text:
Does polyploidy always isolate the polyploids from the diploid source population?
I am receiving conflicting information while researching polyploid speciation. On the one hand, some sources state that a polyploid can only reproduce sexually with polyploids having the same number of chromosomes. But I am also finding information claiming tetraploid x diploid reproduction in orchids, or tetraploid x triploid reproduction of orchids (for example,see  American Orchid Society, AOS.org).
Is polyploid sexual isolation always the case, sometimes the case, or never the case? Can someone clarify this?

Welcome to Biology.SE. That would help if you could link to all your sources.

Ploidy and reproductive isolation in plants
Speaking generally, there is simply no question that for flowering plants there can be a sexual pathway between diploid and polyploidy levels. The question is how wide is the bridge and how much flow is there in either direction. In other words the questions become "How much flow?", "How meaningful the flow?", "How much flow back to the original diploid and polyploid populations?", and "How often over the last 200 million years has such interaction been an important factor in the evolution of flowering plants?".
Examples from Rhododendron
In the following, I will give a number of examples from the plant genus Rhododendron to show how ploidy level can function in relation to sexual isolation. In this taxa, diploid X tetraploid normally produces triploids although occasionally a tetraploid or even a diploid offspring is produced. The triploid offspring of diploid deciduous azalea species X tetraploid deciduous azalea species often look very similar to the tetraploid pollen parent.  'Margaret Abbott', which is a seed fertile tetraploid deciduous azalea, has a fragrant white flower produced by crossing a fragrant pink flowered diploid seed parent with a non-fragrant yellow flowered pollen parent.
Our research on hybrid elepidote Rhododendron indicates that triploids, although reluctant to reproduce sexually, can produce diploid, triploid, tetraploid, and pentaploid offspring when crossed with pollen from diploids, triploids, and tetraploids. 'Phyllis Korn' is an example of a fourth generation triploid. 'Graf Zeppelin', which exhibits polyploid characteristics, is an example of a diploid offspring of a triploid. 'Countess of Derby' is an example of a tetraploid offspring where both parents are triploids. 'White Ginger' is a an example of a pentaploid offspring of a triploid. 'Pink Pearl' is an example of a triploid that has produced diploid, triploid, and tetraploid offspring from interaction with diploids.
In deciduous azaleas triploid X tetraploid crosses often produce aneuploids between triploid and tetraploid. Such crosses can on occasion produce pentaploids.
Our limited experience working with triploids and pentaploids as seed parents indicates that in general pentaploids are better seed producers than triploids.
An interesting finding is neotetraploids can produce diploid offspring in the first generation. In general tetraploids can produce diploids, triploids, tetraploids, and pentaploids when crossed with pollen from diploids, triploids, and tetraploids.
Triploids are common in natural contact zones where diploid deciduous azalea populations overlap with tetraploid deciduous azalea populations. There is strong evidence indicating there is gene flow from the diploid population to the tetraploid population in these contact zones. There is some evidence of gene flow from the tetraploid population to the diploid population. There is some evidence to suggest multi-generational triploids exists in these contact zones.
Worth noting is that the meiosis for triploid deciduous azaleas that do set seed is distributed around 1.5x gametes ranging from 1x to 2x with an occasional 3x gamete. This uneven distributed splitting of triploids is what produces aneuploid offspring between 3x and 4x when semifertile triploids are crossed with pollen from stable tetraploids. Cyril Dean Darlington in the late 1920's and early 1930's documented this uneven distributed splitting of triploids during meiosis. Evidence suggests that neotetraploids can also undergo uneven distributed splitting during meiosis.
Darlington's history of the garden hyacinths showing a triploid pathway from diploid species to tetraploid hybrids parallels the history of the hybridization of the tetraploid elepidote Rhododendron 'Countess of Derby'.
We have some evidence for deciduous azaleas that 3x X 4x can produce aneuploids close to 5x indicating that some of the "3x gametes" are coming from first an uneven splitting of the triploid followed by a failure to reduce in a later phase of meiosis. However this result of aneuploidy near pentaploid has not occurred often enough to be certain that is what is happening.
In general for deciduous azalea species;

diploid X diploid normally produce seedpods and high percentage of
viable seed.
tetraploid X tetraploid normally produce seedpods and high percentage
of viable seed.
diploid X tetraploid normally produce seedpods but a highly variable
percentage of viable seed.
tetraploid X diploid almost never set seedpods.
triploid X tetraploid sometimes produce seedpods and a low percentage
of viable seed.

For hybrid elepidote Rhododendron, 2x X 2x, 2x X 3x, 2x X 4x, 3x X 2x, 3x X 3x, 3x X 4x, 4x X 2x, 4x X 3x, and 4x X 4x are all documented to have occurred.
For deciduous azaleas, we have produced viable seed from 2x X 2x, 2x X 4x, 3x X 4x, 4x X 4x, 4x X 6x, 4x X 8x, 5x X 4x, 6x X 4x, and 6x X 6x.
The flow cytometry for this research on the genus Rhododendon was performed by Dr. João Loureiro, Dr. Silvia Castro, José Cerca, and Mariana Castro
Plant Ecology and Evolution Group,
Centre for Functional Ecology,
Department of Life Sciences,
Faculty of Science and Technology,
University of Coimbra, Portugal.
The ancestry for 'Phyllis Korn' illustrates that triploids can be multi-generational.

The diagram below illustrates how the triploid 'Pink Pearl' has produced diploid, triploid, and tetraploid offspring when interacting with diploids and has produced a tetraploid offspring by interacting with another triploid.

The family tree for the Rhododendron elepidote hybrid 'The Duchess' illustrates that interploidy interaction can be multi-generational.
\
Picture of 'Margaret Abbott' with a quote from Frank Abbott.

Picture showing how much the offspring of a diploid crossed with a tetraploid looks like the tetraploid pollen parent.

Picture showing the successful development of seedpods from crossing a diploid by a tetraploid.

Picture showing the failure in developing seedpods from crossing a diploid by a tetraploid.

Picture showing interploidy hybrid swarm at Audra State Park, WV.

References
Meiosis in Polyploids
by W. C. F. Newton and C. D. Darlington
in Journal of Genetics 1929
The history of the garden hyacinths
by C D Darlington, J B Hair and R Hurcombe
in Heredity 1951
Rules of Engagement: Have Pollen—Will Travel
by John Perkins · Sally Perkins
in Azalean 2010
Frank Abbott's Village of Azaleas
by John Perkins · Sally Perkins
in Journal American Rhododendron Society 2011
Ploidy level estimations in deciduous and elepidote hybrids of Rhododendron
by José Cerca de Oliveira, Mariana Castro, Francisco J. do Nascimento, Sílvia Castro, John Perkins,Sally Perkins, João Loureiro
in Jornadas Portuguesas de Genética, Coimbra, Portugal; 05/2011
Weighing in: Discovering the ploidy of hybrid elepidote rhododendrons
by Sally Perkins, John Perkins, José Monteiro de Oliveira, Mariana Castro, Sílvia Castro,  João Loureiro
in Rhododendrons, Camellias and Magnolias, Royal Horticultural Society, Editors: Simon Maughan, pp.34-48 2012
Untersuchung des Ploidiegrades elepidoter Rhododendron-Hybriden
by Sally Perkins, John Perkins, Mariana Castro, José Cerca De Oliveira, Silvia Castro, João Loureiro
in Rhododendron und Immergrüne , Deutsche Rhododendron-Gesellschaft e.V. , Seite 21: pages 21-42; 11/2013

Very comprehensive and well referenced +1. I edited your answer to bring the general conclusion (for plants) to the forefront, and added a couple of headings. I hope you are fine with my suggestions - otherwise feel free to edit or rollback.

Depending on the species the hability of generating hybrids will be different.
Some can, others don't. However generating a hybrid of a diploid and a tetraploid will give rise to a triploid, usually sterile plants (as it happens with seedless whatermelons, which are a cross between tetraploid and diploid).
This is where most of the isolation comes from, as these triploid hybrids are sterile (they can't undergo meiosis because of the control systems that require an even amount of chromosomes) they are not a viable species, and thus a genetic barrier begins.
I don't know specifically on the Orchids though.


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The role of voltage-gated ion channels in chemical synapses
I am trying to understand the mechanisms underlying action potential generation on
the cellular level.
Typically, there is an emphasis on voltage-dependent permeability changes of Potassium (K+) and Sodium (Na+) channels which lead to the respective changes of the membrane potential.
Also typically, synapses in the brain are chemical synapses (in contrast to the smaller fraction of electrical synapses, e.g. in the hippocampus, which make use of gap junctions for signal transmission).
My confusion is now this: Chemical synapses depend on neurotransmitters to trigger permeability changes. The canonical explanation of action potentials is with reference to voltage-gated channels -- how do these two things go together?

Have you learned about what neurotransmitters bind to?

Yes, so I think to understand that they bind to the receptors/ion channels on the neuron's membrane - but then again, it is the NT binding and not the voltage-changes which affect these channels permeability?

Yes. Those are called ligand-gated channels.

I understand that, but if an AP is dependent on ligand-gated channels, I still don't see how voltage-gate channels fit into the picture

When you learn about voltage gated channels and APs, you probably started with resting conditions and then with some depolarization of undescribed origin: it could be by an experimenter or it just "happens". Next you learn about ligand gated channels, which it turns out provide that initial "kick".

I see, thanks! So what you are saying is that the change in membrane potential which "kicks off" the VGICs is in a first step induced by the ionotropic/metabotropic channels?

