I just counted the dots.

There was 18 black dots on a red/orange elytra.

The location is in Europe (Geneva, Switzerland) and usually we have quite different endemic ladybugs and also the invasive asian ladybug Harmonia axyridis.

I did not found any local ladybugs with such dot counting except articles saying the Harmonia axyridis can be found with a lot of variations (elytra  color, points or stripes, etc...).

The question is: Can I be sure that a ladybugs with 18-points (found in Europe area) is of the genus Harmonia axyridis?

Note that I have a picture of the animal but I want to focus my question on the number of dots exclusively.

No, most of the time you cannot. There is a large diversity of ladybug species (several dozens in western Europe), and many of them can have the same number of spots. Moreover, as you already said, there can be intraspecific variation in the number of spots.

I do not know if there are specific numbers of spots that would be associated to only one species - but for most numbers, it is not the case. For instance, yes, it is common for Harmonia axyrids to have 18 spots (source). But Anisosticta novemdecimpunctata, which  can also be found in Europe - and can also be orange ! - may have between 15 and 21 spots (though it more frequently has 19) (source).

Thus, the number of spots cannot be used as a sole criterion to identify ladybugs: other criteria usually include the general shape, colour of elytra, size, shape and colour of the pronotum, length of antennae, etc. (See here for examples.)

First picture: Harmonia axyridis

Second picture: Anisosticta novemdecimpunctata


What are Expressed Sequence Tags (EST)? I read in an article that ESTs are partial or sub-sequences of cDNA. What are ESTs exactly? Which part of cDNA is cut in order to make ESTs? Why are they so instrumental in genomic research?

The question does not cite the source of the poster’s information, but it might well be the Wikipedia article on ESTs. I suspect the reason that does not answer the first question (“What are ESTs”) is the confusion in how ESTs are generated from cDNAs implicit in the second question “Which part of cDNA is cut…”. I therefore start by dealing with the source of the confusion.

Clarification 1: A Sequence need not have been Sequenced

One source of confusion lies in the word ‘sequence’. One meaning of this (noun only) is “a specific linear contiguous fragment or region of nucleic acid”. When used in this way there is no implication that even the length of this is accurately known, never mind the identity and linear arrangement of the nucleotides. The second use of the word sequence (noun) is the identity and order of nucleotides in a (linear) nucleic acid, with the corresponding verb meaning to determine this. Because today it is so cheap and quick to determine the sequence of a nucleic acid fragment, the student may not realize what a relatively slow and expensive undertaking it was in the last century. I shall use DNA fragment or region instead of the first use of ‘sequence’ in the rest of this answer.

Clarification 2: There are cDNAs and then there are cDNA clones

The second source of confusion seems to be with the cDNA clones. The question does not use the word ‘clone’, but asks “which part of cDNA is cut…”. This implies the poster is thinking in terms of individual cDNA clones in which the inserted cDNA fragment has been characterized — restriction mapped, perhaps sequenced and the protein product even identified. This is the approach adopted when the scientific problem is to identify the mRNA or gene encoding a particular protein — actin, beta-globin, etc. This is not the case with ESTs. Here the only characterization performed on a cDNA clone is a single DNA sequence determined (historically by the Sanger method) from a primer position in the cloning vector. This is because the focus is on producing a bulk library of DNA sequences.

So, what are ESTs and how are they generated?

As an alternative to the standard definition, one might say:

  An EST is a single DNA sequence read derived from only part of a mRNA. Despite its uncharacterized nature, possible redundancy, limited size (perhaps 100-200 nt) and likelihood of errors it is useful in combination with many others from the same tissue as providing a reference to genes that are expressed in that tissue.

So, to reiterate, the answer to “what part of the cDNA is cut…” is “none”. One (presumably) just isolated total DNA from the recombinants in the M13 plaques and ran a single sequence determination from the primer site. And this was because one did not know which EST would be useful, but a collection or library of ESTs would likely contain some that would be useful.

The word ‘tag’ expresses the fact that they act as a handle or reference to the gene or mRNA, rather than being complete in themselves.

Why are/were ESTs important/useful?

The words the poster used originally were “Why are they so instrumental in genomic research?”, but I think that certainly exaggerates their current — if not their past — utility, so I have rephrased the question. Examples of the use of ESTs are given in the Wikipedia article already quoted, so I shall quote from Peter Goodfellow, writing in Nature in 1995.

