Understanding different genetic terminology - Genotype vs SNP I recently came across a study that refereed to variations in genes like this:

IGF1 (CA)19/(CA)19, IGF1(CA)19/X, IGF1 X/X

(From this study: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3274549/)

I wanted to know, as a member of 23andme, how I could check these "markers" (?) against the SNP's listed in 23andme.

I would be very grateful for any help.

Thanks.

The "IGF1" at the front indicates that the genetic variation is in the gene for Insulin-like Growth Factor 1. The notation (CA)n is used to describe n adjacent repetitions of the two-base sequence CA (Cytosine, Adenine) present in a particular IGF1 DNA sequence. Hence IGF1 (CA)19 / (CA)19 is referring to a genome in which both copies of the IGF1 gene have 19 adjacent repetitions of the CA pair of bases, that is, which is homozygous for IGF1 (CA)19.

Such a repeat is usually called a microsatellite or Short Tandem Repeat (STR). They are common sources of variations in genes because the DNA matching process during meiosis sometimes "slips" one or two repeats over.

The type of test performed by 23andMe reports values for selected SNPs (Single Nucleotide Polymorphisms).  SNPs are a different kind of variation from STRs, so the data available from 23andMe does not allow you to determine the kind of IGF1 (CA)n variant present.


Why can we sniff so much? What was the point for us humans (or other mammals) to develop such a strong sense of smell? Depending on the source, we can distingiush from 10.000 to even trillions of smells. But how was the ability to sniff "artificial" smells (e.g. paint or burning rubber) being useful to our ancestors?

Smell samples the chemical composition of the environment, the groups of molecules you are sampling in those examples still exist in nature. It is like asking why being able to taste pizza would evolve, it doesn't, not by itself anyway, it is the inevitable result of being able to taste the things and conditions that make up pizza, carbohydrates, proteins, fats, oils, acids, bases, salts, etc. things that would be important for our ancestors to be able to detect.

With paint you are smelling volatile organic compounds, and many are important biological and/or hazard markers, some are related to rotting meat, others to infection, others to food sources, and others to natural toxic water sources. With burning rubber you have many different smell depending on the rubber, but in each case you are smelling a burning organic polymer which releases organic compounds which again would exist in nature.


What are the highest and lowest amplitude values in ECG for humans? I'm currently trying to parse the records captured from an ECG device and display them on a mobile application. I am wondering what the highest and lowest possible amplitude values for ECGs are in humans? What may happen if they exceed those values?

The QRS complex is the part of the ECG with the largest amplitude.

I scanned a dozen ECG traces across the web, and as far as I can see, the QRS complex has amplitudes of up to 4 mV in a normal ECG:

ECG trace. 1 mm corresponds to 0.1 mV on the y-axis

Amplitudes are relative peak-to-peak measures. If you are asking about absolute values then the minimal voltage versus maximal absolute voltages depend on your baseline value, i.e., the offset in your voltage potential measurement system. Further, artifacts and background noise may add signal amplitudes on top of the ECG proper.

As an absolute minimum estimate, the graphs here posted show that -1 mV would be a safe minimal voltage.


What Is This Tactic Called? (Banishing Adolescent Females) I was watching a documentary about Meerkats the other day and one thing that stuck out to me was how the Mother of a family will banish her daughters once they reach adolescence. If the daughters try to return to the family then the mother will viciously attack said daughter, it's quite sad.

Anyway, the reason for this makes sense (in terms of evolution) because if the adolescent Meerkat were to fall pregnant, she would need more food & support from the clan, thus jeopardizing the original Mother's chance of survival.

I think this is an example of animal behavior/population control where there can only be 1 mature female in the group, like there is with bees. Am I correct in assuming this? Do all animals show this behavior for the same reasons? Also is there a general term that can be applied to this phenomenon?

The reason the dominant female doesn't want her daughter to breed is that she would prefer her own children survive, rather than her grandchildren (the children of her daughter).
I wouldn't call this population control - the dominant female isn't thinking to control the group size, rather, to monopolise the group composition.
The difference with bees is that the genetic relationship between the individuals is more complex (haplodiploid), so the female bees are more closely related to their sisters than to their own offspring!
The general term for the fact that only some animals are taking part in breeding is "reproductive skew".


How to biologically interpret path weight summation in weighted and directed gene regulation network? I've considered asking this question on Bioinformatics SE, Mathematics SE, and Stats SE, however I've judged that my question belongs on Biology SE because I am interested in a biological (domain-specific) interpretation rather than a further development of the mathematics or software.

My question pertains to applying graph theory to biology, so first I will describe the graph in its mathematical properties and how they reflect biological properties.

The graph

Let's consider a weighted and directed graph whose nodes represent genes and whose edges represent the binary relation gene A regulates gene B. The directionality of the edges is imposed in order to reflect that gene A regulates gene B does not imply that gene B regulates gene A. The magnitudes of the weights are to represent some measure of how "strongly"  one gene is regulating another, and the signs of the weights are to represent whether the regulation is upregulation (positive) or downregulation (negative). For this graph, edges with a weight of zero are considered equivalent to 'no regulation' and should be excluded from the graph.

Path Analysis

Restricting ourselves to paths that do not visit the same node twice, what is the biological interpretation of the sum of the weights (of the edges) of a path between two nodes in the aforementioned graph?

I have conflicting intuitions. For example, why would these weights be additive? I'm not imposing that such weights have to be correlation coefficients, for example, but they are commonly used weights in networks that are not additive so it warrants some consideration in the more general case. If they're not additive, then their summation is not necessarily meaningful. Conditioned on being meaningful in the first place, my other inuition is that the meaning of such a summation would reflect the strength of 'indirect' regulation

There's quite a bit of use of graph theoretic approaches in gene regulation, so I'd suggest you start there and Stand on the Shoulders of Giants rather than reinventing gravity:

https://scholar.google.com/scholar?hl=en&q=graph+theoretic+gene+regulation

Although this isn't my area of expertise, I think the thing most obvious to me as a biologist and statistician is:

Sums are misleading in non-linear systems

Biology is very non-linear. You can probably get closer to linear in the graph you are describing if the weights reflect log-transformed ratios: this transformation makes a multiplicative system linear. But even after this transformation, you are making substantial assumptions. The only way to verify those assumptions would be with either a more complex model of the underlying system (since the graph you describe is quite abstracted) or the old-fashioned way: by experiment.


Sequence structure of antibodies It is said that

"When a virus or a pathogen enters the body, the immune-response produces Y-shaped proteins called antibodies to bind to the pathogen or virus".
"Also it is possible to extract antibodies from the blood."
Since antibodies are proteins, is it possible to sequence their structure ?
If the answer to point-3 is Yes, then can't coronavirus antibodies be sequenced, more antibodies be produced from this sequence on a large scale, and then these are administered to the infected people ?

I would like to know any challenges to the above mechanism like "difficulty in figuring out the correct antibody or so" ? Thanks!

Giving a simple answer is difficult as the field of humoral immunology is quite extensive. Here is an abbreviated overview.
Our body produces myriads of different antibodies during an immune response, not just one. It is impractical to isolate and sequence one antibody protein as their sequence differs in very subtle ways. N-terminal sequencing like Edman degradation is not practical as it covers only a few dozen residues at most. Perhaps proteolytic digest of an antibody and peptide sequencing is possible, but again this requires a large amount of a pure antibody. Protein sequencing is not practical.
Instead, people sequence the DNA corresponding to a given antibody instead of sequencing the antibody protein itself. As a given B cell expresses one antibody in large amounts, Milstein and Kohler (Nobel laureates) devised a technique to fuse B cells with tumor cells, creating hybridomas. Each hybridoma thus produces a single antibody. Such hybridomas may be cultured – monocultured in fact - in the lab to large amounts, leading to the production of a uniform, single antibody, termed monoclonal antibody. The corresponding DNA sequence of such monoclonal antibody may be readily sequenced.
I would think it feasible to create a library of individual hybridoma monocultures using a patient’s B cells, and then select the hybridoma producing the best monoclonal antibody from the library, and sequence that DNA. Epitope binning [https://en.wikipedia.org/wiki/Epitope_binning] is one example of a technique to identify the best antibody. The successful hybridoma may then be culture to large scale to produce lots of that exact antibody.
Administering such purified antibodies to a patient is not straightforward as this foreign protein will be itself recognized by the patient's immune system and cleared. There are techniques to reduce the immunogenicity of a given antibody, but that will be a lengthy discussion in itself.


What bacteria shed harvestable energy from root zone organic matter? I recently heard of a successful effort that harvests energy from soil at plants' bases due to apparently bacterial breakdown of wastes from the plants:

  Via photosynthesis a plant produces organic matter. Part of this
  organic matter is used for plant-growth, but a large part can’t be
  used by the plant and is excreted into the soil via the roots. Around
  the roots naturally occurring micro-organisms break down the organic
  compounds to gain energy from. In this process, electrons are released
  as a waste product. By providing an electrode for the micro-organisms
  to donate their electrons to, the electrons can be harvested as
  electricity. Research has shown that plant-growth isn’t compromised by
  harvesting electricity, so plants keep on growing while electricity is
  concurrently produced.