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Changes of permeability and driving force during voltage clamp
An action potential can be understood in terms of voltage changes, and these are fundamentally a function of relative permeability changes, mostly for Sodium and Potassium ions. If for instance the relative permeability of a cell strongly changes in favor of Sodium, the membrane potential approaches the equilibrium potential of this ion, leading to the depolarization of the membrane.
I understand that voltage clamp methods allow us to assess these permeability changes by "clamping" the membrane potential, and equivalently keeping the driving force constant:
$I = g * (V_m - E_{eq})$
with $V_m - E_{eq}$ being the driving force.
Related to that, I have two questions:
(1) Say we are approaching the Na+ equilibrium during an action potential peak, being closer to the Na+-equilibrium means a smaller driving force, hence the ion flux is an interaction driving force x permeability. Hence why the strong emphasis on permeability if the driving force is as relevant?
(2) When we clamp the voltage, say below the Na+ equilibrium at -20mV, we will have a constant influx of Na+. While I understand that this influx consists of only few ions entering the cell, doesn't clamping over a longer period of time change the concentration because the pumps can not keep up with the constant influx of cations, adding up over time?

Relative ion permeabilities determine the equilibrium for a given configuration of ion channels. You can easily understand what is about to happen to the voltage of a cell if you know the permeabilities: if the equilibrium voltage is more positive than the present voltage, then the voltage will increase over time. The rate at which it increases depends on the membrane time constant, which depends on the capacitance of the cell (which is based mostly on membrane area, and stays relatively constant) and the resistance; the resistance is, again, based on permeability.
So permeabilities tell you A) Where you are going, and B) How fast you are going there. This is all relevant if you are living in "voltage land": you can actually ignore currents completely and just think in terms of voltage. This is the situation in 'current clamp' recording and for the most part I would say is the easier way to understand the 'big picture' for a neuron.
If, however, you want to think about currents themselves, then you typically clamp the voltage. Clamping the voltage also keeps the driving force constant (at least over the time scales on which voltage-clamp experiments make sense). In that case, you are right, you can't ignore driving force, however, in that case you are usually setting the driving force (by setting the voltage), and measuring the current. "Driving force" is then only necessary to figure out the permeability.
If you voltage clamp a cell at a depolarized potential for a long time (minutes), eventually yes the ion concentrations will change. Voltage-gated sodium channels tend to inactivate pretty quickly, so you actually won't get much sodium current when you voltage clamp at -20 mV for a long time, at least not in the soma, but you might get more current out in the distal processes that are not clamped well and other ions like calcium. Cells do not hold up well under long-term voltage clamp, however. I believe the main culprit is calcium toxicity, though it might vary by cell type and other particulars of the recording configuration. You can also kill a cell by just disrupting the membrane and making it more leaky: the concentrations change faster than the pumps can keep up with and you get excitotoxic cell death.
I usually recommend Purves' Neuroscience as a basic textbook, and the Methods in Enzymology volume on Ion Channels edited by Rudy and Iverson for patch clamp techniques and related practical wisdom.

Right, that makes sense. So when we do not clamp, driving force is relevant for explaining currents - do I understand that correctly?

@Pugl What do you mean by "when we do not clamp"?

During the action potential, that was what the original post was referring to (I understand that driving force is constant during voltage clamp).

@Pugl It kind of matters what exactly you are trying to look at. If you are recording in current clamp mode with 0 current, then you are just measuring voltage. You don't have enough information because you don't know the instantaneous resistance. But if you were creating a simulation of an action potential, and you are setting the conductances, then yes you could use the driving force to calculate the current in the equation you mentioned.

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text:
What is the resistance of a single human cell?
What is the resistance of a single human cell? I know different cells will have different values, some examples would suffice. I did not find any such information on the internet.

At what voltage? Not only does this differ by cell (and environment), it often varies by voltage (and time due to inactivation).

Welcome to SE Biology. Please insert the term "electrical" in your title and question to make it clear what you are talking about. It would also be a good idea as a new user for you to complete the tour, your lack of the badge for that implies you have not.

Hi poi. Welcome to Bio.SE. Please clarify which type of resistance you are referring to. Also, we ask that you demonstrate some previous effort on your own part to have answered your own question. Please provide such support. Thanks.

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Behaviour of neuron when membrane potential is maintained at threshold potential or more
Via an external electrode the membrane potential of a neuron or group of neurons can be increased from resting potential of -70 mV to -50 mV or more. This will cause them to fire an action potential. What happens if the electrode maintains the membrane potential at -50 mV or more for say 1 minute? Initially it should fire once, but then it will not reach the resting potential, will it stop firing or keep on firing continuously since it is above threshold potential? Will this kill the neuron or make it malfunction permanently?

Before I start, I should point out that in order to change the membrane potential (known as the Vm) of a neuron you really need an internal electrode - so that you can pump current in to it, so increasing the potential above the resting membrane potential (RMP). The RMP is simply the Vm of a neuron at rest, without any external meddling by pesky scientists (or synaptic inputs).
When you depolarise a neuron - in other words, make it less negatively charged, it will fire an action potential once it crosses the spike threshold. This value is different for different neurons, but -50mV is usually not enough to trigger an action potential - normally it's more in the range between -30 and -40. But let's say it does, as it doesn't change the thrust of the question.
The major part of what happens during an action potential is that sodium channels open, allowing the spike to fire. Once closed, these channels have a 'refractory period' - essentially a time out, during which they are less likely to open again. So even though your neuron is still above spike threshold, it can't fire because the channels can't open. (For the aficionados, you can actually think of this as the spike threshold becoming temporarily more positive - going up to, say, -20mV).
So your neuron doesn't fire again for, say, 10ms, until the sodium channels reactivate. Then it does. So you get a train of regularly spaced action potentials at a certain frequency. The more you depolarise the neuron, the faster this frequency becomes until a point where the channels just become totally inactivated and the neuron stops firing. If you hold the cell at this voltage for more than a few seconds, in general it will die.

Edit 2: On second thoughts, maybe secondlevel isn't quite correct. Assuming a the membrane potential is held at -50 mV, using a patch pipette, in whole-cell voltage clamp, then the neuron generally won't fire action potentials. Not as we know them anyway as the cell membrane potential is "clamped". This controls the open probability of ion channels and allows ions to flow in and out of the cell, which can be measured as currents.

Unless the membrane potential is controlled by injection of current, in "current-clamp" mode. This could be controlled in patch-clamp, or done via an external electrode, which would provide local current, but wouldn't be so well controlled.
Secondlevel is pretty much spot on, here's an image of a neuron stepped to approx -60 mV from -78 mV.
The below cell's voltage is not being controlled directly; it is a recording in current-clamp mode, being depolarized by injecting positive current. Action potentials do not occur in a proper voltage-clamp.

Note that the action potentials aren't entirely predictable, there's a bit of variability in the frequency, but they're roughly every 20 ms. Also, this is just one example, from one cell type. Other neurons will behave differently.

Your current clamp example is fine. The OP's question doesn't make any sense if interpreted in voltage clamp terms, because you wouldn't get action potentials in voltage clamp.

Thanks, I was just in the process of trying to clarify. Not sure it makes sense without a thorough understanding of electrophys though.

Since the OP directly said an action potential is fired, and was also initially referring to external stimulus (though like the other answer mentions, it would be nearly impossible to maintain a steady depolarization that way), I think it is safe to assume two things: 1) the voltage is not clamped, and 2) the cell has a threshold no more depolarized than -50mV. I think your answer was more clear without the added explanation of current/voltage clamp.

Also, real life voltage clamp is simply not quick enough to prevent action potentials (usually referred to as action currents) occurring. They do happen in all but the lowest access resistance cases.

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text:
Found Skull(?) in Ontario Canada, help identifying please
skull?...now maybe thinking its a bird pelvis?...(I don't know thats why I'm here!)on the beach in Northern Ontario Canada, have been wondering what it is. Any ideas? As you can see it is very small, fits in the palm of my friends hand.
Thanks so much!
Kimberley,

An old post about Id-ing the same bone,Synsacrum .

Yes, this is a synsacrum, a part of a bird's pelvis. I would say it's from a cormorant, as I have found this comparison of different synsacra online (third from left):
No idea about the exact species, though.

Image source:
https://hiveminer.com/Tags/cormorant,skeleton

but is the OP's specimen large enough to belong to a cormorant? Please research a little more and update your answer with the expected dimensions/size of a cormorant's synsacrum if possible. Thanks!

@theforestecologist how does that help? It might be too small for an adult cormorant (even thought theres a wide range of cormorant sizes among the species), but who says it could not be a juvenile?


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How do we know if a neuron is inhibitory or excitatory?
The textbook examples for an excitatory neurotransmitter is Glutamate, and for an inhibitory neurotransmitter it is GABA.
In my naive understanding, a neuron was inhibitory or excitatory depending on the neurotransmitter it releases onto its postsynaptic partners.
According to this thread, however, a neurotransmitter is not per se excitatory or inhibitory, but this property depends on the postsynaptic receptor it is acting on.
Now this property seems independent of the presynaptic cell - hence, how can we classify the presynaptic cell of being either inhibitory or excitatory (when that is a property of the postsynaptic receptors, which can be either)?
Besides, given that we a huge number of neurons and their connections in each $mm^3$, how can we be sure that the presynaptic's cells action are not mediated by other cells, and the observed inhibition/excitation is not rather a network effect?

In my naive understanding, a neuron was inhibitory or excitatory depending on the neurotransmitter it releases onto its postsynaptic partners.

This is mostly correct. What remains a question is what makes a given neurotransmitter inhibitory or excitatory. To some extent, that depends on the post-synaptic receptors, but also depends on other conditions: one case mentioned in the linked Q&A that I'll repeat is that GABA is actually excitatory at some times, including during development (and the same thing can happen in certain causes of epilepsy). In that case, the reason is because GABA-A receptors are chloride channels, so the reversal potential for chloride is what matters. If the reversal potential for chloride is more hyperpolarized than threshold, GABA-A is an inhibitory receptor; if the reversal potential for chloride is more depolarized than threshold, GABA-A is an excitatory receptor. Chloride ion concentrations are different during certain stages of development so the role of GABA changes (in development it seems like it is important for development of eventually inhibitory circuitry).