  Only 3 per cent of the human genome codes for proteins… the most important
  part of the genome is the protein coding genes and that sequencing these
  will give the largest return of biological information…

After pointing out his own scepticism towards the approach he briefly mentioned one important historical issue:

  Given these disincentives, why have tens of millions
  of dollars been spent on ESTs? After a brief exploratory phase… a major driving force was the hope and the fear that ESTs could be used to patent any gene that had been tagged. Attempts to patent genes via ESTs raised the spectre of an international trade war and the echoes are still reverberating around courts in the United States.

No longer, I hope. Goodfellow then turned to the science:

  It was hoped that large-scale EST projects would define the broad limits
  on the number of genes and the types of genes in the genome and provide a
  snapshot of their expression patterns. It was also expected that enough sequence
  information would be generated to be able to recognize new members of gene
  families of biological and commercial interest.

Coda: Yesterday and Today

Currently the method most used to investigate expression of genes as mRNA is, of course, RNAseq, which is faster, cheaper and, unlike ESTs, comprehensive.


A subtle test for color-blindness Is there a test method of proving a person being color-blind, without letting the test subject know, that he/she is being tested?

E.g. showing the person cards with colored dots like depicted here is not a valid answer.

I am colorblind, but I did not know that before I was 22 (!!). I got to know it by doing the Ishihara test. There are other tests you can do to test for colorblindness, such as the reverse colorblindness test (http://www.cs.unm.edu/~aaron/creative/colorTest.htm), where a "normal vision" person will not see the two patterns shown there.

Anyway, there is no test where you cannot ask "what do you see?" to the subject. On the other hand, I saw a photo where they were showing a northern light in both colorblind and normal vision (https://www.facebook.com/nlblog/photos/pb.236481989828593.-2207520000.1415264974./416457851831005/?type=1&theater) -I hope facebook links are OK in this site-, where I see no difference between the two photos. You could for example show that photo pair to your test subject and ask a set of questions (e.g. which one do you like more?). If he/she is colorblind, then the answer will be "they are the same", so you have a strong indication, or if they are able to point out differences, then they most likely have normal vision.

I could think of an experiment where you just show several photos with different contrasts/saturations, and then add the northern light photo (maybe the author has some other photos you could use), so they are not aware of the underlying question.

I hope this helps


Help identifying fruit This fruit was spotted in Kochi, India on several occassions. Nothing else is known except the fact that it seems to be irregularly distributed through Kerala.

It appears to be a noni fruit (Morinda Citrifolia).


Why do we spend so much time on creating taxonomies? I spent 3 years building a taxonomic database of plant specimens for the Missouri Botanical Gardens (http://www.tropicos.org/). Myself and two other programmers used a modern database and web pages to share the specimens with the research community. Last I looked there are over 3 million specimens included. Anyway I never got a straight answer as to why there is so much time, money and botanist's lives spent categorizing the earth's flora. What is the end goal here? I'm hoping there are professional scientists here that do taxonomic work that can chime in. Thanks.

Biology is about observation and learning from nature. If you categorize the species, it helps you in quickly understand what the species is about, what are some of its common characteristics, phylogenetics, etc. It has applications not just in understanding evolution, but in population studies, ecology. Why do we give humans names? So we can find them quickly and easily and associate them with certain characteristics. It is the basic human nature of using patterns to quickly identify objects.


How early can we know the sex of a human being now? Do we need to wait till a Zygote forms?

Before the zygote, there is no individual for which sex can be defined! However, it is possible to know the sex of the future zygote if you know the gametes that are going to fuse.

In humans, just like in all placental mammals (which excl. kangaroos and platypus), sex is defined by sexual chromosomes, where males are XY while females are XX. A mother can therefore only pass on an X (and have no influence on the sex of the offspring) while a father can pass on either an X or a Y which will determine the sex of the offspring. Knowing the paternal gamete (the spermatozoid), one can infer what the sex of the future offspring will be. Of course, in one ejaculate, there are about as many X-bearing gametes than Y-bearing gametes.

Technically speaking, could typically make a karyotype to infer whether chromosome X or Y is being transmitted.


Calculation of final magnification when using a CCD camera I'm trying to empirically calculate the approx final magnification (mag) of digital images rendered through our confocal microscope. Using a micrometer and the microscopy equipment I have, the following is known:

Objective mag = 63x

Ocular mag =10x

Diameter of field of view when viewing specimen through occular = 320µm

Diameter of field of view when live viewing specimen on the screen = 100µm

What is the final mag of the rendered image on the screen?

This is not a homework question. The manufacturers specification for the degree of magnification that the camera and confocal  (and obviously there is some) provide is unknown.