Apparently there is more research here, and this was particularly interesting (a PDF) as it states more clearly that we are indeed talking about bacteria:

  The PlantPower concept is based on the cooperation of plants and
  microorganisms to produce in-situ electricity. Plants take up carbon
  dioxide and water and capture light energy. This energy is stored in
  the chemical bonds of sugars produced, using carbon dioxide and water.
  Part of this chemically stored energy is transferred to the roots of
  the plants. This energy present in the root zone can then be captured
  by the so-called electro-chemical active bacteria. These organisms are
  capable to oxidize the organic matter present in the root zone and
  transfer the energy rich electrons to an electrode. The energy carried
  by the electrons can be used as electrical energy, after which the
  electrons react at another electrode with oxygen to form water.

I would like to understand this process as far as what bacteria or "micro organism(s)" are being leveraged here.  It seems that they are supplementing the soil with some kind of bacteria that acts in this specific way of releasing additional electrons that can then be harvested.

Any idea as to what kind of micro organisms or bacteria have this kind of reaction wherein they release or excrete harvestable energy (and apparently CO2 + H+) upon consumption of plant "excretions" (C6H12O6)?

After doing a bit more digging, I have found some, perhaps, interesting information from Wikipedia:

What ultimately confuses me here is that the other method noted earlier does not really emphasize any particular kind of plant and therefore I can't help but think that perhaps there are some other more useful bacteria for this scenario...

Short answer
It is known that a great variety of soil micro-organisms is able to use solid anodes as electron acceptor for their metabolism, thus creating some electrical current. Geobacter spp., Clostridia and Deltaproteobacteria are among them (1). However, I could not find any extensive list of these microbes. It is likely that a large number of these microbes is not identified yet.
A review on Plant Microbial Fuel Cells was recently published and might interest you (2).
Long answer
Plant Microbial Fuel Cells are a special case of Microbial Fuel Cells
The system presented at your first figure is being developed by the Dutch company named Plant-e and falls within the concept of Plant Microbial Fuel Cells (PMFC).
Simply put, a Microbial Fuel Cell (MFC) is a device in which chemical energy contained in chemical bounds of organic substrates is converted to electrical energy by microbes. Microbes consume the organic substrates while using the anode as the final electron acceptor of their metabolism. Microbes capable of using anodes as electron sinks for their metabolism are called electrogens.
PMFCs are a special case of MFCs, taking advantage of the microbe/plant interactions. Organic substrate is supplied to microbes directly by the plant and you get two benefits: plant biomass and electricity production.
Complex interactions between plant and microbial communities
As you noted in your last sentence, no particular species of plant was cited. Indeed various PMFCs strategies were implemented, based on various species of plants, such as Glyceria maxima, or Oryza sativa (rice) (2). The plant species is not the only key factor for efficient PMFCs: the nature of the organic substrates provided by plants to microbes, the soil's characteristics, the electrodes' characteristics, and the nature of the inoculum are crucial factors too.
Regarding the microbiological aspect, it appears that pure culture (single species) PMFCs are not necessarily the best alternative. Plants provide microbes with a variety of chemical compounds, which may not be all consumed by a single species. Only a well adapted microbial community is likely to be able to take advantage of all these compounds and to include efficient electrogens. The path from plant products to electrical current is more likely to be a complex microbial food web, rather than a single species' metabolism. In practice, most studies seem to rely as soil as the incolum (2).
So, concerning your initial question: we might not have identified yet every soil electrogens. Several are, however, already well known, such as Geobacter sulfurreducens. But, what is important is that most (P)MFCs strategies rely on microbial communities as a whole, in a 'black box' way.

References
(1) Dunaj, S.J. et al. Relationships between Soil Organic Matter, Nutrients, Bacterial Community Structure, And the Performance of Microbial Fuel Cells, Environment Science and Technology, 2012, 46 (3), pp 1914-1922
(2) Nitisovarut, R., Regmi, R., Plant microbial fuel cells: A promising biosystems engineering, Renewable and Sustainable Energy Review, 2017, 76, pp 81-89


Are all of my ancestors from 400 million years ago fish? Say you have your family tree for the last 400 million years or so, back to the Devonian, the age of fishes. You take the set of ancestors that are about 400 million years old (which will be across multiple generations). The question is are they all fish?

Or, is it more complex than that? Can there somehow be non-fish in that set?

Note added later: this question is not a duplicate of another question.
In the context of that other question, howewever, my question can be stated as "Is Dawkins correct in stating that my 185th million ancestor was definitely a fish, with no exceptions?"

Yes they all were because there weren't any land vertebrates, vertebrates were all fish at 400 million years ago.

It is a close call based on fossil evidence from 395 million years ago, there are footprints of 3 meter tetrapods from littoral/seaside fossils. https://www.sciencedaily.com/releases/2010/01/100107114420.htm

The earliest land vertebrate skeleton is from 375 million years ago. https://en.wikipedia.org/wiki/Tiktaalik

It is technically still a fish, so probably yes, the ancestral species of all land vertebrates were still fish. There are various experimental early quadrupeds, some with 6 fingers, which are cool reading.

They still exist in the form of lungfish.

Here are images of the earliest land vertebrates


Western Blot: Fischer ECL substrate 2:1 instead of 1:1? i recently developed a b-actin-ab-incubated PVDF-WB-Membrane with the Thermo Scientific Pierce ECL Kit. According to the manufacterers orders i mixed Reagent 1 and Reagent 2 1:1. But unfortunately i got kind of "unbalanced" bands (on the right side of the picture). Then someone gave me the tip to try to mix the reagents 2:1. For this substrate i got the result on the left side which actually looks much better.
Has anyone of you had the same experience and can anyone explain to me why this is so?
Is it "legal" to do so, or does it alter somehow the results of my experiment?

Yours,
p1ssn3lk3

Well usually in an ECL kit, one of the reagents is the substrate and the other one is hydrogen peroxide, which activates the substrate for breakdown using the HRP on your secondary antibody (Ab) so I genuinely doubt what you are seeing is the result of ratio difference. In order to make that conclusion you need to run your samples twice (on two separate membranes) and do a 1:1 and 2:1 ECL and if you observed such a difference then you are on firmer grounds.

I suspect what has happened in the above experiment is that you have done a 1:1 (with 1Ab and 2Ab not distributed equally on the membrane) then after perhaps not a very thorough wash, you have done another 1Ab and 2Ab incubation using the a 2:1 mix. I suspect what has happened is that in your 1:1 the left hand side has not received the Ab mixtures very well and when you did the 2:1 since the right hand still Ab attached to it (if you didn't strip the membrane) so the left hand side was "forced" to get the Abs hence again the Ab mixture and ECL not equally bound. It is obvious since one image is opposite the other so its the Ab incubation step that has gone wrong. Otherwise if you have done the second ECL incubation mixture straight after the first and didn't do a wash step, the same can result if the membrane did not receive the initial ECL mixture equally since you can get a blocking effect by the old ECL mixture and perhaps what has happened is that the H2O2 or the substrate was present in excess in the second incubation step hence amplifying the signal in the sections of the membrane that did not receive the ECL mixture very well in the first place, relative to the rest of the membrane, which still has ECL liquid on it from the last experiment (again if you haven't washed the membrane well as ECL can be active for up to 24 hours in some kits but after a few hours the activity usually reduces but can still be observed)

What you need to do is after ECL, wash the membrane with TBST for a few minutes followed by TBS, leave the membrane in the sun to dry so that the Ab slowly denature (although that doesn't always happen specially with high affinity Abs such as anti-tubulin and actin). After at least 24 hours, strip the membrane from Ab and redo the Ab incubation. The best thing to do is to do all the incubation steps in a sealed bag then make sure the membrane receives the ECL mixture equally and do the visualisation. I would say however since the membrane is unequally "contaminated" with the Abs then the best thing to do is to redo the experimental run and re-run the gel. Its a pain but you need to get to the button of this!


How is the diploid chromosome number maintained at mitosis? A normal human cell is diploid that contains 46 chromosomes in 23 pairs. Thus, when the cell undergoes mitosis, the cells still has the full chromosome with the two sister chromatids. What is it doing in interphase when it produces the other chromosomes?

I thought that the sister chromatids were pulled apart and, in interphase, the single sister chromatid grew another one. How is this possible if a human diploid cell contains 23 pairs of 2 chromosomes each?

The terminology of "chromosome" during this process is confusing, but here it is:

There are 46 chromosomes in the cell (23 pairs)
Before division, each chromosome has two sister chromatids, joined in the middle (92 chromatids in total)
During division, the chromosomes split and each daughter cell gets 46 chromatids, one from each chromosome
These chromatids are now known as chromosomes
Each one of these new chromosomes only has one "chromatid"
During interphase, the new chromosomes replicate and now they have two chromatids each, joined in the middle

So whether a chromosome has one or two chromatids it is still called a chromosome. I hope this helps.