I digress a bit, but I think you've really already encountered all you need to know: labels like "excitatory" and "inhibitory" for a neurotransmitter itself are generalizations that satisfy human preferences for heuristics. It's convenient to talk about GABA as an inhibitory neurotransmitter, because in most cases the major systemic effect of GABA is inhibition. Same with glutamate in the direction of excitation.
Most of the inhibition caused by glutamate is the presynaptic inhibition type discussed in a previous Q&A; that is, it is suppressing the release of glutamate itself. In that sense, glutamatergic inhibition is only as effective as glutamatergic excitation is: the net effect of glutamate will always be excitatory in that system.
Therefore, it is straightforward to consider GABAergic and glutamatergic cells inhibitory and excitatory, respectively.

how can we be sure that the presynaptic's cells action are not mediated by other cells, and the observed inhibition/excitation is not rather a network effect?

The principle way is by pairwise recordings: you record from the presynaptic and postsynaptic cell at the same time, activate the presynaptic cell, and measure the voltage in the postsynaptic cell. These sorts of pairwise recordings are a common tool in neuroscience.

Cancedda, L., Fiumelli, H., Chen, K., & Poo, M. M. (2007). Excitatory GABA action is essential for morphological maturation of cortical neurons in vivo. Journal of Neuroscience, 27(19), 5224-5235.
Owens, D. F., Boyce, L. H., Davis, M. B., & Kriegstein, A. R. (1996). Excitatory GABA responses in embryonic and neonatal cortical slices demonstrated by gramicidin perforated-patch recordings and calcium imaging. Journal of Neuroscience, 16(20), 6414-6423.
Thomson, A. M., & Deuchars, J. (1997). Synaptic interactions in neocortical local circuits: dual intracellular recordings in vitro. Cerebral cortex (New York, NY: 1991), 7(6), 510-522.

"The principle way is by pairwise recordings: you record from the presynaptic and postsynaptic cell at the same time, activate the presynaptic cell, and measure the voltage in the postsynaptic cell." --> But this is still a correlation analysis. Say you activate cell A and record A and B, how can you exclude A acting on C,D,E...with all kinds of non-trivial interactions then leading to changes in B? Then while A would still be relevant for B, the excitation/inhibition might arise from more complex mechanisms.

@Pugl No, it's not a correlation analysis: you stimulate and measure the response. A correlation analysis would just measure activity in both and relate the (spontaneous) spiking times to the voltage. You can base conclusions on latency, use brain slice recordings where spontaneous activity is very low (such that only the cell you are activating is likely to be firing, and especially only that cell is firing time locked to every stimulation trial), in some cases record directly from dendrites and even axons in special synapses.

You can use pharmacology to test which transmitters and receptors are involved, directly puff neurotransmitters onto the post synaptic cell and see the same results, you can use imaging to monitor voltage or calcium in real time, you can activate presynaptic terminals with calcium uncaging. Basically decades and decades of neuroscience research.


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Why do I have two kinds of pubic hair?
I feel silly even asking this question, but there's a quirk of my anatomy that I find interesting, and I can find nothing about it online.  I am looking for information on whether this quirk is documented, and whether it has any biological role.
I am a Caucasian male, and my quirk is that I have two different kinds of pubic hair.  On my genitals and immediately above, I have a dark wiry kind of hair like that which I find under my armpits and on my chest.  Above this, there is a second bundle of hair which is fairer (similar color to the hair on my head) and curlier.  The color difference between the two hair types is marked.  There is also a small amount of hair continuing up to my navel, which appears to be of the first type (same as chest, armpits, and genitals).
So my questions are:

Is this a common feature?
If not, is it documented at all?
Does it serve a biological purpose?

My reason for asking 3, in particular, is that I've heard multiple explanations for the existence of pubic hair.  One theory is that it indicates sexual maturity.  Another is that it is related to hygiene.  My anatomy seems to suggest both might be true: Hair under armpits is presumably for some practical purpose, like wicking sweat out of an otherwise dank crevice, and the hair on the genitals would appear to have the same effect.  On the contrary, colored hair like that on the head is presumably a secondary sexual characteristic, and the fact that I have a bunch of colored pubic hair above my genitals (where there is no apparent practical purpose, as with the hair below) would seem to serve the same purpose.

Relatively interesting evolution question --- hypothesis regarding reasons for certain evolutionary traits can be debated (this particular question, scientists seem to have many theories). However, here is one possible explanation:

Pubic hair near the sexual organs is likely for hygiene function; especially for women infections from parasites were common in those areas. The hair would act as a protection barrier, and hence the different texture of that hair being a little thicker.
Pubic hair in arm pit regions may keep pheromones, or chemicals your body produces that send subconscious messages to other humans. Often, these chemicals are released from sweat, and hence it would make sense to have hair in those regions to trap them there. The texture of the hair in those regions probably evolved to be more effective in keeping oder.

https://www.self.com/story/why-you-have-pubic-hair
https://blogs.scientificamerican.com/bering-in-mind/a-bushel-of-facts-about-the-uniqueness-of-human-pubic-hair/

what you are describing the the difference between terminal hair the coarsed darker hair an vellus hair the fine hair. Yes all adults have both.
 Vellus hair covers basically your entire body, Terminal hair mostly develops during puberty as a secondary sexual characteristic and only covers certain areas. the function of terminal hair and pubic hair is hotly debated and may differ from area to area. Proposed functions include friction/chafing prevention (armpits), scent retention, or even just as a maturity signal.


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Finding All of the Genes in a given Genome
I'm interested in finding the start position of each nucleotide in a given genome.  I first went to EcoCyc and wrote a scraping script for their E coli data, but I can't find the same web page layout for other specimen.  So wondering if there is a database with more consistent formatting and such things.  I've been looking around BLAST (?), but got confused with the resources, and rather than spinning my wheels, thought I'd ask for some pointers where to start.

Are you working with annotated genomes? Is there a reason you can’t just pull a .gff file from NCBI?

"I'm interested in finding the start position of each nucleotide in a given genome." Do you mean the start position of each gene? And by "gene", I'm assuming you're restricting it to protein-coding genes? What algorithm will you be using to call genes, as just searching for start codons won't work.

@acvill I'm not opposed to any format, just fairly new to this work, and looking for good pointers to start off with; I'll read through the documentation you linked and some examples.  Any other resources you might suggest?

@MattDMo "each gene" is just a good place to start, to start working with stuff, as I'm fairly new to this kind of work.  For example, on the EcoCyc I link to, it has the position of the start of each gene in the given E coli genome.  Are there libraries of the genes in a given genome?

I think @acvill's point is that this work has already been partially or totally completed for quite a number of organisms...

Yes, there are numerous gene databases in NCBI and elsewhere. This is turning into an XY problem, though. What exactly is your goal in doing this work?

My goal here is to take a set of organisms (of any domain in life) and take down the locations of each gene start position; then doing so, making a bead-and-chain model, where a ball with a gene is of some type (maybe sub-types, etc), and a ball without a gene is of another type (and a ball corresponds to some few kilobases of DNA (or less)).  Ultimately the models should be more sophisticated, but this is the initial toying around step

Why would you want to break it up in such a way. Each part - even if it is not coding for any gene still has an immense role to play in coding for the genes and other things?

I would suggest using the FTP at NCBI to download GFF files for whatever organisms you are interested in, as suggested by commenters. GFF files will have annotations for the genome for genes and also for many other features (figure 1).

Not entirely clear about the goals of this, but if you want annotated coordinates of things in genomes GFFs are a good place to start.
Note that many/most genomes will not have assemblies at the chromosome level, but only at the scaffold/contig level. Depending on your application that may be an issue.
If you want to go to a specific genome/organism, you can search it here. You can access the FTP through the interface for each genome there.


text:
Questions about Cohesin - what does the ATPase domain do, and any suggested PDBs to look at?
I've been reading about cohesin lately, and I'm confused about the head subunit interactions.  I've read a few papers, and also found this nice figure from wiki that demonstrates the crux of my question (note: SMC here corresponds to Cohesin, or am I mistaken?  I'm pretty sure this is correct, or pretty much correct):
From reading around, I'm aware generally the head subunit is an ATPase, yet from this diagram (and from the typical putative "use" of Cohesin in TAD maintenance), I'm not sure what exactly is the ATPase motif so useful for, it seems that the ATP is sort of "glueing" the the two head domains together, but that seems opposite of what ATPase would typically do, ie catalyze ATP -> ADP.  This makes me think I'm just misunderstanding something, and wondering what is the function of the Walker A/B ATPase motif.
Also, I'm wondering if there are any nice PDB files that show a cohesin loop, or elsewise are generally the most instructive about Cohesin.  I've searched through a few, but would like more informed advice about some good structures, and maybe why they are nice.

This article :
Prakash Arumugam, Stephan Gruber, Koichi Tanaka, Christian H. Haering, Karl Mechtler, Kim Nasmyth,
"ATP Hydrolysis Is Required for Cohesin's Association with Chromosomes",
Current Biology,
Volume 13, Issue 22,
2003,
at
https://www.sciencedirect.com/science/article/pii/S0960982203008042
Their conclusion is:
"Conclusions: Cohesin complexes whose heads have been connected by Scc1 must hydrolyze ATP in order to associate stably with chromosomes. If chromosomal association is mediated by the topological entrapment of DNA inside cohesin's ring, then ATP hydrolysis may be responsible for creating a gate through which DNA can enter. We suggest that ATP hydrolysis drives the temporary disconnection of Scc1 from Smc heads that are needed for DNA entrapment and that this process is promoted by Scc2/4."