Assuming that the FOV that is captured by the CCD on the screen is 100µm wide as determined by the micrometer, and you are viewing the 920 pixel wide image on a standard 96 ppi monitor, the zoom would be approximately 2434 times.

$$\frac{920p}{96p/in}/100µm \approx 2434$$

Additionally, you should ensure that the minimum resolution on the micrometer is at least twice as large as each pixel on your microscope CCD.

The reason that the pixel size must be at least 2 times smaller than the minimum resolution present in the image is due to the Nyquist-Shannon sampling theorem.

This being said, all microscopes (and arguably all measurement devices) should be calibrated against a standard. This paper explains the usage of a standard to calibrate confocal microscopes.

A similar technique used to calibrate normal optical microscopes using a stage micrometer standard can be used if you do not possess such a standard. First calibrate the normal microscope, then image an identical sample using both microscopes in order to obtain the size of the field of view.


Why does sulfonamid not inhibit the growth of Rickettsia? Sulfonamid is an antimicrobial agent, why has it no effect on the growth of Rickettsia?

Sulfonamides competitively inhibit the enzyme dihydropteroate synthase, which is involved in the tetrahydrofolate synthesis pathway in most bacteria. Rickettsia lack this enzyme target, and thus possess a natural resistance to the antibiotic. As tetrahydrofolate is an essential compound, it is believed that Rickettsia possess an alternative enzymatic process which is not susceptible to sulfonamides, or the bacteria simply acquire the compound (or its immediate precursors) from their environment.


What species is this black, blue and white bird? I think this species is native to Edmonton, Alberta, Canada, as I see it regularly, especially around the urban locality (Downtown Edmonton).

Season: Early Spring

Date: May 18, 2017

Basic Description: Medium sized bird, and I was not able to observe a characteristic chirp from the bird while I was taking a photograph. Most distinctive feature is the bright royal bluish gradient on the tail and tips of the wings.

That bird is commonly called a magpie. The only species found in Alberta is Pica hudsonia. You can see a reference image on the left and their distribution throughout Canada on the right:

[source]

Interestingly, it is one of the only non-mammals studied that is able to recognize itself in a mirror. In fact, these and other corvids are thought to be some of the most intelligent species on Earth.

You mentioned that you didn't hear them chirp. These birds are actually quite loud and about fifty of them used to wake me up every morning. Have a listen (not my video).


What flower is this? (Dolomites, Italy) I took this picture a few days ago in Val Rendena, in the dolomitic Brenta group (2000 m). The whole plant was 15 cm tall at most, and it had a single leaf on the stem. What flower is it?

I had a look at white-flowered plants flowering in July in a site about the flora of the French Alps, and the best I could find was Parnassia palustris:
http://www.florealpes.com/fiche_parnassie.php

At this developmental stage, it looks quite similar to your photo, with the same kind of structures at the base of the petals.
The site says that there are heart-shaped leaves at the base, plus one on the stem. This last leaf matches your description. The site says it can grow up to 2500m.

The Italian Wikipedia says:

  In Italia è presente solo nelle regioni settentrionali e centrali, nonché in Campania.[2] In montagna si spinge fino a circa 2000 m, ma sulle Alpi è stata segnalata anche a quote superiori (3000 m sul versante svizzero del Monte Rosa).

This means that it can be found in the Italian Alps too, including at 2000m.


What is the difference between eugenics and evolution by natural selection? So with the working definition of Eugenics: "the aim to improve the human gene pool". What are key features that distinguish Eugenics from evolution by natural selection?  I mean, besides that natural selection occurs naturally.

Selection is a mechanism of evolution which favours specific forms of traits over others, this can cause the spread of beneficial mutations through a population.

Natural selection is the spread of beneficial traits/genes through populations as a result of the natural variance in their effect on reproductive output (a function of life history traits like lifespan aging and reproductive rates). A classic example is that of Darwin's finches, where different variants of bill length and shape have evolved in populations based on what food resources (types of seed) are available to them and their ability to utilise those resources.

Artificial selection is selection imposed on a population by humans to deliberately affect specific traits. Examples of this would be milk yield in cattle (we want more efficient production and better quality milk), dog breeds (selection on a whole host of traits like colour, beardedness, height, length) and crops like wheat and barley (selected for higher efficiency and  quality output).

Eugenics, coming from the greek for "well-born" or "good" race, is the application of artificial selection principles to humans. Just as with cattle or crops, there is an aim, it may be to increase height, remove genetic diseases, or promote a certain set of traits like blonde hair and blue eyes. Historically we can associate with a number of radical political ideologies, such as Nazism. Even here in Sweden (people tend to think of it as a very progressive and equality driven country) there was a program of eugenics until very recently, achieved by forcibly sterilising or coercing people in to it, for various reasons (racial purity, health, and antisocial behaviour). Here's an interesting example of a girl designated as being genetically inferior because her family had a history of alcoholism (that page gives a good history of eugenics too). The social and ethical problems of eugenics are obvious.