The following link contains a more complete explanation of mitosis. The first picture explains this point quite succintly: http://biology.tutorvista.com/cell/mitosis.html


what is the margarine metabolism in our body? margarine is commonly used food ingredients that contribute to both inflammation and

obesity , but actually I want to know the margarine metabolism in the human body

I can find some resources talk about its impact on health but I can't get the idea of its metabolism.

As pointed to by @Chris the Wikipedia link for margarine explains that these are formulated upon vegetable oil-based fats. Their melting points and other properties are adjusted by industrial hydrogenation of the unsaturated fatty acids in the vegetable oil.

Most unsaturated fatty acids present in nature are in the cis conformation at the double bonds. The hydrogenation process, if it is not carried to completion, produces the trans isomers of fatty acids. These so-called trans-fats are blamed for the undesirable side effects of consuming margarine, or other foods containing hydrogenated oils.

Most of the fatty acids present in margarine (i.e. cis unsaturated and saturated fatty acids) are metabolised by the normal route (β oxidation).


Primer design and BLAST E value stringency When searching for misprimings I have been told that an e value that is higher than 0.01 is ok and will produce no significant amounts of mispriming. Yet I searched some and it would seem that the e value threshold limit is dependent upon the "amount of information" in the database.  Indeed I found that some papers cite as values lower than 0.07 to be significant already.

What are the criteria you use at times to judge this issue, and how do I know when to lower or increase my stringency when running a routine BLAST for the purposes of designing primers?

I never used BLAST for primer design, but often for finding out where a sequence came from.

From the FAQ of the NCBI:
http://www.ncbi.nlm.nih.gov/blast/Blast.cgi?CMD=Web&PAGE_TYPE=BlastDocs&DOC_TYPE=FAQ

"The lower the E-value, or the closer it is to zero, the more "significant" the match is. However, keep in mind that virtually identical short alignments have relatively high E values. This is because the calculation of the E value takes into account the length of the query sequence. These high E values make sense because shorter sequences have a higher probability of occurring in the database purely by chance. For more details please see the calculations in the BLAST Course.".

What they say in the papers is true, the size of your database matters in deciding how significant the match is. I can imagine that for primer design you want to be more careful with the E-values, as they often fall under: "because shorter sequences have a higher probability of occurring in the database purely by chance".

I hope this helps to make your decision for deciding your threshold, otherwise please give more information.


Additive genetic variance $V_A= 2pqa^2$ ... what is $a$? Reading Falconer and Mackay looking at equation $V_A = 2pqa^2$ (equation 8.5, page 126).

I am trying to write a clear explanation of how additive genetic variance is defined and calculated, but I keep getting twisted up in the books I am working from.

Just what is the term $a$ and how is it calculated?

This information is given in p.118.

In essence $a$ represents the deviation from the population mean due additive genetic effects.

Say a trait is controlled solely by locus X with the effect alleles X impacting the phenotype Y in an additive manner (no dominance and epistasis effect), then we can calculate the effect size of carrying the X allele, called $a$, and representing the distance from the population phenotypic mean of homozygote XX. Based on this definition, the distance from the mean for individual with the following genotype is given by:

XX: $a$
Xx : 0
xx: $-a$

This makes more sense using the genetic model:

$P=G+E=BV+I+E=A+D+I+E$ (parameters listed at the bottom)

In the example, the locus has only an additive effect then D=0 and assuming there is no epistasis then I=0 as well which gives $P=BV+E=A+E$ therefore $BV=A$

In this case $a$ can be computed directly from the BV, with p=f(X) and q=f(x), as:

$BV(XX)=2qa$
$BV(Xx)=(q-p)a$
$BV(xx)=-2pa$

Now for the complete case of both additive and dominant effects, i.e. $BV=A+D$, you can refer to table 7.3 in p.118 which describe that XX individuals are given the value $a$, Xx -> $d$ and xx -> $-a$ with the corresponding relationship to the BV given by (care here it's not $a$ but alpha $\alpha$):

$BV(XX)=2q\alpha$
$BV(Xx)=(q-p)\alpha$
$BV(xx)=-2p\alpha$

with $\alpha=a+d(q-p)$

P=phenotype
BV=A+D=Breeding value
G=Genotypic effect
E=Environmental effect
A=Additive genetic effect quantified by $a$
D=Dominant genetic effect quantified by $d$
I=Epistasis effect


Questions on DNA damage I'm not strong in biology, so bear with me on this:

I've been reading that as we age, our DNA is damaged by internal (e.g. errors during replication) and external (e.g. sun damage or radiation) factors.

If you take, say, an 80 year old, can you find DNA in their body that's the same as when they were a newborn? What kind of cells would have undamaged DNA?
Is DNA damage distributed evenly across the body or will some parts have more damage than others?
Is there any published data on how much DNA damage an average person accumulates over their lifetime? I'm not sure how this can be quantified, but I'm wondering if there has been any study on gauging damage.

Excellent question!

You would definitely be able to find quite a few sequences of DNA that are undamaged (in fact most of them would be undamaged), but it is very unlikely that any cells in his/her body would have a perfect copy of the entire original genome.
I'm sure that cells closer to the skin (exposed to more radiation) would have more mutations, but beyond that most everything depends on where you live, your habits, etc. (if you're a smoker you will obviously have more mutations in your lung cells).
Under regular circumstances (low levels of mutagens), about 3 nucleotide mutations occur in the human genome per cell per division (DNA replication) (from http://www.ncbi.nlm.nih.gov/books/NBK26881/). The rest of the math would be a very rough estimate, seeing as you'd need to make a lot of assumptions (cell division rate average, other mutagens an organism may encounter, life span, the list goes on), but however you want to do it, there's the number you need to start with.

I hope this helps.

CDB


Identify this insect (looks like part of a tree)? I found this insect and thought it was part of a tree at first, then it moved and so I knew it was an insect. I've never seen it before though so I am posting here hoping someone knows what it is.

The location is North East US, during the day, in a tennis court surrounded by trees. The insect was clinging to the cover seen above (which covers the tennis court fence).

Any idea what this insect is called?

Alight, best guess, based on it being the most common species, a decent match in pictures, and a decent match to the description on Wikipedia is Diapheromera femorata, the common walking stick.


Bird identification: Warora, India These photographs have been taken in Warora, India. Could someone please help identify this bird?

This is a pond heron or paddy bird. The de-facto source for identifying Indian birds is Birds of the Indian Subcontinent by Richard Grimmett, Carol Inskipp and Tim Inskipp. The book is remarkably complete and contains the vast majority of species found in the Indian Subcontinent.


Can Two Opposite Running Action Potential Cross Each Other without Annihilation in One Axon Can two opposite travelling action potential cross each other annihilation in an axon?
My answer would be affirmative. If the propagation mechanism is linear as described by https://en.wikipedia.org/wiki/Cable_theory or even https://en.wikipedia.org/wiki/Telegrapher%27s_equations with approximately constant coefficients, the waves are then linearly additive and each signal should propagate unperturbed. The refractory period on each end of the axon can not possibly prevent the other end from being excited at the same time since the signal has not arrived yet.
This question is inspired by the question Can a single axon propagate multiple simultaneous action potentials?

Combining the lecture notes on the interchannel and channel  electric potential leads to a description of the propagation of the action potential $V$. Specifically, substituting in $I_{\text{ion}}=I_{\text{ext}}$ of equation (6) of cable theory by equation (1) of Hodgkin-Huxley model gives the full propagation equation. A linearization of the Hodgkin-Huxley model leads to a system of linear partial differential equations. I will write out the full formulation and the linear approximation later. That allows complete superposition of action potential. The original non-linear system of partial differential equations under a set of functions/parameterizations at least close to the linear version should permit two opposing wave to cross each other though with interference. So it is not true that all parameterizations of the Hodgkin-Huxley model prohibit two-wave-crossing.
It would of course be intriguing to investigate the existence of a particular form/parameterization where the model does extinguish two opposing waves with its initial condition being two pulses close to a dirac delta function at each end of the axon.
Here is a paper M. Argentina, P. Coullet and V. Krinsky, Head-on Collisions of Waves in an Excitable FitzHugh-Nagumo System: a Transition from Wave Annihilation to Classical Wave Behavior a special case of the Hodgkin-Huxley model. Just as I expected, the waves do not always annihilate each other, but rather may cross, annihilate or even coalesce or even coalesce then re-emit, all depending on the particular values of the parameters of the model. Another paper Oleg Aslanidi, O. A. Mornev, Can Colliding Nerve Pulses Be Reflected? on the numerical simulation of a full-blown Hodgkin-Huxley model reporting crossing of colliding waves. This paper Follman et al, Dynamics of Signal Propagation and Collision in Axons reports under their particular set of parameterization of Hodgkin-Huxley model, two colliding waves annihilate. This paper by Alfredo Gonzalez-Perez et al demonstrates Penetration of Action Potentials During Collision in the Median
and Lateral Giant Axons of Invertebrates based on the soliton theory of nervous signal propation as described in On soliton propagation in biomembranes and nerves by Thomas Heimburg and Andrew D. Jackson.
The wikipedia page on autowave has some interesting information including references for propagation and collision of nonlinear waves in excitable media.