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Why might the chirality of gastopods be dominantly dextral?
This wikipedia page on gastropods provides a definition of chirality, and briefly describes the genetic mechanisms behind why a shell is wound left (sinistral) or right (dextral) handed. It also mentions the fact that there are more species of gastropods that are dextrally wound than sinistral. What the page does not offer is why this might be so with regards to evolutionary pressures.
Does anyone have an explanation of why gastopod species have wound up dominantly dextral?
This question relates to my question about a specific species of gastopod that is found in equal proportion of both chiralities, and both in the question and answer there are suggestions of a chiral relationship between predator and prey and perhaps ease of mating. But it really doesn't answer my general question.
If it's a predator-prey pressure then is there any evidence across a larger sample of species that supports this explanation? Or of the left and right handed species of gastropods, anatomical evidence across a large number of species that shows mating advantages? Or likewise any other explanations that offer evidence?

Possible duplicate of Does the species of snake that eats Amphidromous inversus have chiral dimorphism?

I don't think the question per se is a duplicate, but @Remi.b's answer covers this nicely.


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What exactly is "chromosome topology"?
I've been reading a lot about Hi-C lately, and this has been bothering me.  So far as I can tell from reading around, the topology is related to the conformation of the linear chromosome.  This seems like a fairly pointless description however, as they should all have the same topology.  A "conformation", in my understanding, is the chromosome being folded into a particular geometry.
On the other hand though, I guess if two genes were brought together to form a loop, they would also form a "hole" (the gap in the loop).  But this seems like a weak connection to make, just because two chromosome regions are paired doesn't necessarily mean they were bound and formed a loop.  It seems the "topology" would "best" be seen after a 3D reconstruction from the pairs data, showing the predicted geometry, and from there you could see how many putative loops and such there are, and thus start to determine the topological properties.
The last possibility I was thinking was that this is in reference to network topology implied by a contact matrix.  This seems the most likely to me, but also the least implied (to me, at least) in the literature I've ever read.
All of this has me wondering if I've missed something about the meaning of "topology" here, as opposed to just "conformation".  I'm wondering if there is a consensus on the precise meaning of topology in the genomics/Hi-C context.

'topology' can just mean 'shape' . "the way in which constituent parts are interrelated or arranged."   whether it is point-set topology, algebraic topology, network topology, chromosome topology. It is the study of the shape of something.

Conformation (chromosome) refers to the spatial organization of chromatin in a cell. A wide range of eukaryotic organisms fold into higher-order chromatin domains. These are affected by TADs (topologically associated domains), LADs (lamina-associated domains), NADs (nucleolus associated domains), constitutive and dynamic.

Topology isn't just about shape though, but about the properties of a shape that are conserved under continuous deformation, ie folding, which all chromosomes would share (w some special case exceptions).  As wiki states: 'The motivating insight behind topology is that some geometric problems depend not on the exact shape of the objects involved, but rather on the way they are put together.'  Linearly, all chromosome (of same type) are put together the same way.  I can see how perhaps there is a network topology interpretation of Hi-C data, but it doesn't seem like the implied interpretation

To use the coffee cup/donut example, there are many ways to deform a donut that maintain the same topology (such as into a coffee cup), and it would be confusing to call all of these different conformations "topologies".  However, you could deform the donut so that regions that aren't adjacent on the surface are adjacent in 3D space, and you could get unique "network topologies", but again, this interpretation doesn't feel like the implied one.  The one exception is if you consider loops in chromosomes, but that also seems correlated, but not great, with Hi-C data

*I shouldn't say "the one exception", I mean the primary exception/caveat

Could be relating to where genes are relative to each other. This affects their activity.

I can see how that might work, the issue is that this would, within one organism, every chromosome should generally have the same chromosomes, just with different chromsome configurations and gene up/down-regulation.  This would change with gene transposition, or gene insertion/deletion, but this topic is not brought up in the literature when talking about topology, or really Hi-C in general (and if it is, those are exceptions, not the rule).  Generally, chromosomes are thought of all as "the same" organizationally, as is shown by comparisons of chr region's characteristics between cell types

@user8243 You are hung up on a mathematical terminology. Your quote about continuous transformation refers to the mathematical term for topology, then the disambiguation goes on to mention discrete , network, electronic layout and geospatial topologies. It's not a word that came from math. Math uses that word because it means "shape" and no one says "shape theory".  I am not sure why mathematicians feel like they own the word... they don't use this with english words 'category', 'field' or 'group' probably because those are far more used in english language than "topology".

I never see a mathematician critique the idea of a 'football field'  by asking why 'Field' is used for that concept when the elements or operations or the identity elements aren't even clear. But I see mathematicians do this all the time about other areas using the word 'topology' .

no one asks about the genus of a chromosome topology just like no one asks about the order of a finite football field. Just about any chromosome topology reference that uses the word 'genus' is referring to the taxonomic level between 'family' and 'species'.

See comments in the answer below, but as an example: "field", "category" etc are very colloquially used terms.  However, something like "algebra" and "geometry" have very obvious mathematical connotations. In terms of linguistic clarity and scientific precision, using such words to mean something else, based on a "non-technical" but non-colloquial definition of a word is extremely confusing for anyone trying to figure out what it actually means.  This is especially the case when this is scientific field, it would be common sense for someone to think the mathematical definition is relevant here

It's important to emphasize also that, as I have mentioned, I am okay with fields using words as they please.  HOWEVER, as indicated by Maximilian Press's answer, and my own confusion, it is not clear that there is a consensus on what topology actually means.  Why not just shape?  Why not just say conformation?  These questions lead people to look up what topology means, which likely leads them into the lap of mathematics, which leads to serious incongruity with it's use here, and its mathematical meaning, which leads to confusion and lack of precisely explicated meaning.  This isn't elitism

As they please* so long as the definition is connected to something meaningful (as it seems to be here). The use of "topology" here isn't nonsensical (and is technically valid), just very confusing, is my point

@JimN hey hope all is well.  I think I found a satisfactory solution, I posted it, let me know what you think

I think that there are a few things going on in this question, I'm going to try to answer the ones that I think are most pertinent:

We should not expect "topology" as used in the Hi-C field to have a rigorous mathematical interpretation. Most of the people thinking about it are ultimately biologists who are interested in biological problems. As suggested in the comments, they are basically interested in the shape of DNA in the cell; e.g. which pieces of DNA are close together and which are far away. You can use this information for a lot of different purposes of course, but most people using the technique are satisfied with viewing topology as "the set of pairwise distances between all DNA chunks" (and whatever things you can infer from that set).

Your sense (from the comment) that the linear chromosome ordering is the main interesting feature of topology is (IMO) absolutely correct. However, it is not a given that every chromosome is put together the same way. This is related to the most useful application of Hi-C data that I know of, which is to either (A) scaffold genomes (put discontinuous sequences into the right order) or (B) deconvolute mixed populations of genomes into groups of sequences that belong to the same cell. The linear order of DNA is by at least an order of magnitude the dominant signal in the data, and is therefore the most trustworthy thing in there.

Network topology is sometimes implicit but generally central as a feature of algorithms using Hi-C data. I don't know that we can say that all workers in the field are thinking of this when they talk about topology, but I certainly am. Some random papers that make it fairly obvious: here, here, here.

(Full disclosure: I work for a company that sells Hi-C kits and services.)

Thank you for your reply.  My question is in part critical of (what I believe is) an unecessary and ambiguous use of the word.  Technically, "geometry" seems to be a better word, but was more frustrating was that "conformation" often seemed not only appropriate as well, but redundantly used alongside "topology".  I'm critical of this though not out of a sense of "elitism", but because it is genuinely confusing.  Anyone trying to understand the "topology" part here will be seriously confused if they end up reading about actual topology.  Your answer is helpful in clarifying its use here

This ambiguity is compounded when its use varies, from a "network" sense to a "shape" sense, that the sense of its use is rarely explicated clearly, and that the term is used so promiscuously.  HOWEVER, this is not to say that using the word "topology" is monopolized by mathematics - I do recognize when a field uses a shared term, it is possible it has different connotations (the point of this question, and you gave a good answer I think).

Still, all of these considerations together mean that the use of "topology" here is very vague and almost inexplicable in its general definition, having very idiosyncratic use going from paper-to-paper, or even year-to-year.  Not even in terms of linguistic use, but even just in terms of scientific clarity, this seems like an unfortunate flaw.

Also, I appreciate those paper links.  I see what you're saying about the uses there

accept the fact that the english word "topology" means anything referring to shape. Another dictionary definition: "1: topographic study of a particular place
specifically : the history of a region as indicated by its topography". Another dictionary: "the way the parts of something are organized or connected:"  Every field of study is entitled to use an english word as it suits their needs

As I said, "this is not to say that using the word "topology" is monopolized by mathematics - I do recognize when a field uses a shared term, it is possible it has different connotations".  What is confusing about topology is that, unlike "category", "field", "group", the word "topology" is no longer (if ever, I do not know) colloquial.  These words do not require anyone to look up a definition in a dictionary.  HOWEVER, the word "topology" does.  And in doing so, you also run into a formal mathematical field.  This seems needlessly confusing when "conformation" can and DOES DO the same job

I think I found a somewhat satisfying solution here, that explains the original use of "topologically associated domain".  I'm not sure if this was the original intent of the semantics, but it works kind of, enough to make the use of topology seem more reasonable.
Topology is, according to Wiki, "concerned with the properties of a geometric object that are preserved under continuous deformations, such as stretching, twisting, crumpling and bending, but not tearing or gluing."
In population Hi-C at least, Hi-C emphasizes/shows the high frequency contacts.  As an example, imagine these as contacts that form a loop (there are other conformations, but this is the simplest case).  The particular loop geometry can vary, but the contact that Hi-C can measure won't vary.  Think about a tied shoe - the shoe can move, the loop of a knot itself can have all sorts of various geometries (imagine squishing it, folding the loop with your hands, etc.).  Regardless, the knot will stay the same; the "string loci" that are adjacent in the knot will always be adjacent, which is an observable that relays that the topology is probably staying the same, ie a "loop" (not to get into knots and stuff, just considering strings touching each other as creating a hole, ie the loop).
Thus, the contact matrices are almost a histogram of the observables which relay topological features, at least for population Hi-C.
For single-cell Hi-C, because we don't have multiple samples, the contact matrix is not a histogram.  Regardless, you can think of it as one term in a histogram, and thus still part of this indirectly topological description.
Let me know if this is unclear.