Under normal conditions a persons reproductive output is largely determined by their own choices and actions whereas under eugenics that choice is taken away and made by someone else and specifically with the aim of "improving" the quality of the population.

So in summary:

natural selection is the result of natural variance in fitness linked to traits
artificial selection leads to a change in traits, in a specifically targeted direction, decided and imposed by another organism (usually humans, I know of no other species which does this)
eugenics is practice of artificial selection on humans enacted by humans with the specific aim of improving quality: often for social, economic, or political reasons and is generally accepted as being against human rights these days.


How isolated are different areas of the brain? I'm interested in understanding how isolated different parts of the brain are from each-other. I'm trying to understand the way that different sections of the brain work together.

More specifically, I'm interested in whether or not the different sections are all intertwined together into a wild mass, or work in a more isolated way:

Do different specialized areas of the brain have specific, consolidated connection areas where they exchange information (sort of like they do their job and pass on the necessary information to the other modules)?

Or do they instead mesh very thoroughly, connecting freely to other parts of the brain sort of like tangled string, with no obvious points of consolidated interaction?

Well, to answer your question, both your hypothesis are true, at least partially true.

The brain has several known specialized connections called neural pathways that connect specific areas of the brain and are responsible for determined functions.

For instance, when you move your leg, the stimulus starts at the motor cortex and travels through the pyramidal tract to your leg and then back.

However, one can argue that the stimulus didn't start at the motor cortex. Why? you thought about moving, then made the decision and only then perform the real action of moving your leg.

And here's a more complex (and maybe humorous) example:

You see a dog running ferociously at you.
The stimulus travels through your visual pathway to your visual cortex.
The image of a dog forms in your brain.
It then travels to your Hippocampus.
You realise that's a dog and also remember a traumatic childhood experience with a dog.
The stimulus travels to your amigdala.
You feel fear
The stimulus activates the sympathetic system.
You're now prepared to fight or flight
The frontal lobe is activated
You decide to kick the dog
The stimulus goes from your motor cortex to your cerebellum
Your cerebellum "remembers" the karate classes you had as a kid
The stimulus goes to your leg
You kick the poor dog. He runs.
Nucleus accumbens is activated
You feel good with yourself

So, in short, the brain has pathways that connect specific areas of the brain but, in a sense, all parts of the brain are connected either directly or indirectly. Like the saying "all roads lead to rome!"

DISCLAIMER: I do not endorse animal cruelty.


Genetic Models for Natural Selection? My question is simple:

Given that evolution is described by random genetic mutations allowing certain members of a species to gain a reproductive advantage over others that coexist in the particular environment- I am curious- single genetic mutations do not seem to really explain complex morphic changes such as the length of a giraffes neck. Instead it appears it must be a compilation of many such mutations. So what are the statistics for mutations? How long does it really take for so many to favorably compile? How does this compare with the reproductive time of the species?

The rate of mutation has been studied since the early 1900s, which is when your question was put to rest in a prescient paper by JBS Haldane (1949). Essentially the answer is that it varies a lot between organisms and environmental conditions, but for any given gene a mutation occurs once in about 50,000 sexual replications. That is equivalent to, in a human, several hundred new mutations in each person born. Impressively, Haldane's calculations have since been confirmed by a variety of other methods (e.g. Nachman & Crowell, 2000; Xue et al., 2009).

Faster rates of evolution have been recorded in other organisms, and there have been many, many studies looking at the rate of increase in sizes of the whole body or of particular organs of a wide variety of animals and plants.

For example, Azevedo et al. (2002) look at the rate of mutations affecting size (trying to select for decrease in body size) in C. elegans, and found mutations affecting size occured at a rate of ~0.0025 per haploid genome per generation.

In another example, with a result more definite regarding your question, Keightley (1998) investigated the rate of change in average body weight under conditions of selection for increased body size, over 50 generations in mice. They recorded an average increase of 0.23-0.57% body weight per generation from new mutations. That's pretty huge, and demonstrates how rapidly a complex trait can change by mutation under selection.