Why do our eyes "wrap" hue from UV to IR? On the high-wavelength side of things, we see almost-infrared as reddish, with a slight tinge of magenta. On the low side, we see violet fading into the same magenta color. Why is that?

You can see it clearly on any hue chart. There's an unbroken flow from one to the other, even though the wavelengths are literally as far apart as they can be while still remaining visible.

I understand that color vision is limited due to several biological factors(cone receptivity, absorption, etc), but why do the colors on both side fade into each other? Is it just our brain making things "neat" and continuous?

Basically.  You are most likely looking at the electromagnetic spectrum, which is linear and conveniently makes sense... except for magenta.

Colors as we perceive them are additive and made up of Red, Green, and Blue; this is opposed to subtractive color we learned about while finger-painting in kindergarten (Red, Yellow, Blue).  The three types of cones in our eyes each are sensitive to one of these colors, and it is from the combinations of Red, Green, and Blue that we see all the colors we see.  Yellow, for example, is when the red and green cones are both stimulated.  Purple/violet is from red and blue stimulated together.  This is the single special case, as you point out, because red and blue are at opposite sides of the spectrum from each other.  Our brain has two options:

Use the color smack-dab in the middle aka Green
Make a new one as if they wrapped around

Green is far away and already taken, so our brain intelligently invents Magenta.  This produces, instead of a linear EM spectra, a circular color wheel that looks very intuitive.


Can 'human' become a genus due to space colonization? I have read that during the Second World War, some mosquitoes got trapped in the London underground railway system. The mosquitoes never got out and eventually they became a new species by themselves.
I had a similar thought. In the next few centuries, if humans could, in theory, colonize other planets like Mars, Proxima Centauri and beyond, then the environments there are not the same as Earth. So, in the long term, humans who would be born and who would grow up on Mars, for example may become more and more suited to Martian conditions than Earths.
Now, when early humans explored and ventured into new geographical areas, they did change characteristics, but we are still one species Sapiens. But living extraterrestrial, is a whole new thing. The gravity alters, the entire atmospheric composition does. So that is going to have some significant changes on humans.
So, my question is: is it possible that in millions or even billions of years, if humans expand to space, there may arise separate species of humans? And would this new emergence of human species actually result in humans moving one step up the taxonomical ladder: becoming a genus?
EDIT: To avoid confusion and create speculations at the answers, I should specify that I am talking about a very particular case: if Sapiens are living in different planets, then is there a chance that Sapiens will become a new genus, and that Homo can be taken one step higher in the taxonomical order? There would still be Sapiens on Earth, but considering the environmental changes that could happen here too, humans then can be drastically different from humans now. So the question is: can 'Sapiens' become a genus?
Thanks to @tyersome and @jamesqf for pointing this out.

The concept you are referring to is speciation and it has been well studied in a wide variety of different natural organisms. I suppose here we are talking about the biological species concept.
The overall answer is yes it is possible, but critically depends on a few different factors. The reality of speciation in the wild is very complex, but these are some things to consider:
Genetic isolation
If two groups, such as your Martian colony and humans on earth isolate from one another, then for speciation to occur, there needs to be a significant level of genetic differentiation between them. This means substantial differences in the kinds of genetic variants found at positions along the genome.
Genetic differences are eroded by post-isolation gene flow – in your example, that might mean a spaceship flying back to Earth with Martian colonists, who then have offspring with people on Earth.
Although there is plenty of evidence that speciation with gene flow can occur, the general rule of thumb is that increased gene flow means a longer divergence time is required to fully speciate.
In nature, this is often caused by some kind of geographic barrier to gene flow, such as mountains or rivers forming, but it can also be caused by morphological differences, such as variation in sexual appendages. Of course, in our example, this barrier to gene-flow would be the large and difficult to traverse distance between the Earth and Mars.
Divergence time
You alluded to some kind of separation time, and you are right to be talking on the scale of millions of years. Speciation can occur extremely quickly; in Lake Tanganyika cichlids, it has occurred probably within the last 15,000 years. Humans have created whole new species of crops, such as maize, within the past 10,000 years. There is even evidence of some fish speciating in 3000 generations.
However speciation is often a much longer process. For example humans and chimps were thought to speciate in 4.5 millions years.
Of course, there is an interaction with several other factors. All other things being equal, less post-isolation gene flows results in a shorter time to speciation and vice versa. Stronger selective pressure between the different environments leads to a more rapid accumulation of genetic differences.
As Konrad Rudolph correctly points out, divergence time is strongly related to generation time, with all other things being equal, a shorter generation time, results in faster speciation.
Selection pressures & differing environments
I think the last main factor governing speciation is how different the Martian colonists environment was from that on Earth.
Different environments can lead to natural selection occurring in opposing directions in the two populations, leading to ecological speciation. Speciation can proceed without differing environments, where neutral drift in allele frequencies can eventually cause speciation, but this will be a long process.
Speciation will occur much more rapidly if there is a start difference in environment and selection pressures between the two groups.
So in conclusion, given enough time, genetic isolation and differential selection pressures (or some combination of the above), it is plausible that a new species of human could form. However, given the time-scales required, it seems a bit unlikely to me.
EDIT
I think it is worth pointing out what @Jaquez said in the comments. If current terrestrial humans split from an extraterrestrial source to form another species, it would be named as another species within the Homo, such as Homo extraterrestrialis, for example. The addition of a new species does not move the group Homo up to become an e.g. Tribe or Family.


Are there any disadvantages to HRP conjugated PRIMARY antibodies I need to detect a FLAG tagged protein on a western blot and have to order an antibody. I'm not expecting to see a massive amount of my protein. To keep analysis time to a minimum  I am considering a HRP-conjugated anti-FLAG. Are there any disadvantages to it (e.g. sensitivity)? First hand experiences/problems?

You can compare directly coupled antibodies to the classical indirect primary-secondary systems:

Directly coupled antibodies

Advantages:

quicker workflow as only one antibody is used
eliminates the chance of a cross-reacting secondary antibody (possibly less background)
possibility to use differently labelled antibodies on the same blot

Disadvantages:

lower sensitivity because the signal is not amplified
only few labels are available
directly labelled primary antibodies tend to be expensive and you need relatively high amounts of them
the labelling can damage or reduce the immunoreactivity of the
antibody

Indirect Primary-Secondary Antibody systems

Advantages:

the secondary antibody amplifies the signal (which is especially
interesting for weakly expressed proteins)
differently labelled secondary antibodies can be used on the same
primary
primary antibodies from different species can be used simultaneously
one secondary antibody can be used with different primary antibodies
(for example for the protein of interest and the loading control)
the labelling reaction does not affect the primary antibody

Disadvantages:

cross-reactivity of the secondary antibody can lead to non-specific
bands
the method takes longer, as more steps in the process are necessary

For me the most important point is the higher sensitivity of the indirect method, for comparision see these images (from Life technologies):


What determines the influx of calcium ions in the voltage-gated ion channels? Calcium channels play a crucial role in neuronal signaling by helping the synaptic vesicles to fuse through the synaptic active zone and release their neurotransmitters. My question is, at a given moment, what determines the influx of calcium ions in these channels? Where are the ions coming from and what is their source? Is the influx determined by the source by changing the ion flow, or the ion flow is constant and the influx of ions into the synapse is only regulated by opening/closing of the channels?

So, let's use a neuron to neuron connection as an example.

Calcium is released into the neuron when voltage gated ion channels, specific to calcium, open. These channels can only open when there is a significant depolarisation in the axon terminal of the neuron.

Where do the calcium ions come from? The majority of them are outside of the cell by the plasma membrane and adjacent to the synaptic vesicles.

I'm not too sure what you mean when you ask what the calcium ion's "source" is. It is common for calcium ions to sit outside the cell, not just in neurons, to help maintain potential difference for example.

And yes, the influx of calcium in a neuron is determined by the opening of voltage gated calcium channels.

Sources: https://web.williams.edu/imput/synapse/pages/IIA1.htm , https://en.wikipedia.org/wiki/Calcium,  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3249630/


Detecting food fraud There's undoubtedly more than one way to do this, but if a DIY biologist were to attempt to detect food fraud (e.g. as done by students from Stanford University and Trinity School, Manhattan with respect to fish samples from markets and sushi restaurants), then what would be the minimum steps and equipment?

(I know barely anything about molecular genetics, but have been reading about DremelFuge, OpenPCR, and Blue Transilluminator, and wondered whether they - or things like them - might get such an investigator some of the way towards the goal above; and what else would be required.)

There are several ways you could go about identifying species through DNA. If you want to do everything yourself, the simplest option in terms of equipment needed consists of evaluating fragment lengths observed during gel electrophoresis after amplifying specific DNA sequences using PCR.

If you are content with some outsourcing, you can also send DNA samples to a commercial company for sequence analysis.