Can you add your sources? The link to the wiki page etc.?


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How animals know which is carnivorous and herbivorous?
Deer ran away from tiger or cheetah, but not from giraffe or zebra.
where did deer learn this?
How animals know which is carnivorous and herbivorous?

Tinbergen's famous goose/hawk paradigm and subsequent work would be a good place to start.

They probably don't know and probably don't need to. They tend to run away from potential danger and predators in the same evolution environment because those who don't run away will have fewer offsprings that exhibit similar behaviors.
If an animal suddenly sees a predator that his ancestor has never seen before, then it may not run away from it, to its own detriment. Dodo Bird thought humans were harmless.

It is definitely not that easy and the answer will depend on the species of interest. There is probably an important part of culture. There is also probably various reaction depending on the smell or the color of the animal  that is perceived that might be adaptive. One cannot make a general case saying "they just run away from anything".

I agree, deer just do what deer do when they see a predator. To imply that they know or are conscious of their actions carries a huge burden of proof. In fact they are almost certainly acting unconsciously in order for the reaction to be fast enough.  It sounds silly but that's what evolution and natural selection pressures do. There probably were many kinds of deer that didn't run from predators, and they died at various times in history, and we don't call then deer now.

@ebrohman: Yet this "run away" reflex is not what you observe in nature.  If you come upon a deer while out hiking, as I often do, it will often stand and look at you, apparently evaluating whether or not you're a threat.  If you live within a game refuge, as friends of mine do, they don't even bother to run from humans, as they usually do where hunting is allowed.  So it seems that, at least with larger mammals, there is a good degree of learning in threat recognition.

@jamesqf humans aren't the deer's natural predator so I don't think it's surprising that some deer do not flee when they see a human. Humans may hunt deer now but that's more recent in terms of evolutionary time scales. The predators that deer evolved alongside of run on all fours, or fly (large birds of prey).

In zoology, the word "Naive" means an animal which is suddenly put into a terrain/ecosphere which its evolution has not prepared it for, or when a new animal arrives which can destroy the terrain/ecosphere. For example, if an island has no predators, then the animals on it would have no sense of fear and thus not be prepared if a predator suddenly comes along. That is how the dodo became extinct - because it was not scared of humans. Source

Higher predators usually have the eyes in front of their head to see stereoscopically and judge distance visually. Prey usually has eyes on the side of the head to visually analyze the most possible area, giving up stereoscopic distance information.
This puts human in the predator, carnivorous category. That being said, I am not sure that it is used by animals to judge unknown species.

Hello! Might be better suited as a comment. As you said ("I am not sure that it is used by animals to judge unknown species"), you don't actually answer the question.


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What is meant by nucleated in this context?
Hi I am little confused in one of my classes; because the teacher will say that " the actin is nucleated by the ARP 2/3 complex" or "microtubles are nucleated by the centrosome". Unless I am misunderstanding, I don't take this as having anything to do with the nucleus as in the nucleus inside a cell. ( or does it). so what does this really mean than?
Thank you

http://en.m.wikipedia.org/wiki/Nucleation

Cytoskeletal nucleation refers to the de novo formation of cytoskeleton filaments. If microtubules are nucleating, that means microtubules are being polymerized from lit. "From the beginning" by α/ß-tubulin dimers. So literally, and we see in the image below, Arp2/3 complexes act as progenitor sites so to say for new actin filaments by the "nucleation" of actin:

From wikipedia for Nucleation: "Nucleation is the first step in the formation of either a new thermodynamic phase or a new structure via self-assembly or self-organisation."

In this context, i feel nucleated means being a "core structure", a substrate for the organization of one or multiple polymer chains.


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Why can newborns swim?
I am wondering for someone to discuss the phenomena that newborn babies (humans) are able to submerge underwater up until a few months where that ability is lost again? What is the explanation for this?

Have a look at the answer here the bottom portion of it.

It's called the Diving reflex, also known as the bradycardic response. It goes away around six months.
From https://www.breatheology.com/articles/mammalian-dive-response/

Another action of the diving response can be observed in infants when they are under water. The windpipe by the vocal chords spontaneously closes to prevent water from entering the lungs. This reflex is initiated as soon as there is contact with water. However, it disappears when the child reaches the age of roughly six months.

This is answering the 'how' but not the 'why' (not sure that this can be answered fully though)

When the face of an infant is exposed to cold water, the heart slows down and blood is shifted away from the peripheral muscles to conserve oxygen for the brain and heart, and they typically hold their breath. The reflex is the same one that protects babies from getting milk in their lungs. The reflex kind of reroutes the entire circulatory system to save blood for the heart and brain, and not pump it through the rest of the body.
http://www.ncbi.nlm.nih.gov/pubmed/12022304


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How to use a published phylogenetic tree?
I would like to know how should I use a phylogenetic tree from an already published article, to put it on my own article so I can analyze the evolution of a trait. Is there any software I can use, or do I only have to "edit" the tree with a traditional image editing software?
I've seen that using trees from other authors is a common practice. Many times they summarize the trees. But no paper seems to tell you how they did it.
Thank you!!

Have you looked at the supplementary material?

Can you explain what you mean be "use" the tree? Do you mean just getting the tree into a usable (e.g., Mesquite) format? Or do you mean do you have the right to use a published tree?

If you'd like to reproduce the image, contact the publisher. If you'd like to reference the data in your analysis to publish, cite the author appropriately. If you'd like to obtain the raw data so you can do something with it, you can do what @Remi.b notes and check the supp. materials for a table or something, or you can contact the author, and cite the author.

Thanks Remi.b and CMosychuk.
My answer is more in the way that says CMosychuk, I mean that I would like to take a tree from the paper "A" and include it on my own paper "B". The tree from "A" will be modified to adapt to my analysis, for example by changing fonts, size, and adding images representing characters in some taxa. I do not mean to modify it on its structure, nodes, or distances.
I do not know how to explain it better.

I don't know how generalized this is, but some journals require the authors to deposit the trees in a database, like treebase. In this case, papers should indicate the accession numbers of their trees.
You then need the appropriate software to load the tree, manipulate it and print it, for instance ete.


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While preparing Jam we use sugar.Why? (can you elaborate in science language)
Actually I was trying to find out the basic necessity of adding sugar in preparing jam.

Welcome to Biology.SE. Because people like it this way. It is still good with little to no sugar but it then called a compote and not a jam and is typically eaten differently. There is not much science to talk about here! Note that sugar will also increase preservation of the jam but I am not sure this is what you are interested in. Is this a homework question? If, yes there is probably a context in which the question was asked. What is this context?

@Remi.b The sugar is actually essential to the prolonged shelf life of (especially opened) jams, which is the point of making jams in the first place.

Well... the historical interest in making jam should not be discussed here (but I am sure it was not so much your goal). I asked in my comment whether his question had to do with preservation (end of the comment). I suppose the question the OP is trying to ask is "Why adding sugar improve preservation?". The OP would need to clarify that

Someone had asked a Q before and you'll find your answer there.

I'm voting to close this question as off-topic because it is not about biology.


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What is this strange worm-like creature?

Hi! While I was in my front yard this morning, I happened to look down and see this little guy wiggling thru the grass. He isn't like anything I've seen before.
He is about 2 1/2 inches long. He has a small horn coming out of his back near what appears to be his behind. His belly is a light green color. Also, he starts to flick around when I touch him (To catch him, I scooped him up in a small pot.)
I live in north west Mississippi in the hills near the delta. I am also surrounded by a large forest with all kinds of both pine and normal trees, if it helps.
Thank you in advance!

A picture of the underside or a profile would probably be nice if you still have it around. Most likely a caterpillar or another larva. A giveaway that it is an insect larva is if you inspect the legs, you will see that there are 3 pairs of true legs, near the head, and any other leglike things along the rest of the segments of the body aren't really true legs.

Sorry, but I put it back where it was little while ago!

Also, it had really stubby legs, if that helps.

The horn on the last segment is caterpillar-like. "stubby legs" too. Searching for "caterpillar with horn" led me to species of this genus: https://en.wikipedia.org/wiki/Manduca, but the photos of caterpillars I got didn't look like yours. The colour of yours is not a familiar caterpillar colour for me.

I believe this is some sort of Cranefly larvae, see here:  I've found these guys both directly in streams and along the banks of rivers, but also underneath rocks far away from major sources of water. There are different types of cranefly larvae, but they all have the same characteristics, (bulbous bodies, worm like, not easily noticeable arms, alien encephilization)

It may also be deer fly larvae ( a type of horsefly ) but they typically are more "spiky" on the sides.


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How can you design a drug to modify apoptosis to treat a disease such as cancer?
How can you design a drug to modify apoptosis to treat a disease such as cancer? Im in highschool so can someone please explain in simple terms. Thankyou.

The new cancer drugs are custom designed antibodies that have a cell-killing agent attached to them. These antibodies specifically attach to the cancer cells, and kill them. Other methods, like traditional chemotherapy target cells that are actively dividing, like hair in addition to cancer. Cancer cells are defined by uncontrolled cell division. But traditional chemotherapy, in simple terms, stresses the body to near death, differentially killing actively dividing cells. The new targeted methods are much less toxic.


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Are the sister chromatids exactly the same?
I'm having doubts about whether the sister chromatids are exactly the same or not. I know that they are the arms that carry the information genes (the alleles), but I don't know if they are exactly the same and / or in what these arms differ, since in a partial exercise they ask me the following:
Explain briefly why the sister chromatids are not exactly the same and the homologous chromosomes are different. To answer, consider the origin of both structures.
Nor do I understand quite well when the statement clarifies "take into account the origin of both structures."
Thank you very much for the help!

Well, what is the origin of the sister chromatids? In other words, by what process does a cell go from one chromosome consisting of one DNA molecule to one chromosome consisting of two DNA molecules (two chromatids)?