I wrote a small piece of python code to calculate the increase after x generations at the same rate (the formula is very simple)...

initial = 1
rate = 0.35
generations = 1000
result = initial * (1.0 + rate) ** generations
print result
>>>20.10655586861808

Thus if we assume that approximately the average rate found in the mouse study (0.35%) could be the rate at which giraffes' necks might increase under strong selection, after 1000 generations the mean neck length would be over 20 times the original length. A low estimate for wild giraffe longevity is around 20 years, thus for giraffe necks to increase around 20x might take 20,000 years. Of course this basic estimate is making a whole lot of assumptions, but the point is that rates of mutation are actually very high, easily enough to explain the diversity of traits we see in the world.

References

 Azevedo RBR, Keightley PD, Laurén-Määttä C, Vassilieva LL, Lynch M, Leroi AM. 2002. Spontaneous Mutational Variation for Body Size in Caenorhabditis Elegans. Genetics 162: 755–765.
 Haldane JBS. 1949. THE RATE OF MUTATION OF HUMAN GENES. Hereditas 35: 267–273.
 Keightley PD. 1998. Genetic Basis of Response to 50 Generations of Selection on Body Weight in Inbred Mice. Genetics 148: 1931–1939.
 Nachman MW, Crowell SL. 2000. Estimate of the Mutation Rate Per Nucleotide in Humans. Genetics 156: 297–304.
 Xue Y, Wang Q, Long Q, Ng BL, Swerdlow H, Burton J, Skuce C, Taylor R, Abdellah Z, Zhao Y, et al.. 2009. Human Y Chromosome Base-Substitution Mutation Rate Measured by Direct Sequencing in a Deep-Rooting Pedigree. Current Biology 19: 1453–1457.


How to attract Cyanobacteria? I would like to attract cyanobacteria in one spot on an object (e.g. cloth,) instead of having it swim in the media. my current method is to pour it on the object in a beaker and wait for some of them to become attached (very pour attachment yield).
Now, I am thinking of making the object emit light. Do you think that the bacteria will swim all the way to the cloth because there are attracted to light?
is there a better method to help the bacteria get attached to the cloth?

It might work, many cyanobacteria are reported to be phototaxic. https://www.pnas.org/content/115/52/E12378


Why are these trees leaning, but no trees around them are? This was observed in Florida.The trees on the left have a distinct lean to them, but none of the other trees in the area are leaning, why is this?

I'm not sure what other information is pertinent or what else I should look for.

There are several reasons as to why a tree might lean. Normally, it is a combination of some/all of the points below:

Weight distribution: Depending on the diameter of the trunk and especially the height of a tree, gravity can create problems. So the main question is how the weight of the crown is distributed over the tree's trunk.
Species variability: Different species of trees have different root systems, some go deeper and others don't. The depth and width of the root system are factors to consider when assessing a leaning tree.
Environmental factors: There are a variety of environmental factors that will contribute to a tree leaning. For example, a
tree that leans because it has grown towards the sun often has a curved trunk. The trunk curves due to the tree's ability to adapt over time to the changing
availability of sunlight. Its root system will grow to accommodate the “off center” weight distribution, up to a point. Additionally, storms or constant wind can obviously cause a tree to lean.
Structural damage: Leaning trees that don’t have a “sweep” (caused by wind) but tend to have a fairly straight trunk generally have a history
of structural damage to the root system or storm damage that has
caused the root system to slip, break, sink or simply fail to support the
tree in some fashion. If the trunk appears to enter the ground without
a mound of soil on the side away from the lean, then the root system
has sunk, either from rot, mechanical fracture, physical cutting of the root plate or soil subsidence. If the mound does exist on the back side of the lean, that's a sign that the root plate is being tipped
out of the ground and the roots have failed - either through mechanical wounding or structural failure. As roots break under stress from wind or off center crown weight pushing the trunk away from the soil holding the roots, the up-wind side of the root plate will tip out of the ground.

In addition, it may be worth mentioning that time plays an important role here too. Older trees will have been exposed to the forces of nature and plant pathogens for longer than younger ones so it certainly makes sense to take the life cycle of a tree into consideration, some live longer than others and thus may have been subject to wind while the other surrounding trees weren't "tall" enough to shield off any of the wind etc.

Sources: Georgia Forestry Commission - Leaning Trees - What's up with that


Cytochalasin B in cell movement In an experiment by Pollard, T.D. and R.R. Weihing, amoeba cells injected with  Cytochalasin B were inhibited of movement, while the control group amoeba cells did move. A hypothesis was made that Cytochalasin B blocked polymerization of actin monomers into actin filaments, thus preventing the cell from moving. To validate this hypothesis the experiments were made again with cycloheximide (inhibits new protein synthesis), and dinitrophenol (inhibits new ATP formation), and colchicine (inhibits polymerization of microtubules Here are the results:$\\$

$\begin
Condition:                                  % of cells that didn't move
No drug                                      3
Cycochalasin B                            95
Colchicine                                   4
Cycloheximide                             3
Cycloheximide + Cycochalasin B    94
Dinitrophenol                               5
Dinitrophenol + Cycochalasin B      85$
$\\$

Question: Why were these control important? How did they help validate the hypothesis?
Note: this is for self-study.