A compromise between these options in terms of information obtained, is to do study Restriction Fragment Length Polymorphism (RFLP) by amplifying DNA fragments and using restriction enzymes to cut the fragments, before analyzing the fragmentation pattern using gel electrophoresis. To perform RFLP analysis, you would need to obtain restriction enzymes in addition to the chemicals mentioned below, and they can be a bit pricey.

The minimum equipment would consist of a PCR machine, one or more pipettes with matching pipette tips, a gel electrophoresis tray with power supply and a transilluminator (preferably blue-light/non-UV). A centrifuge is not strictly necessary, but can be useful for processing/filtering your DNA source.

Some chemicals will also be needed: Polymerase and dNTPs for the PCR reaction (or a pre-made "master mix" containing both), electrophoresis-grade agarose and running buffer for the electrophoresis, along with a DNA dye specific to the type of transilluminator (Usually UV or blue light). For a blue-light transilluminator, GelGreen is a suitable DNA dye. You will also want to use a "loading dye" to mix in your DNA sample before applying it to the electrophoresis gel. This can either be purchased or prepared yourself by mixing sugar and food coloring in water.

You need some form of heating to dissolve the agarose - a microwave oven is convenient for this, but take care to avoid over-heating, glass explosions or flash boiling. It is convenient but not strictly necessary to have some lab glassware. Preferably use a screw-top bottle to mix your agarose solution. Always leave the top off when heating bottles.

Photographic equipment can be also useful for documenting results of gel electrophoresis.

Finally, you will need single-stranded DNA oligomers (primers) specific to the DNA regions you want to amplify. DNA primers can be bought from a number of companies, but it varies how easy it is for non-affiliated individuals to order and make payments. Macrogen has been my choice: They both deliver DNA primers and perform DNA sequencing.

You may be interested in the following thread on the DIY Bio e-mail group: https://groups.google.com/forum/#!topic/diybio/cPzfEuiZH58

I have collected some of the primer sequences mentioned in the thread on a page on OpenWetware: http://openwetware.org/wiki/User:Jarle_Pahr/Meat


Hybrid, Japanese or European larch please? pictured in NE Scotland 29th April

To tell these larches apart from each other the shape of the scales on the cones is a good place to start.

European larch have cones with scales that are straight, rather than curving outwards.

Japanese larch have cones with scales that curve markedly outwards as in this photo below.

From Wikipedia - Larix kaempferi

Hybrid larches, being a cross between the European and the Japanese, have cones that are in between. But as this Forestry Commissions publication,
 "Know your conifers", mentions there is some variation so it is useful to look at cones from more than one tree across a stand.

Summary: Your photo shows a cone with slightly curved scales or bracts, so I don't think that it is European larch. But it could be, it is slightly misleading as the seeds (the thinner bits are protruding).

Japanese larch cones are really curved, which when I was being taught tree ID were described as 'like roses'. So a definite, not Japanese.

So in my opinion it is most likely to be a Hybrid larch, but as the cone is not fully mature and open, and there is only one to look at it could be a European larch.

When looking at cones, I find it best to find old cones on the woodland floor that way you can see them at there most fully developed, and the differences between the species are more marked.

There is another ID feature between European and Japanese, and that is the colour of the stems. The former are straw-coloured and the latter are darker, brown/purplish colour. This becomes more obvious as the season progresses.

There are quite a lot of photos of cones on the web that have been given the wrong names, which makes it quite confusing. Best stick to Forestry Commission literature, or educational institutions.

When looking for photos I came across this YouTube video by Harper Adams University which is good and actually features the Japanese Larch photo that I found on Wikipedia.


Is it possible to see the microbes on your hand without using UV light or a microscope? I know that black light (UV) is often used to see the microbes (colloquially referred to as germs) on people's hands but is there any way by which we can examine the microbes on people's hands without having the surroundings be completely dark (what is required for black light to work) or using a microscope? I am trying to show a roomful of people the microbes on my hand but the surroundings aren't going to be completely dark and there is no way I can use a microscope.

Given your constraints, the only solution available would require some amount of preparation. If you are so inclined, you can purchase sterile, ready-to-use agar plates online, which you can then inoculate with microorganisms from your hands by simply touching the agar surface with your palms, and letting the plates incubate at room temperature. A day or two's time should be sufficient for plenty of microorganisms to grow, allowing you to demonstrate that your hands have "germs" (although some of the microorganisms you'll find on your agar plate may very well be airborne contaminants if you don't take some precautions).


"Most bacteria have at least one cell wall" In the first answer to How do we find antibiotics? @Ashafix claims that

  Most bacteria have at least one cell wall

Does this mean that there are bacteria with more than one cell membrane? Which are those and how does that look/work? Are there different milieus in the different compartments?

Cheers

I agree with @Maximilian that the phrase you quote is unclear, and we can't understand if it's talking about the number of cell walls of about the presence of cell walls:

  Most bacteria have at least 1 cell wall, meaning that some bacteria can have more than 1

This is wrong, as @Maximilian explained. But this:

  Most bacteria have a cell wall, meaning that some bacteria doesn't have any

Is correct. Tenericutes, a group of Eubacteria, don't have cell wall:

http://onlinelibrary.wiley.com/doi/10.1002/9781118960608.pbm00025/abstract

Reading the answer, it's clear that the user was talking about the outer membrane in Gracilicutes.

However, it's good to emphasize that all bacteria have only 1 cell membrane, because the outer membrane is not defined as a "cell membrane" (despite being a phospholipid bilayer): http://www.nature.com/nrmicro/journal/v13/n10/images/nrmicro3480-f1.jpg


How is chewing gum processed? There is the common belief that

  Chewing gum takes 7 years to digest

But is this actually true? Does it really stick to your intestines for 7 years, or is it processed like all foods, except it isn't broken down and is excreted soon after digestion?

Purportedly White House Spokesman Sean Spicer consumes (chews and swallows) at least 35 pieces of gum every day.

Mastication breaks down the components and carbs, oils and alcohols are digested accordingly, but the rubber is pushed through by your intestinal muscles. You might enjoy this article which goes into detail about the breakdown and digestion of "gum" constituents. For the most part tho the rubber in gum passes through like corn, peanuts and such.

So, no - no "seven years" to digest. I remember hearing that as a kid. I think it is the kind of thing kids are told to discourage them from swallowing outright instead of chewing gum.


Small non-coding RNA (sRNA) vs. micro RNA (miRNA)? What are the differences between micro RNAs (miRNA) and small non-coding RNAs (sRNA)? Are these two terms used interchangeably?

Small non-coding RNAs are NOT generally abbreviated as sRNA but as sncRNA, if anything. I say "if anything" because the "small" part is subjective and just a portmanteau descriptor. The straight answer to your question is as Forest has written: miRNAs are a specific type of small non-coding RNA, some of which appear to function in the regulation of gene expression — others remain to be characterized. Another problem with the 'small' epithet is that miRNAs may only be 20 nt in length, but are formed from pre-miRNAs of up to 1000 nt.

Other categories of small non-coding RNAs include:

tRNA (transfer RNA) - originally abbreviated sRNA (for soluble RNA) - involved in protein biosynthesis.

5S rRNA - a component of the ribosome

7SL RNA - a component of the signal recognition particle involved in recognizing the signal peptide of secreted and membrane proteins.

snoRNA (small nucleolar RNA) many of which act as guide RNAs in ribosomal RNA modification.

snRNA (small nuclear RNA) many of which are involved in the splicesome, the ribonucleoprotein complex which removes introns from precursor mRNA (these have names like U1, U6 etc.)

SINE RNA: RNA transcribed from the short interspersed nuclear repeats (SINEs - Alu sequences in humans) which are thought to be 7SL signal recognition particle pseudogenes.

And, no doubt, there are some I (and science) have missed.


What exactly is Tinnitus? What exactly is tinnitus? What is it's cause, and why do some people hear it and others don't?

Although tinnitus is usually described as a ringing in the ear, there's a whole range of tunes, buzzes, whooshing sounds, humming and hissing sounds that are described of as tinnitus. The sounds can either genuinely be there or be perceived to be there. If it is genuinely there it suggests muscles ate at play or some blood vessel disease if the sounds are in time with your pulse, but usually its the latter perceived to be there that presents.

Tinnitus that is perceived and permanent usually suggests damage to your hearing nerve (called the auditory nerve or cranial nerve 8 or vestibulocochlear nerve). The common cause for this we see is patients that have been exposed to loud noises or drugs like certain strong antibiotics which cause damage to the nerve. Other drugs also have a side effect of causing tinnitus. However any ear problems really may cause tinnitus including ear infections, too much wax, getting older, a disease called Mennieres, tumours, neurological diseases, vitamin deficiencies and lots more.

If you're really interested, keep reading. There's a number of reasons why it might occur. Usually patients presenting with it have some degree of hearing loss. Its thought that somewhere along the line the structures are getting more sensitive to sound because through a feedback mechanism. Think of it this way, you speak to someone but they can't hear you so you speak louder and louder until they can. In the same way its thought that the sensitivity is increased and increased to try to restore hearing but the result is audible nonsense sound from abnormal activity i.e. tinnitus.