Then the sister chromatids would be formed from the DNA replication?

Yes exactly. Now, is DNA replication perfect or are errors introduced?

I suppose it is perfect or is it possible that there are errors?

A new chromatid is synthesized by copying the other chromatid. As such two sister chromatids are (quasi) perfectly identical.
Why did I say quasi? Because there are sometimes "errors" when replicating DNA. These "errors" are called mutations. As far as I know, most mutations occur during meiosis though and only very few occur during mitosis. So, to a pretty good approximation, yes sister chromatids are identical.

Ohh ok, with this I understood what canadianer means. Thank you very much for the explanation!


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What genes are the muscles, nerves, bones and blood?
I have a question about genes. The question is that bones, muscles, nerves and blood are each made on which genes. Father or mother genes? Does the person take any of the characteristics of the mother or father? Thank you.

The question is very unclear. I don't know either what you mean by mother and father gene. You are maybe referring to maternally vs paternally inherited chromosomes. Then, the answer would be both. You should just have a look to a intro to genetics.

Most genes case:
Let's state back what a gene is: it is a portion of the genome, numerous versions of a gene exists (called alleles). But one individual can only have two alleles in the same time (one from his mother and one from his father). So gene coding for nerve, muscles are present in both your mom and dad, and you will inherit of half of their allele (1 from each). There it is 50/50!
The exception
You maybe know women and men have a slight difference in genome: the sexual chromosome, men have XY and women XX. So the only case I could see a gene only inherited by your father would be that this particular gene is present on the Y chromosome.


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Microscope parameters for whole blood alalysis
I wonder, what are the minimum requirements for a microscope for blood cell analysis. I'm interested in:
-Counting erythrocytes
-Counting and differenciating all typed of leucocytes
-Counting of thrombocytes

What is the minimum magnification of the objective required?
Which type of objective is sufficient?
What is the minimal price-class of such an objective?

As I found out in medical lab-groups, the most lab-workers use 100x Objective (oil or dry Leica objectices) and 10x ocular. This results in 1000x and the images like the below.
My idea was to use 20x objective (as it is much easier to handle) and 14MP camera. The erythrocyte should have the resolution about 60x60 pixels then, which should be enough for the differentiation.


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why is DNA better for storing genetic info while RNA better for transmission of it?
I do know that RNA cannot be used for transmission since it is unstable, but how does it prove to be a better transmitter of genetic information?


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c4 cycle in photosynthesis occurs in monocots or dicots
the biosynthetic  portion of the c4 cycle occurs in the bundle sheath cells and i have studies that bundle sheath cells are present only in dicots and not monocots.
according to this, the c4 cycle shold be occuring in dicots and not monocots (due to the absence of bundle s. cells).
but important examples of pants following the c4 pathway like maize and sorghum are monocots.
i dont understand if there is a confusion on my side regarding presence of bs cells in dicots or if there is somewhere else that im going wrong.the following link is contradicting my answer as to presnce of bs cells in dicots

I had the same confusion but monocots do not lack bundle sheath cells.

monocots don't lack bundle sheath cells.  In fact, they are much more likely use c4 respiration than dicots.  There are actually about 10 times more c4 monocot species than c4 dicot species.  the c4 cycle is really primarily a monocot adaptation.  I think that the confusion often comes from the fact that dicots appear to be "more sophisticated" than monocots when you look at them, with their pretty, well organized vascular bundles and branching veins, which makes it intuitive to assume that they would be the ones using the "higher tech" c4 system.

C4 photosynthesis occurs in bundle sheath cells. And bundle sheath cells are present in dicots as well as in monocots. But anatomy is different in both types.
The bundle sheath in dicot leaf is present in single layer and made of colorless cells. On other hand in monocot, the bundle sheath is made up of single or double layer and made of colored cells because of chloroplasts.
The bundle sheath of dicot leaf is made of parenchyma cells whereas the bundle sheath in monocot leaf consists of sclerenchyma cells.
(Via:  https://vivadifferences.com/monocot-leaf-vs-dicot-leaf/)


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Why don't self pollinated crops show inbreeding depression?
Being continuously self pollinated means the fusion of same/similar genes from time to time, then why don't they show such a decrease in productivity?

Yes, self pollination does lead to inbreeding depression:

However, we found substantial inbreeding depression, with seeds per fruit, progeny survival and progeny growth being lower after self- than after cross-pollination. Progeny arising from self-pollination also had a higher frequency of certain traits ... which were associated with lower rates of survival. ... high inbreeding depression has also been reported in other self-compatible trees ...

--Self-pollination and inbreeding depression in Acacia dealbata: Can selfing promote invasion in trees?

Inbreeding depression is one of the leading factors preventing the evolution of self-fertilization in plants.

--Inbreeding depression in self-incompatible and self-compatible populations of Leavenworthia alabamica.

The strategy for breeding F1 hybrid squash is to develop parental lines through self-pollination. However, it increases plant mean homozygosis, which is not the natural genetic state of a cross-pollinated species, and can cause "inbreeding depression".

--Depression by inbreeding after four sucessive self-pollination squash generations
So why don't all crops that self-pollinate show decreases in productivity? In part, they do, but the reduction in productivity caused by inbreeding is outweighed by the increases in productivity caused by inbreeding (i.e. selection for productive traits via inbreeding leads to both positive and negative results, and the total outcome is the sum of the positive and negative effects).
And partly because the deleterious effects of inbreeding can be partially overcome through "purging". The negative genes that lead to inbreeding depression when homozygous can be removed from a population as the affected individuals die (or fail to breed) and take their negative genes with them. Purging is most common when a population has a moderate degree of inbreeding over a longish time, which is what you'd expect with a crop that typically self-pollinates. It's an effect in many but not all common crops:

Several plant species, E. g alfalfa (M. sativa) carrot (D. carota) , hayfield, tarweed etc show very high inbreeding depression. ... Many crops species, such as maize, jowar, bajara etc. shows moderate inbreeding depression. ... Several crop plants, E. g onion (A. cepa), many cucurbits, rye (S. cereale), sunflower (Hannus), hemp etc show only a small degree of inbreeding depression. Only a small proportion of the plants show lethal or subvital characteristics. The loss in vigour and fertility is small; rarely a line cannot be maintained due to poor fertility. The reduction in yield due to inbreeding is small or absent. Some of the inbreds lines may yields as much as the open pollinated varieties from which they were developed.

--Degree of Inbreeding Depression

Interesting question, but the answer might not be very simple. I'm not a big expert, but will try to give some clues.
So, first of all in many cases there is inbreeding depression. For example, some crops that are highly inbred (like tomato for instance) have a big problem of genetic diversity, which is very low among cultivated variants. This is sometimes solved by introducing introgressions from wild relative species. Otherwise you end up with crops that suffer from low biotic and abiotic stress tolerance.
Also note that in some cases, the seeds that are sown by farmers are not inbred lines, but rather the F1 result of a cross between two inbred lines. This is common for instance in maize, where all commercial cultivars sold by seed companies are hybrids. This leads to a phenomenon called Heterosis or Hybrid vigor, in which the progeny of the cross (the hybrids) have improved phenotypes over the parental lines.


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Mathematical Biology Jobs/Prospects?
I'm a junior math major starting to take his first courses in Algebra, Analysis, Topology, Nonlinear and Partial Differential Equations, etc.
I am just considering my career options at this point and somebody told be biotech/biology could have some interesting work. So I have come here to hear some advice if that is okay! Is there anything highly mathematical about the search for anti-aging or achieving the whole "biologically immortal" thing? I just don't know about any of this stuff so please inform me :)
PS: I also know Prob/Stats at a decently advanced level. So there's that too. Thanks!!

Off course you can! Here are career paths for you as per my limited knowledge:

BioStats

There are lot of applications in this domain. For example in Microarray Gene Expression or Proteomics analysis (for example, this paper).

Bioinformatics

Sequence alignments use common techniques like Dynamic Programming, Probabilistic or Heuristic methods, etc.

Computational Biology

There are lot of applications like Lagrangian and Eulerian Mechanics (Computational Anatomy), Computational Phylogenetics (Computational Evolutionary Biology), etc.

Systems Biology - In Systems Biology, you can have applications in:

1-) Probability and Hypothesis Testing - usually used to find associations between genes (Ref: S. Krawetz (ed.), Bioinformatics for Systems Biology, DOI 10.1007/978-1-59745-440-7_8, Chapter 8)
2-) Stochastic Modelling of Biological Patterns - ODEs,PDEs (applied to lot of problems), Markov Chains, HMM, PSSM are common mathematical implementations in this domain.
3-) Population Genetics - uses Statistical models (for example Genetic Distance), exponential equations (for example, Cumulative Effect of Mutation)
P.S: Here are some tools you might be interested in:
1-) Bioconductor - one of the main reasons why R is preferred language by BioStatisticians.
2-) BioPython
Wish you best of luck with your career!


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How big is the change in proteins due to alternative splicing?
How different can the proteins be that are coded from the same DNA-sequence but undergoe alternative splicing?
What I am trying to wrap my head around is why we are so fixated with the DNA-sequences and what they are coding for, if the outcome can differ a lot due to alternative splicing.

For your first question, They can vary dramatically.
I did not originally post as a formal answer because my statement below is hard to cite a source and would therefore be somewhat subjective, although I am pretty confident in the assertion. It is based on my own experience in both GWAS and EWAS literature reading. My research concerns methods for analysis of such data.
To answer your second question, the main focus has shifted from genetic variation (still done though) to expression variation and epigenetic variation. The expression research focuses exactly on the type of issue you are discussing with alternative splicing, and this is largely possible because of the decrease of the cost of RNAseq. We aren't as fixated on sequence anymore; the advent of GWAS, once thought to be a panacea for the explanation of disease susceptibility has only ended up explaining a fraction of genetic heritability estimates. Not to say it isn't focused on, just in the context of other types of variation and environmental exposures.