The other inhibitors work on other processes, as you already noticed. There is almost no difference between the conditions when they are added and the corresponding condition when they are missing, suggesting those other processes play no role in the observed phenomenon. Eliminating those other processes makes it more believable that actin polymerization is important, rather than being one of multiple factors.

Moreover, often cell will adapt to an inhibitor by increasing or decreasing other kinds of activity. For example, it could be that actin polymerization inhibition prevents amoeba from eating. In this case, because any imaginable motive mechanism requires energy, starving amoeba may become unable to move, even though it was not using actin for movement. In order to refute such scenarios, where actin polymerization is not directly inducing movement, and where cytochalazine does not inhibit movement directly mechanism, supplementary experiments were performed.

DNP induces something similar to starvation, yet, in these experiments, did not abolish movements when given alone. Nor did DNP rescue movement, because the combination (DNP + cytochalazine) is virtually identical to cytochalazine alone. In both circumstances, DNP did nothing, thus showing that ATP depletion is not influencing movement. This is proof that actin polymerization is directly causing amoeba movement, and not an indirect ATP-mediated effect. Similarly, cytochalazin's effect is independent of protein synthesis, once more supporting the hypothesis that actin polymerization is important on its own.


Genetic variation and sensitivity of wild cabbage 1: Is it true that the genetic variation of kale plants is smaller
  than wild cabbage?

I think so, because of human selection of the kale plants.

  2: Are broccoli and cauliflower more sensitive to changing
  environmental conditions than wild cabbage?

I think so, because domesticated crops have a lower genetic diversity than wild varieties. Genetic diversity is useful for adaptation

  3: Is it a good recommendation to grow new Sprout plants from the
  seed of wild cabbage plants?

I don't think this is the best idea, because genetically engineered Sprout plants could be much better.

I am going to assume that Kale is a plant derived from wild cabbage and has been selected upon for certain attributes by humans for 1000's of generations.

1 There are two principle reasons why genetic (allelic) diversity might be lower in the kale subgroup than in the wild cabbage. Firstly, strong selection imposed by humans may have diminished allelic diversity. Strong selection can drive alleles to fixation. Secondly, if the kale has come from a small sub-population of the wild cabbage it may have been through a genetic bottleneck, this is likely to reduce allelic diversity because, unless all alleles from the original population are captured in the founder populations, some alleles will be lost by genetic drift.

2 Generally allelic diversity is a "good" thing in an unstable environment. It allows different trait combinations and variation in traits to occur. If the environment changes drastically then it could impose severe selective forces on the population, those with high allelic diversity are likely to come up with a combination of alleles that survives.

E.g. Humans only allow the cabbages over 18cm in diameter to reproduce in to the next generation. 5 loci affect cabbage size, each having a "large cabbage" (C) allele and a "small cabbage" (c) allele. Having 5 c alleles gives a cabbage size of 15cm. Each C allele adds 1cm. If a population has fixed the c allele at 3 loci (i.e. there is low genetic diversity) then none of the cabbages will be >18cm. If a population has both the C and c allele at all loci then some of the population will be over 18cm.

3 The final question is difficult to answer, it depends on what you define as "a good recommendation,"  that is very subjective. If the aim is to maximize allelic diversity then yes, if it is to maximize cabbage size it is probably no (because the "genetically engineered" plants have been selected upon for large cabbages - they might have the C alleles fixed in the populations!)


How do you sequence a tree genome? I'm writing a grant proposal, and part of the research will involve sequencing and comparing DNA from trees in America and Japan. How does one analyze the genome of a tree and compare it to a conspecific?