If anything doesn't make sense, please do say :)


Is it possible to induce erysipelas to treat cancer, under the condition that the patient is to be given antibiotics to control the erysipelas? Dr.William Coley was one of the first to attempt fever therapy on cancer patients. He did this experiment: artificial erysipelas to treat cancer.
Coley injected Streptococcus pyogenes directly into the tumor.

My question is: if we repeat a similar experiment today, (under the condition that the patient is to be given antibiotics to control the erysipelas to avoid the ethical debacle), is it possible to develop this as a cancer immunotherapy treatment?

Before any experimentation on humans, any treatment undergoes an extensive testing on animal models.

Besides, there must be some degree of confidence in the potential curative effect of a remedy in order to start experiments in the first place. An experiment like the one you describe would not be approved by your institute's animal ethics commission (there is such an unpleasant but important thing) unless you prove with some line of evidence and prior knowledge that the suffering of the animals is likely not going to be in vain.

It is now also customary to provide an official approval from the ethics commission during publication submission. [You would not need such an approval for flies or worms, but for rodents (which would likely be your first test object in the case in question) or primates you would.]


where i can download reference MSU7 rice genome? I am working with RNA Seq data analysis. I have to download MSU7 rice genome. somehow i downloaded from

"http://rice.plantbiology.msu.edu/pub/data/Eukaryotic_Projects/o_sativa/annotation_dbs/pseudomolecules/version_7.0/all.dir/ "

. But i am not able to find Annotation (.gtf) file and reference genome (.fa) file . so how can i find and how can i download..help me

You can find this on the phytozome website. You will have to make a free JGI account to access it


what is allelic sequence variation? When DNA polymorphism occurs mutations can take place.  If these mutations occur in the germ cell and do not destroy its capability to reproduce, it is said that the mutation might move on to the next generation. My book says it might lead to allele sequence variation. But what does it mean?

Can you please give a direct quote? I am pretty sure your textbook did not say exactly what you said!

  When DNA polymorphism occurs mutations can take place.

In genetics, polymorphism just refer to the existence of genetic variation among individuals in a population (often referring to a specific locus).

Mutations is the ultimate source of polymorphism. It is not polymorphism that allow mutations to occur.

  If these mutations occur in the germ cell and do not destroy its capability to reproduce, it is said it might move on to the next generation.

Indeed!

  My book says it might lead to allele sequence variation.

'allele sequence variation' is just some kind of another generic term for polymorphism. For this expression to make sense to you, you should start by looking up the definition of allele


how to find full mitochondrial genome of plants in GenBank? I am searching for full mitochondrial genome of a species of Malvaceae family.
To be more specific, I need the genus Corchorus. But I could not find the location where it is in gene bank. After searching in google, I found this, but here I did not found anything for plant.
Can you help me to locate its actual location?
Scientific classification from Wikipedia:
Kingdom:    Plantae
(unranked): Angiosperms
(unranked): Eudicots
(unranked): Rosids
Order:  Malvales
Family: Malvaceae
Subfamily:  Grewioideae
Genus:  Corchorus
L.

Is this one? http://www.ncbi.nlm.nih.gov/genome/38606?genome_assembly_id=233326

What I did was Google: "search mitochondria genome BLAST"

and clicked the first page for me "Organelle Genome Resources". I then selected

"Browse by Organism" on the lefthand side, which took me to a new page.

I then entered in the top left text box the phrase "Malvaceae" and up came a scroll down list from the text box of choices for the text field.

I chose the first "Malvaceae (taxid:3629)" and upon clicking that, 26 entries came up for organelles. Two of which were from Mitochondria under the "Type" column.

The other entry being: http://www.ncbi.nlm.nih.gov/genome/10704?genome_assembly_id=233221

Sorry if I  was totally off base, I am just a undergrad.


How did the activities of protocells become inheritable? I have learned that first a protocell came to exist and its characteristics came to be passed on by genetic material. So how come genes for all the activities come to incorporate into genetic material? Did genetic material come first and random sequences made random proteins that were used to make cells ?

The sequence is believed to be opposite of that implied by the phrasing of the question: the inheritance of structures supporting inheritance came before protocells.  The important point is that you need a system of reproduction before building more complicated structures (such as a cell).  Without replication (reproduction), a cell would be little more than a soap bubble, and would disappear without a trace before long.

The initial (or very early) form of replication is thought to be based on a simple form of RNA. The reason for this is that (1) RNA does encode genetic information in a way that is replicatable, and (2) RNA can take on shapes and chemical structures that act as an enzyme (called a ribozyme) that catalyze chemical reactions.  The hypothesis is that an RNA molecule formed that catalyzed assembly of copies of RNA chains, including itself.

After such replication was established, probably some kind of enclosure like the cell membrane evolved to contain the chemicals, making the reactions more efficient.  After (or maybe before) this, RNA catalyzing assembly of simple protein-like molecules whose sequence was encoded by RNA sequences evolved, leading to protein-based cellular machinery.  This mechanism is still evident in life today in that protein assembly uses a ribozyme-based molecule assembly (the ribosome) to translate messenger-RNA into proteins.


Mathematical model about the relationship between two animal species I'd like to relate a mathematical model with  two animal species. This is the model:

$$
\begin{split}
\frac{dN}{dt} & =rN-\frac{rN(N+M)}{k} \\
\frac{dM}{dt} & =r'M-\frac{r'M(N+M)}{k'}
\end{split}
$$

The model means that there is competition within the population of the first species ($N$) and the population is also affected by the population of another animal species ($M$).

Something similar occurs with the population of species $M$.

My question is:

  What kind of animals would fit this model?

I was thinking about white sharks as $N$ and whales as $M$. Clearly the first equation would be correct but the second equation would be saying that the population of whales is affected by sharks, which I think is not true. Is it?

The model you present here is a special case of the Lotka-Volterra competition equations, where the two species have the same effect on each other (i.e., symmetric competition). Some things to think about in interpreting this:

each species has a negative effect on the other (i.e., increasing the density of either species lowers the other's population growth rate), hence this is a "negative-negative" interaction; it makes more sense for two species that are competing with each other (for resources, space, enemy-free space, etc ...) than for a predator-prey system such as the shark-whale example you give.
In contrast, in predator-prey (or more broadly "enemy-victim") systems, one species (the predator) benefits from the association - its population growth rate increases when the density of the other species (the prey) increases - and the other species (the prey) suffers (its population growth rate goes down when the predator density increases)
the fact that the competition is symmetric (this happens because you are using the sum of the population, $M+N$, and not using a competitive asymmetry parameter, e.g. $M+\alpha_{MN} N$) means that this would be most suited to modeling the competition between species that were very similar to each other (e.g. the same size, resource-gathering ability, etc.)


Organ donation compatibility based on DNA As far as I know, multiple tests are made before organ transplant to determine matching. Would it be possible to do the matching based on the DNA of the patients, rather than the actual serum antigen/antibody? If yes, is it any better/cheaper/easier?

@zeller

The better answers are being sought in a field called Regenerative Medicine.

A number of techniques have been tried, among them 3D printing of organs and dissolving the cells from a donor organ leaving the collagen scaffolding, then reseeding the organ with a patients stem cells in a bioreactor.

Most of these technologies, unfortunately, are in the proverbial 20 years from now category, which means that there are an incredible number of technical and biological challenges to overcome, but the ideal result would be organs with the patient's own cells and therefore no rejection or need for immunosuppressant therapies post transplant.

A nobel prize was awarded a few years back to Shinya Yamanaka for creating Human Induced Pluripotent Stem Cells. A technology like this would be the likely source of the stem cells necessary to seed these organs, however there have been problems with these cell lines including their tendencies to become neoplastic and form cancers.

So for at least the near and medium term the best alternative is to find organs that are as close a match as possible for Major Histocompatibility Complexes, and as Moderator Chris said, the best way to do this matching is to test for the cell surface proteins, as these are what will be the targets of immune cells. Also an organ has a very short life span after the donor dies to be usable. Sequencing is much slower than the protein screening that is in place today. You run into ethical questions regarding keeping someone on life support for the sole purpose of harvesting their organs.

And we still wouldn't be 100 percent sure that even people with the same alleles for these molecules express them in the exact same way as there may be slight differences in the post translational modifications that are made. The human immune system has evolved to detect small variations and as such we would still need to test the proteins, even if we found allelic matches. People get autoimmune diseases all the time, so there is no guarantee that even allelic matches would not be rejected.


Difference between vacuolar and symplast pathway what is the difference between Vacuolar  Pathway and Symplast Pathway ? Is the symplast pathway does not take into account the vacuole to vacuole movement?

The vacuolar pathway involves the movement of water between vacuoles of neighbouring plant cells. The symplast pathway, on the other hand, involves the movement of water from the cytoplasm of one cell to the cytoplasm of a neighbouring plant cell without it entering a vacuole inbetween, so the symplast pathway has no vacuole to vacuole movement.