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Does urea at different concentrations (5 or 0.5M) have different effects on proteins?
The problem is to explain why each additive gives rise to the distribution of the protein (RMAS) as shown in the Western blow below:

In each case, the homogenates were subjected to high-speed centrifugation and the supernatant/pellet fractions were resolved separately by SDS-polyacrylamide gel electrophoresis. The gels were blotted and probed with an antibody raised against RMAS.

I am specifically stuck on explaining the effect of the 0.5M urea vs 5M urea on the soluble and insoluble proteins represented by the pellet and supernatant respectively. My thinking is that at low urea concentrations (0.5M) the pellet protein is destabilised by urea and solubility increases showing a band. However, soluble proteins are denatured and show no band. However, at 5M urea, the pellet proteins are reversibly soluble and therefore do not show as a band whereas the soluble proteins are OK and so show a 'normal' band. I don't know if this is the right explanation, so could someone please explain it to me??

What you need to do is compare the relative amounts of the protein in the insoluble (pellet) fraction to the soluble (supernatant) one. This way you can determine how soluble the RMAS has become through the effect of the indicated compound.
DTT breaks disulfide bonds, but does nothing else to solublize the protein, so it's all in the pellet, with none detectable in the supe. NaCl is a salt that increases the ionic "strength" of the lysis buffer, but doesn't really do anything to solublize the protein, so again all of the target stays in the pellet. On the other hand, detergents like Triton and SDS free the protein from the insoluble fraction and move most of it into the supernatant, leading to the pattern you see for them. Depending on the exact subcellular localization of the protein of interest, and the amount and combination of detergent(s) used, you may see essentially no protein at all in the pellet, as it has all been solublized.
Urea and guanidinium hydrochloride are chaotropic agents, disrupting hydrogen bonding, van der Waals forces, and weakening hydrophobic associations, causing the protein to denature and separate from other proteins in the pellet, thereby putting it into the supe. This effect is generally seen at relatively high molarities (e.g. GuHCl is often used in the 6-8 M range), which explains the difference in effect seen with 0.5 and 5 M urea. At low concentrations, there is just not enough urea present to effectively denature the protein. I am a little surprised that nothing showed up in the 0.5 M lane, however, this is just a simulated Western showing ideal results - in real life things are almost never quite this cut-and-dried.


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Why are dogs so selective about choosing a spot to defecate?
Anybody who walks a dog knows that dogs are normally selective about choosing a spot to defecate. They sniff around for a long time, while I just want to be on my way.
I understand about marking territory with urine. Is it the same with feces?

As a dog owner, I personally don't find dogs so complicated to please for pooping spot. They sure investigate the ground for good peeing spots though.

Well then your experience is very different from mine, which was the reason for the question.

I don't see where I admitted that Charles. Perhaps you could clarify. That was absolutely not an opinion-based question, and I have no doubt it has a research-based answer.

I can't say that I've ever noticed this, but it seems possible that what the OP observes might happen when the dog is walked (quite possibly on a leash) in a peopled/built up environment, and therefore is related to house training?  Whereas my dogs, and my friends, generally run off leash while we're hiking or riding in wilder places, and don't seem to be at all choosy/


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Why don't humans typically drink human milk after infancy?
Does any human culture routinely do this? Typically taboos have some evolutionary basis. So what would that be? Does any mammal drink the milk of its own species, besides nursing?

I guess your question should be the other way round. Humans I guess are the only species that drinks milk after infancy. We drink cow/buffalo/goat milk. This is an interesting read regarding lactase insufficiency and gene-cultural co-evolution. https://www.americanscientist.org/issues/feature/2010/2/gene-culture-coevolution-and-human-diet/1

I understand about lactose intolerance. And it is interesting that we drink milk from other species. But that is what brought me to the question in the first place.

@KarlKjer As you explained to Polisetty, your question is not about human drinking milk of other species at adult age but in case it is of interest anyway, I want to point to the post Are humans the only species who drink milk as adults?.

Q1: I don't know. Q2: presumably because it's not in the mother's interest to provide direct high-quality nutrition (very energetically expensive) over an extended period of time; additional cost of this parental investment wouldn't pay off in increased total (inclusive) fitness. [HOWEVER: not posting this as an answer because it's speculative/tautological ...] Q3: don't know (but see linked question by @Remi.b)

On might speculate that it's simply a matter of there being a very limited supply.  But it does happen: search "breast milk cheese" for some examples.

@charles. Humans. Because we have a culture that is often linked to evolution, and everyone reading this is human. The other species just came up as something that might support a universal rationale.

It is only in our modern times that human milk is not consumed. I don't see how you could say for sure that our prehistoric ancestors never consumed human milk as adults.

Giving a woman food for her to inefficiently convert to different food is a waste of time and energy; it only makes sense for infants that can't eat much else (and even there, plenty of people find substitutes so the woman can get back to work).
Turning grass, which people can't eat, into a food people can eat makes a whole lot more sense.

I see your point. But in a capitalist society. if there were profit in it, it should happen. But it doesn't because ...ew... yuck. Why?

@KarlKjer Humans were not capitalist for most of their history, which is the context in which they evolved. Only after thousands, maybe even millions of years under our modern capitalist society can you pose the question you have.

@swbarnes2 Well, it is also inefficient to feed grass to a cow and drink its milk, instead of just growing beans on that meadow and eating those, and yet dairy is a enormous industry.

You don't have to "grow" grass.  It grows on its own with no effort.  Crops take work.  The fact that for millennia people who knew perfectly well how to grow plants did cultivate cows for milk is really good evidence that it really is worth the effort.


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GWAS terminology "Tag" vs "Lead" vs "Index" SNP
I'm trying to get my head round the correct GWAS terminology. I keep seeing the terms like "tag", "lead" and "index" SNP to be used almost interchangeably and I would like to get a clarification from someone inside the field.
My (limited) understanding is as follows:
Tag SNP - the SNP included on the genotyping microarray. Once we have a compendium of SNPs for a given sample we can use reference haplotypes to impute the rest of the SNPs.
Lead SNP = Index SNP - the SNP assigned the highest association significance after we've run association analysis for all the imputed SNP. The other SNPs in high LD with the lead SNP will form the associated locus.
Am I correct in my understanding? Any other / better terms I should be aware of?
Many thanks!

Hi. One question for clarification: have you read the wikipedia article on "Tag SNP"?

I did. It explains "Tag SNP" quite clearly, but it doesn't really touch on "downstream" terminology, even in the GWAS section. Thanks for bringing it up though - it's a useful link to have in this question.

I found a review paper that addresses your questions, see
Schaid, Chen, Larson (2018): From genome-wide associations to candidate causal variants by statistical fine-mapping
Tag SNP. You correctly identified tag SNPs. From the paper:

[T]he SNPs on microarrays, called tag SNPs...

Lead and index SNP. These are apparantly synonyms. From the paper:

This allows one to focus on the SNPs with the smallest
  (that is, most significant) P values in distinct regions,
  sometimes called the lead or index SNPs.


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What type of insect in this?

Can anyone tell what of kind of insect is in this image ? They have been showing up in my room for the past month; never happened before that. The room is generally hot during daytime.
Thanks

Wow i saw same bug hour ago!

Where was it found and when? That is basic info for species identification questions.

This question has previously been asked/answered here: Identification of an insect from midwest US. A post about their smell can be found here: The smell of the shield bug (aka stink bug).

Brown marmorated stink bug (Halyomorpha halys):

Source: Brown marmorated stink bug (wikipedia)

That is a "shield bug" in the order Hemiptera. They're often called stink bugs because they release noxious chemicals for defense. I agree that it does look like the brown marmorated stink bug, but there are several species that look similar. Depending on where you live, the brown marmorated stink bug may be an invasive species. The links below show how to distinguish them, and give info about the invasive species. They're showing up in your room because they over-winter in houses, and become active at warmer temperatures. They can become a serious problem due to forming large colonies, so you may want to look for obvious places they could be getting in, and seal up the entries. Once they start hanging out in your house, they attract others with scents. The Farm and Dairy article has a simple, inexpensive cleaner recipe to remove the chemicals they release to attract more stink bugs.
Identifying stink bug species, including marmorated stink bug: http://www.stopbmsb.org/stink-bug-basics/look-alike-insects/
The brown marmorated stink bug as an invasive species: https://hort.uwex.edu/articles/brown-marmorated-stink-bug/
How and why stink bugs get into your house, and how to keep them out: https://www.farmanddairy.com/top-stories/simplest-way-to-eliminate-stink-bugs-indoors/373786.html


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I am looking for examples of polyandrous insects?
This is for a homework assignment, and yet I am not able find any references that can help me find example of polyandrous insects.
Does anyone have any references or suggestions on where to look?

https://www.ncbi.nlm.nih.gov/pubmed/10973716 what about this one

The concept is sort of difficult to apply to insects, since they dont form pairs. However, females mating with multiple males is common (maybe the norm).


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what is CpG coverage? DNA starting material?
referring to this quote from an article about predicting methylation states:

"Because of the small amounts of genomic DNA starting material per
  cell, single-cell methylation analyses are intrinsically limited by
  moderate CpG coverage"

can you please explain it to me?
What is exactly starting material? and why it's small per cell?

Please try to find the meaning of common English scientific phrases by an internet search. And think about how big a single cell is and how much DNA there would be in it.

Can you please link to the document you're citing from? Without a context, it sounds rather difficult to interpret this sentence.

https://link.springer.com/article/10.1186/s13059-017-1189-z

The comparison the authors are making is between bulk and single-cell sequencing.  Currently, single-cell sequencing is becoming very popular as it allows much finer grain analyses of the biological expression.  For example, tumor sub-populations can be determined.
However, single-cell analysis lose a great deal of genomic material, causing the resultant measures (expression most often) for each cell to have very minimal and sparse values.
Therefore the starting material is simply the DNA in each cell, which is limited by the single-cell process.