In journal articles, they are doing many studies every year describing the state of the art tools and procedures for sequencing plant genomes.

by researching 5 minutes you have results of this kind:

http://www.pnas.org/content/95/16/9693.full

  Protocols involved commercially available kits (e.g., Qiagen’s RNeasy Plant Minikit), non-commercial RNA extraction lab protocols (e.g., CTAB, acid phenol) and hybrid methods that combined components of both commercial kits and lab protocols. The detailed protocols used for all isolations are available online in Appendix S1.
  http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0050226

  Tissue and organ samples for Northern blot analysis of gene expression patterns were taken during the growing season and frozen in liquid nitrogen, then stored at −80°C. Shoot-tip samples are the terminal 1–2 cm of succulent stem tissue from elongating branches and terminal leaders. Immature xylem was harvested with a vegetable peeler from the surface of woody stems after removal of the bark, and includes cells with primary cell walls derived from the cambial zone through the zone of radial cell expansion. Compression wood and side wood immature xylem RNAs were those used for preparation of the libraries, whereas vertical immature xylem denotes samples taken from stems of control trees growing vertically. The tissue described as “phloem” was collected from the inner surface of the bark of vertical stems and actually includes periderm and other tissues as well as active phloem. Planings were collected from the surface of vertical woody stems with a wood plane after immature xylem was harvested and includes cells that have formed secondary cell walls strong enough to resist harvesting by the vegetable peeler. Needle samples were partially expanded juvenile needles.

here are some more texts for you to check

http://www.pnas.org/content/106/31/12794.full

https://bmcevolbiol.biomedcentral.com/articles/10.1186/1471-2148-7-214

From_field_to_film_Rapid_sequencing_methods_for_field-collected_plant_species

It took me 5 minutes to find these informations by searching articles for

  plant sequencing methods


Species Identification: large shiny black beetle, Detroit USA What sort of beetle is this? I live in a suburb of Detroit and found a whole bunch of these living under my lawn when I was replacing a section of it. I'm assuming these are also the source of the grubs I found as well. Are these harmful?

You found a stag beetle (family Lucanidae).

Although the males are much more readily recognized with their large "stag antler" shaped mandibles, these species are often sexually dimorphic with females having much smaller mandibles (e.g., see here). However, in some species the males' mandibles are likewise diminished and not stag shaped.

According to the Wikipedia page:

  Currently, the only means of identification of world species is the illustrated text by Mizunuma, T. and S. Nagai. 1994. The Lucanid Beetles of the World. Mushi-sha, Tokyo. 337 pp. based on the work Catalogue illustré des lucanides du globe in Encyclopédie Entomologique (series A 27: 1-223) by Robert Didier and Eugene Seguy.

So without this guide (and without known dimensions of your specimen), an exact identification will be very difficult.

However, your species looks very similar to a male specimen of Lucanus placidus.

Additional pictures (such as the one below) can be found here.

According to Wikipedia, L placidus is 22–35 mm long, has two or more teeth on its jaws and has dark femora. The species is sometimes found in soil and it does live in Michigan:

We can rule out Lucanus capreolus because the color is wrong:

  [L. capreolus is] dark reddish brown in color with a smooth, shiny elytra; [their] femora are orange-brown.


How do neurons find each other? Neurons form complicated networks in brains, but their connections can't be random (at least not entirely). Brains function similarly among all members of individual species, and that functionality is largely dependent on neuron organization. Furthermore, various brain regions have predictable functions, and there are even parts of the brain where specific cells carry out specialized functions (place cells are an interesting example).

Great! We know neurons can organize into very complex networks, but how? They need to find each other, somehow.

The best I can guess is that either:

Neurons find other target neurons with specific chemical signals.
Neurons don't "find" each other, exactly, but grow in predetermined shapes from from set locations. In this case, the connections would simply be due to neurons bumping into each other as they grow in their predetermined paths.
Or both.

In the first case, there would be a mechanism for searching each other out. In the second, there would be a mechanism for staying in one spot (and growing from there). What are the names of said mechanisms? How do I find out more about them?

Q: We know neurons can organize into very complex networks, but how?

The answer is your first guess: Neurons find other target neurons with specific chemical signals.

Q: What are the names of said mechanisms?

This process is called axon guidance, by which the growth cones of developing axons are directed to reach their targets. This process depends upon a slew of cellular and molecular cues. The first axons to grow in any particular brain region are called pioneer axons and are the most dependent upon these cues. Later axons are able to follow (and diverge from) previous axons by the interaction of cell adhesion molecules on their surfaces. Dendritic development is also important for your question, but dendrites tend not to travel as far.

Here are some of the molecules that we know to participate in axon guidance:

Cell adhesion molecules and substrate adhesion molecules, including IgSF CAMs and cadherins
Some chemokines, e.g. CXCL12
Netrins, ephrins, and semaphorins
Slits, via the Slit-Robo cell signaling pathway
Developmental morphogens, e.g. Wnts and Hedgehog

The list goes on, and this is an area of active research. Each of these cues is recognized by one or more specific receptors on the developing neuron, which upon recognition of the ligand molecule either attracts or repels the axon from (or both, depending on the context). Recognition can function either short-range (by direct contact with a ligand) or long-range (e.g. by detection of a concentration gradient), depending on the molecular cue.