In what forms do plants and animals excrete sulfur? Sulfur is part of the amino acids cystein and methionin, plants take up sulfur in the form of $H_2S$. These organisms will also need a way to get rid of excess sulfur, how? In what compounds?
Judging by the smell of some farts, I guess $H_2SO_4$ plays a role, but I can't imagine that one get'S rid of all the sulfur this way.

Sulfur is $3^{rd}$ most abundant mineral element in the body. Carnivores obtain it from Cysteine and Methionine in the animal protein which converted in to Glutathione.
Excess of sulfur is stored into Glutathione or oxidised to sulfate by sulfite oxidase which is eventually eliminated by urine.

[1]: Nimni ME, Han B, Cordoba F (2007). "Are we getting enough sulfur in our diet?". Nutr Metab (Lond) 4 (1): 24. doi:10.1186/1743-7075-4-24

[2]: Wikipedia on Sulfur metabolism


Why is carotene in carrots? Internet says that the carotene is an important pigment for photosynthesis and UV-protection. That explains its accumulation in leaves. I suppose colored fruits are more appealing to animals, so that explains the fruits. But why roots? Why is carrot full of carotene? The only reason I can think of is human cultivation. Is there any specific reason carrots synthesize so much carotene? Are there other similar examples of so vividly colored roots?

Carrot (Daucus carota) is a biannual plant that accumulates massive
  amounts of carotenoid pigments in the storage root.

The root of the carrot was not orange before domestication.

  Although the root of carrot plants was white before domestication,
  intensive breeding generated the currently known carotenoid-rich
  varieties, including the widely popular orange carrots that accumulate
  very high levels of the pro-vitamin A carotenoids b-carotene and, to a
  lower extent, a-carotene.

As stated in the comments people did this to give a better taste to the roots. This is simply economical more beneficial because otherwise only the leaves of the carrot could be used for consumption (and not the roots which are a major part of the carrot), wasting this root would result in a lot of waste (and thus a lot of money waste) and because of an increase in carotene (and other compounds which contribute to the flavour) this would save money and provide more tastefull and appealing roots.

  It is likely that wild carrot plants had uncolored roots of a bitter
  taste and a woody core but were initially cultivated because of their
  aromatic leaves and seeds.

So the only reason (as far as I can find) is that this is ineed because of cultivation by stimulating a flux in the direction of the carotenoid biosynthesis

I think this picture will explain it all:

   (source)

I'm not sure how familiar you are with biology so I described this not in that much detail about the genes and expression of them etc. If you would like to know this I would highly recommend to read these articles:

Biosynthesis of carotenoids in carrot: an underground story comes to light. (which I mainly used to write this)
New insights into domestication of carrot from root transcriptome analyses


What do the numbers in Photosystem I P700 and Photosystem II P680 stand for? Is it the optimum wavelenght? The maximum wavelenght? I am a bit confused about this because my teacher and english Wikipedia say it's the wavelenght the Photosystem is most reactive to; my textbook and the german Wikipedia say that it is the maximum wavelenght the Photosystem can absorb :-/

I'd first like to briefly mention what the P700 and P680 refers to. These are the reactions centers of the photosystems. The Photosystems are where the light is absrobed and converted to the form of electrons. The light is absorbed by the chlorophyll molecules and the energy is transferred to the reaction center which transfers that energy into an electron from a water molecule. Tha elecron is transport tmake ATP and NADPH, which is important for carbon fixation.

The numbers specify the wavelength of light that the reaction center are most reactive to, and therefore, the wavelength where they absorb the most light. That's what's meant by the maximum absorption. So everybody is right, your teacher, the textbook and Wikipedia. They just say it differently.


Why did the urinary bladder evolve? Sure it's convenient to decide when to urinate but not essential for survival or reproduction, as I understand. But just convenience is not a drive for evolution.

Does the bladder serve any essential purpose? If not why did bladders evolve?

Here are just a few points that might apply:

Urine is used for scent marking by some species, so the ability to store urine could be useful.
At the opposite side, controlling the release of a strong scent would help in stealth for both predators and prey.  (In addition, a single strong scent might temporarily overload a predator's sense of smell making tracking more subtle scents more difficult.)
Flushing an excretion point (single point reduces opportunities for invasion) under some pressure could help avoid blockage and parasitic invasion/accumulation.  (Providing a tube from the extraction organ to the excretion point allows more flexible (and protected) placement of the organ, but also increasing the benefit of a flushing mechanism.)
Flushing could also reduce contact with skin. Urine might act as an irritant and a nutrient source for parasites.
Adding a buffer is a common technique for any pipelined operation to allow smaller resources to handle temporal variation in input and output rate.  Without a such a buffer, all stages have to be sized for the maximum utilization rather than something closer to average utilization.
Avoiding potential contamination of food and water may also be a benefit of controlled urination (or excreting might have a fertilizing or pest-deterrent aspect for plants).

Since terrestrial animals presumably retained urinary bladders developed by their marine ancestors, benefits associated with terrestrial lifestyle would only provide selective pressure to retain such a feature. However, if somehow a line of terrestrial animals abandoned urinary bladders, it is not entirely implausible that even scent marking benefits could increase the selective pressure enough to overcome some peculiar opposing selective pressure.

Initially, the animal might apply scents by scratching at an area of skin irritated by urine release against some surface. Then this scratching might be preferentially located (i.e., a scent marking behavior is developed). Having such a behavior would then obvious bring benefits to storing a significant amount of urine and eventually to being able to squirt the urine (allowing the scratching behavior to fall away).

The above are just somewhat reasonable speculations about what selective pressures might encourage the development (and retention) of a urinary bladder.  Hopefully, someone with actual knowledge will provide a better answer documenting established theory and evidence for how urinary bladders actually developed.


Is Infra Red light safe to use on your scalp? I own an Anodyne Infrared therapy device which I use to treat ligament/tendon/muscular pains and it works nicely.

I see other infrared products used to combat hair loss (e.g. https://www.amazon.com/dp/B01B29PCUU), but I don't know the nuances of different infrared devices. Is it safe to use the device intended for the above uses on my scalp? I'd rather not purchase a separate infrared device for my scalp if I own the necessary technology already.

These are entirely different devices. First off, the Anodyne product is truly far-infrared, emitting at 890 nm (infrared is above ~650-700 nm). However, the hair loss product you linked is far-red/near-infrared, with laser diodes emitting at 650 nm (which is why it glows red). If you put the Anodyne product on your skull, you'd just heat up your brain, possibly burning any hair you have left. (Well, maybe not, but it sounds kind of funny.)

I would strongly suggest you don't try regrowing your hair using an instrument designed to relax your muscles. I will give you a recommendation - read the small print very carefully. The hair product is only recommended for a certain type of hair loss called Androgenetic Alopecia. Please consult with your doctor to determine if you actually have this condition, otherwise your investment of US$600-700 will be completely wasted.


Division of proteins This textbook states

Proteins determined by a single gene may divide to form different proteins with various physiological actions.

First how do proteins divide? Second if it's just fragmentation then what is this process called? Third since my textbook doesn't explain it could anyone explain with an example of how different parts of original protein( considering that protein has divided by fragmentation) perform different physiological actions?

This is not a very helpful passage, I agree.  Some proteins are cleaved by other proteins (a protein that cuts another protein is called a protease).  Other proteins cleave themselves.  Otherwise, proteins are quite stable and don't just fragment wily-nily.

In the case of the first group (proteases acting on other proteins) the coagulation cascade may be a good place to start for you.  Precursor proteins in this pathway are converted to active enzymes by a chain reaction of protein 'division' and other protein modification.  This page has other interesting cases of this process, such as in food digestion, which may be what you're looking for.

Some of the second group are self-cleaving such that an intervening sequence is removed, and the ends are pasted back together.  (This is analogous to how introns are spliced from messenger RNA and the exons are spliced together.)  Such intervening protein sequences are called 'inteins'; the removal of one intein can generate one functional protein, so this isn't protein division.    However, some viruses encode self-cleaving regions that will split the mother protein into two or more pieces.  A famous example of this process, now used widely in biotechnology, is the 2A peptide, which is used to 'split' a single transgenenically-expressed protein into 2 (For instance if you want to express a protein and a marker such as GFP simultaneously, you could employ the 2A peptide to link these together.)

The first group may be of more interest to you because of the known role of these proteases in human health.  Also, in your question it sounds like you also may be referring to random 'fragmentation' of proteins, which is not currently known to be an important contributor to protein breakdown in the human body, even in the stomach.  Enzymes such as pepsin are responsible for digesting proteins.


Does melanin protect against nuclear radiation? It is known that melanin protects against UV radiation.

But say a nuclear bomb dropped somewhere would more people of dark complexion survive the radiation burns because the melanin would protect them?

Or as another example, suppose there was a meltdown and someone had to swim into the reactor to pull out the core, would it be best to send the light skinned or dark skinned person to ensure maximum chance of survival? All other things being equal.

The absorption of gamma and x-ray radiation by skin is negligible, so the amount of melanin present is irrelevant. Stopping high energy photons requires a lot of mass, not a few microns of melanin.