You write "the starting material is simply the RNA in each cell". Perhaps you can explain how you can measure DNA methylation starting with RNA.  The poster actually quotes what the starting material is: "genomic DNA" but appears unfamiliar with the English expression "starting material". As for "CpG coverage" it would appear that both his scientific knowledge and his English is deficient. But you ignore that part of his question.

I know the English meaning of the words "starting material". My question: what is that starting material? and why it's not enough?

specifically, is CpG coverage the number/percentage of C-G sites covered in sequencing? or it's something related to methylation?

CpG coverage is a general term, but thinking about it as the fraction of methylated CpG sites over the total number of CpG sites is accurate.  To get the number of CpG sites, accurate sequencing of the genome needs to be accomplished.  As I tried to explain, the single cell method limits the amount of DNA (edited the answer to be correct) able to be sequenced, and therefore the number of CpG sites is not well known, and the CpG coverage as well.

Also the question states "What is exactly starting material? and why it's small per cell?" nothing about CpG, therefore I did not include an answer about CpG.


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Camera and the eye (filtering information)
How does a camera recreate a very similar perceptual stimulus (through the photo) for us to see compared to the person directly viewing the object of interest with their eye?
My questions stems from what I've already learned about the visual system:
1) The retina receives information from the external world, but not 100% of the photons (the form of this information).
2) This information is then passed to the superior colliculus where further filtering, and changes to this information occurs.
3) It is next passed to the thalamus and then relays it to the occiptal lobe which interprets this information (another filtering process) causing us to perceive the external world in a particular way.
Is it that the camera captures the light information on the film that would otherwise have made contact with our retina? And then upon seeing the photo, that same information (or similar since the camera would not exactly capture it, but enough for us to notice that we are seeing what we expected to see) finally makes contact with the retina and then the process occurs as described in the points above?
If so, how does the camera do this!? Because I thought the camera would also be selective in which light it uses to recreate these images. And I'm incredibly doubtful that a camera simulates the filtering processes of the human brain. Moreover, it doesn't make sense that we would perceive the expected image in the photo if it was already based on the filtered information.
I am very curious and very confused. :)
-N

I'm voting to close this question as off-topic because you are asking how a camera works, not about biology.

I disagree. This question came from a friend who disagreed with the above explanation that the light information that encounters the retina is no longer the same once it reaches our visual cortex. He couldn't believe that our vision of the external world is not a true representation (whatever that is!).
So he then argued my original question in this post. If it isn't a true representation of the external world, how is it that a photo is able to provide a stimulus for almost the same visual response of an object of interest.


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Where are all the seagull nests?
Seagulls are common. I live on the shore of New Jersey (U.S.), but I have never seen a seagull nest. Where are they?

Seagulls in urban areas tend to build their nests on rooftops instead of ground nesting. I'm not sure if that's New Jersey's case. I've also seen gulls' nests in sea cliffs but the area wasn't as populated as New Jersey.

Breeding season
Chances to see nests will be higher during breeding season which normally occurs once a year. Eggs will be laid in early May but they will be built in the previous months.
Area
In densely populated urban areas gulls may build their nests on rooftops instead of ground nesting. In the case of New Jersey I found the following brochure:
https://www.nj.gov/dep/fgw/ensp/pdf/bnb_brochure.pdf
If you mean seagulls as in all Laridae, then you have two members of that family (black skimmer and least tern) in that brochure that actually use NJ's beaches and even have their own designated space for that.
Googling 'seagull rooftop nests' brings a decent amount of pictures of rooftop nests. 'Seagull nests' brings a lot of cliff-placed nests, rooftop and ground nests. I assume the choice depends mostly on food availability and predator population density. I remember in Spain a few years ago there was a big enough problem to appear on local TV news related to seagulls attacking people. They would nest on every roof and attack people that would go out on the balcony with a sandwich.

Sources:

Habitat Selection and Nesting Biology of Roof-Nesting Glaucous-Winged Gulls
Kees Vermeer, Damian Power and G. E. John Smith
Colonial Waterbirds
Vol. 11, No. 2 (1988), pp. 189-201 https://www.jstor.org/stable/1521000?seq=1


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What is the reason for cats not liking water?
I have two cats myself, a Siberian and a Maine Coon, neither of which like water. In fact, they detest it - like most cats. I was wondering what the reason for this was and if any of you have any interesting theories as to why this is the case.
Thanks in advance!

Quick note here : I agree with the questioner, and the accepted answer. I don't like to bring an old question out of zombie land but ... I recall seeing images of a tiger (i think it was) very happily charging into a pool of water when chasing after prey. No hesitation. So I wonder if different species have different levels of fondness? I know this is the case for dogs ~ we had a newfoudland, and she was impossible to keep dry if even the smallest puddle was seen, she was in it ! Other dogs are somewhat less aquatic, we now have a chihuahua that only likes to paddle ~ she doesn't like rain !

First, some cats do like water. But it seems true (from personal observation and most people's opinion) that most cats don't.
The question has already been asked many times online. Just Google your question!
I doubt one will find peer-reviewed papers on the question but below is a summary of what seem to be the most often mentioned possible reasons I could find. Of course, these bullet points are very hypothetical and I don't know of any research presenting evidence for or against these hypotheses.

Their fur is not really adapted for the water and will very quickly become waterlogged and heavy making it uncomfortable.
Cats are generally speaking quite skittish
Cats may not like the odour of chemicals we put in the water.
Cats love to groom themselves. It is an aweful lot of work to do the grooming after a bath.

Note also that domestic cats are descendent from cats living in very arid areas. The most closely related species with cats are the African Wildcat living in Northern Africa, the Near East and around the periphery of the Arabian Peninsula.
Source
My non-peer reviewed sources are

http://www.petful.com/behaviors/why-do-cats-hate-water/
http://www.animalplanet.com/pets/healthy-pets/do-cats-really-hate-water/
http://www.petguide.com/blog/cat/why-do-cats-hate-water/

Thanks a lot for this helpful and comprehensive answer :)

My answer is inspired from three different sources (incl. the one you cite), none of which are peer-reviewed. I doubt one will find a peer-review paper on the question. Nothing is presented as a fact but is rather hypothetical. I doubt one could find a peer-reviewed document on that question. The question has been asked thousands of times online so I guess we can either vote to close as homework question (as it lacks effort from the OP) or rephrase an answer along the same lines as other answers online. I just tried to clarified these points.

A series of hypotheses has never been considered uncacceptable as long as they are logical, plausible, not based on false opinions and is clearly presented as a series of hypothesis and not as supported by any evidence. Consider this post for example.

Well, I am sorry you chose not to answer. Hypotheses are accepted as answers here (if labelled as such). Regurgitating what others say, is pretty much what we all do when answering a question. This is the whole point of saying things that make sense. We just have to be clear about whether we are giving hypothesis, loosely supported hypothesis or extremely supported hypotheses. IMHO, this is pretty much the only  type of answer one can provide. Btw, I read more than one webpage and their hypotheses were often quite related.

You can open a meta.biology.SE post if you want to discuss whether my answer is on-topic by its nature or not but let's not further our discussion with more comments. It'll be interesting to see how other users see this issue.

@Charles I added the sources. These are not the original webpages I used (I just don't quite remember what source I first used) but they are making the same claims and all are using the same vocabulary. The main interest in adding these sources is to avoid to be called for plagiarism.


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How to determine the height/bits in a sequence logo?
I am trying to create a sequence logo, and I am completely confused by how to determine the height/bits for each column. So, for example I understand how to create the flat sequence logo: (add up all the letters, the letters should represent their ratio for that position) but not the normal sequence logo:.
I have been reading this paper "WebLogo: A Sequence Logo Generator" again and again and I can't figure out how to determine the bits/height for each given position.

It's http://weblogo.berkeley.edu/Crooks-2004-GR-WebLogo.pdf

Wikipedia has a page on sequence logo which discusses the calculation briefly.
The "bits" here are related to those used in Shannon entropy. This is an information-theoretic equivalent to the Boltzmann entropy from thermodynamics. This is a measure of how "disordered" the position is, or more precisely how specific the distribution is.
The general formula for the total entropy (expressed based on probabilities/fractions) is
$$ S = -k \sum_i p_i \cdot log( p_i ) $$
where $i$ ranges across all the various states (e.g. each nucleotide).
The difference between Shannon entropy and Boltzmann entropy (aside from the contexts where it's used) is the value of the constant (one for Shannon, Boltzmann's constant for Boltzmann entropy) and which logarithm used (the natural logarithm for Boltzmann entropy, and typically base-2 for Shannon entropy.) As it uses base-2 logarithms, the Shannon entropy is typically measured in units named "bits".
The wrinkle is that the entropy of a distribution isn't really what you want to display in a sequence logo. Instead, you want something that gets larger (not zero) when the sequence becomes more defined. As such, the values displayed are not the entropy itself, but the "entropy loss" from a completely random (maximal entropy) distribution.
That's how you get the total number of bits at a position (the total height). The height of the individual letters comes by taking the total height and multiplying it by the probability of each state. This might not have rigid theoretical justification (you can't attribute the entropy loss to individual nucleotides like that), but it fulfills the display purposes of making the more prevalent nucleotide identities larger in display size.

For example, if you have a position with 70% G and 30% C, then you have
$$ (4 \cdot -0.25 \cdot log_2(0.25)) - (-0.7 \cdot log_2( 0.7 ) + -0.3 \cdot log_2( 0.3 )) = 1.12$$ bits of total height. G gets a height of $1.12 *0.7 = 0.78$ bits, whereas C gets $1.12 *0.3 = 0.34$ bits.

I don't understand the example: what is (4⋅−0.25⋅log2(0.25)) ? I would replace this part with 2 since it is log2(4)−S @R.M.

@Manuela (4⋅−0.25⋅log2(0.25)) is the entropy of a random sequence: 4 possibilities, each with a probability of 0.25.

ok perfect thank you !