For more information, you may want to read Sanes et al., Development of the Nervous System.


What is a membrane potential? I know this may be silly, but I am confused to what a membrane potential actually is. I understand that at resting membrane potential is -70- -80 mV. But what does that exactly mean and how does this all tie into diffusion potentials and equilibrium potentials.

The existence of membrane potential is just that: as long as they are alive, cells try to keep their cytosol different from the outside soup, mainly by expelling sodium ions. There is a longer story, with cells pumping other ions in or out, or leaking ions due to the imbalance, but resting membrane potential really revolves around sodium. There is an imbalance in sodium across the membrane, and that makes sodium naturally try to balance out, by trying to leak back in.

I am sure you have heard about the famous sodium/potassium ATPase. It expels sodium ions, while letting in fewer positive ions. It is just the most studied way the cells are going about making sure their innards poorer in cations, that is, negatively charged when compared to their environment.

All these pumps are ATP-dependent, and you would know ATP is the main energy store. So as long as cells live and make ATP, they can maintain this difference between their innards and the environment. Once they die, ATP is gone, pumps stop, and there is no sodium disequilibrium - no membrane potential.

Diffusion potential is an artificial concept that we use in order to make sense of the membrane. We imagine a membrane that opposes sodium movement alone, and we calculate how hard will it be (how much energy must be spent) to keep the asymmetry of low sodium inside - higher sodium outside, were a hole punched in the semipermeable membrane. Luckily, we can use some physics and maths, and figure that this energy is dependent of the ratio of sodium concentrations ([Na]in divided by [Na]out). For typical cells, there are 150 mM Na outside and 15 mM Na inside a cell; physics tells us it will take 62 milli-electronvolts to hold a Na ion out once some hole is found.

If you don't provide those 62 meV and you don't close the doors for leaking, sodium ions will fly in. And that is indeed what happens in depolarization, when sodium gets a chance to move.

These electronvolts are a unit of energy, or work. We can think of a few ways of performing this work on a Na ion that tries to leak in: heat the cell until ions stop caring about direction of movement, hold the outside Na in some tight  chemical structure etc. But the simplest way is to apply an electric field. If you add to the concentration imbalance a 62 mV electrical difference in electrical potential, you stopped the flow of sodium either way. Get a bit less than 62 mV, and the Na ions will carry on their old ways and try to no avail to leak into the cell. Get a bit above 62 mV, and the flow of sodium will be force in the opposite way. Stay on 62 mV and you achieve equilibrium potential: neither direction will have the upper hand.

The picture is way more complex once you factor in the other ions, but the facts are:

resting and action potentials are voltages one can measure across membranes, quite often during cells' lives
diffusion potentials are part of an abstract model
equilibrium potential is something one could impose on a cell - not something that you'd find in natural frequently, yet not plain fiction.


Is it possible to affect a brain with electromagnetic waves? A human brain can generate electrical signal. So it generates magnetic field as well. Is it possible to affect a brain with electromagnetic waves?

One can use transcranial magnetic stimulation to modulate neural activity. This is effectively inducing a current in the tissue under a magnetic coil.


Exhalation while holding breath If you inhale to your maximum capacity and hold your breath for an extended period of time, it begins to feel uncomfortable; slowly releasing your breath at this point seems to provide relief from this discomfort.

Is there a biological reason why this is so, or is this something psychological?

The exact causes of the discomfort relief  after the breath-hold breakpoint  is unknown yet.

It has been stated that breath "pacemaker" continue to work independently of voluntary breath holding. Thus, while breath holding, the breath center is trying to activate the diaphragm and the afferent feedback from the diaphragm normally causes the feeling of discomfort. Thus, upon starting breathing again, i.e. actual diaphragm movements, the discomfort will diminish and the subject will feel relief.

Breath-holding and its breakpoint. Experimental Physiology Volume 91, Issue 1, January 2006.

full text of cited article


PCR enzyme units or concentration? When performing PCRs, usually in every protocol enzyme amount is specified as 1.25 U as optimal per 50 uL reaction. Then, when running 25 uL PCR reaction should i use 1/2 he amount the enzyme or should i respect the value on Units thus using the same volume as in 50 uL reaction?

You have to scale amounts of all PCR components proportionally depending on the volume of the reaction. The polymerase is no exception in this respect, the only difference is that you measure it in terms of activity - units. So in your protocol you have 0.025 U/µl and you have to maintain this concentration when changing the volume.