Are Humans Considered Keystone species? Do humans have a huge impact on the ecosystem ? is it possible for other animals to live without us ?

I am voting to close as homework question.

I felt like I would give you a few hints though.

  is it possible for other animals to live without us?

Life on earth have existed for almost 4 billions years. Animals have existed for about 600 millions years. Modern human (AMHS) have existed for 0.2 million years.

  Do humans have a huge impact on the ecosystem?

Here are just a few pictures taken by airplane of agricultural lands

and a koala searching its home after a rapid man-made deforestation


What is "Peripheral Dogma"? The book, Introduction to Bioinformatics, by Arthur M. Lesk, 3rd edition; Oxford; low-price-edition; in its chapter-1 (introduction), page-no. 6 ; provided a paragraph, entitled "Dogmas: Central and Peripheral".

As-if; there exist a contrasting term for central dogma.

But while thoroughly going through that paragraph (and other chapters linked(mentioned) in that-paragraph; I couldn't found the mention of the term "peripheral dogma" or such.

From the paragraph; it looks like the term "peripheral" has been used to indicate all information-flows other-than genetic codes, and including Junk-DNA and  protein-folding-variations. No mention of epigenetic codes found.

In Web too; I could found only 1 website  used the term "peripheral dogma" in context with biology. which, too, does-not mention the definition clearly.

So, What is peripheral dogma?

P.S. this is purely a terminology question; which is looking for authoritative reference about usage of a term.

I think the author was just trying to make a point that while the "central dogma" is indeed key, there is more to it than that and that understanding of molecular biology has advanced beyond being simplified to that one tenet. Without having the passage in front of me, the ideas you gleaned from the paragraph make sense, though others such as epigenetics seem like they would fit as well.

As you've noticed, this term is difficult to find anywhere else, it isn't a standard term and therefore doesn't really have any meaning unless it is defined in the source. I wouldn't recommend using it yourself unless you plan to define it. The Wikipedia page for central dogma that you linked has a whole section on information transfer not included in the "central dogma" - I think you can safely assume the author was referring broadly to these items.

This all may be a bit of a joke, as well, given the definition of "dogma" and it's somewhat inappropriate use in the context of the central dogma of molecular biology - again, the Wikipedia article you linked talks about the problematic use of the word "dogma" in this scientific context.


Are Oct4 and Oct3 the same protein? Are the transcription factors Oct4 and Oct3, who are encoded by the POU5F1 gene, actually the same protein, or alternative spliced products from said gene?

The best review I can find is the one by Wang and Dai 2010, conveniently titled starting with "Concise review".
From the beginning of the abstract:

The human OCT4 gene can generate at least three transcripts (OCT4A, OCT4B, and OCT4B1) and four protein isoforms (OCT4A, OCT4B‐190, OCT4B‐265, and OCT4B‐164) by alternative splicing and alternative translation initiation

and from later on, in the introduction:

It is well established that OCT4 gene (official symbol POU5F1, also known as OCT3, OCT3/4, OTF3, and OTF4) functions as a master regulator in maintaining the properties of pluripotency and self‐renewal of ES cells

I take from this review that OCT4, OCT3, OCT3/4, whatever you want to call it, all refer to the same gene. However, this gene does have splice and translation variants. It seems that when talking about these variants, you will see them differentiated using A/B/B1. An older paper and some that cite it, Takeda et al, 1992, refers to the splice variants as OCT-3A and OCT-3B. If not noted, you can expect that the paper is considering them all together regardless of whether they call it OCT3 or OCT4.
I did find one thesis that treats Oct3 and Oct4 as separate proteins, renaming them from the A/B terminology, but they cite only the Takeda paper for this, which does not do the same. It seems more likely to me to be a mistake.

Takeda, J., Seino, S., & Bell, G. I. (1992). Human Oct3 gene family: cDNA sequences, alternative splicing, gene organization, chromosomal location, and expression at low levels in adult tissues. Nucleic acids research, 20(17), 4613-4620.
Wang, X., & Dai, J. (2010). Concise review: isoforms of OCT4 contribute to the confusing diversity in stem cell biology. Stem cells, 28(5), 885-893.


DNA synthesis companies: cost per base, turn-around time, codon-optimization algorithms I would like to synthesize a 3.4kb gene (originally isolated from soil bacteria) and transform it into E. coli. There are several companies (DNA2.0, GeneScript, BlueHeron) which will synthesize the gene for you. I would like to know how these companies (or others) compare with each other in terms of:

Codon optimization - most of the companies are going to codon optimize the sequence and thus increase the protein expression in the desired host. Recently I learned that there are different algorithms that can be applied. I am mostly interested in how the codon-optimization is performed in the different companies and whether there are some direct comparisons of protein expression between them.
cost per base - I would like to find the cheapest one. In general, the cost of gene synthesis usually depends on the size of the fragment, as well as the complexity of the sequence. But on the other hand, DNA2.0 can synthesize 1kb fragment and 5kb fragment for the same price.
Turn-around time - which company will synthesize the fragment the fastest? I think that this mainly depends on size. Of course I have an option of ordering 3 x 1.1kb fragments and joining them myself, but then I have to sequence-verify the final product. So, I need to find the trade-off.

Please, keep in mind that I am not asking about your favorite company, but about specific characteristics of the companies.

Are you working in academia? It might be worthwhile to call the companies directly and see if there is a discounted rate for your institution (another lab or department may have already set something up).

You won't be able to get information on the different algorithms if they are proprietary.  However considering that codon usage data is public and shared knowledge, I can't imagine that the different algorithms are that much different. I think there are some tricks for choosing certain codons near the transcription start site in some organisms? From what I hear, the algorithms are constantly changing. I could tell you how my E. coli optimized gene from GenScript worked two years ago, but they'd probably design it differently now.

Okay - GenScript calls their algorithm "proprietary", so they are not sharing the details. DNA2.0 says their algorithm is patented, so it's out there for inspection. They published a PLOS paper on their E. coli algorithm: Welch et al..

Although, maybe all they do these days is spit out codon sequence randomly:

  The results obtained in this study indicate that the codon
  randomization method is a superior strategy for codon optimization. A
  significant improvement in protein expression was obtained for the
  largely established process of chymosin production, showing the power
  of this strategy to reduce production costs of industrial enzymes in
  microbial hosts. (Menzella 2011)

Stitching smaller synthesized fragments works well if you're pressed for time, but it's usually more expensive. However, sometimes these companies do special pricing on synthesis for <1kb, which makes stitching a great choice. Turnaround is generally faster for three 1kb fragments than one 3kb fragment.


programmatic fast search of 100-1000 short reads to a public server and obtain list of nearby genes What are the options for programmatic fast searching of 100-1000 short reads to a public server and obtain list of nearby genes where the reads map?

Input: ~100-1000 short reads

Output: GFF list of genes it maps to or nearby genes

Genome UCSC is restrictive to the number of searches and AFAICS it won't allow programmatic use.

Any ideas? I've asked this question to another forum without much luck:
https://www.biostars.org/p/114124/

This can be done offline and wont require too much of computational resource.

What you will need:

A fast short read aligner such as STAR or even bowtie (STAR is faster)
Genome sequence (you will have to build index for the genome for your aligner)
A GTF annotations file (get it from GENCODE or any other standard genome repository for your organism of interest)

Before you align remove redundant reads. Keep their counts if necessary.
Align the reads using any of these aligners and obtain the alignment co-ordinates. The default output is SAM format for STAR and a tabular format for bowtie (bowtie also gives SAM).

Column-3 of SAM shows the name of the reference sequence
where alignment happened (chromosome)
Column-4 is sequence start
Column-10 is read sequence. Add the length of this to column 4 value to get stop site.

The columns are tab separated

Now define a window that you define as proximal/nearby (lets say 500nt).

Now all you have to do is find genes that lie $\pm500nt$ from your start/stop sites. In your reference GTF parse for the lines that have the feature "gene".

I am giving an example using awk. You can use any programming language you are comfortable with. Check the GTF format also.

Assuming that you made a file (reads.txt) from your SAM output in this format:

Chromosome <tab> Orientation (+/-) <tab> Start <tab> Stop

I am giving an example awk script:

example.awk

#!/bin/gawk

BEGIN{FS=OFS="\t"}

NR==FNR{
    a[$1 FS $2][$3 FS $4] # store the co-ordinate information from your reads file
    next
}

$3=="gene" && ($4 FS $7) in a{ # quick parse for reference chromosome and orientation

    i=$4 FS $7
    for(j in a[i]){
        split(j,jj,FS)
        if(jj[1]>=$4 && jj[2]<=$5)
            print $0";contained"

        else if($4<=jj[2]+500 || $5>=jj[1]-500)
            print $0";partial overlap/proximal"
        }
}

call it like this:

awk -f example.awk reads.txt annotations.gtf

NOTE: In the above script I have not considered antisense proximity. If you want to allow that then don't parse for orientation. Also gawk version < 4.0 doesn't allow multidimensional arrays. So install gawk>=4.0

The output is by default a GTF because you are printing selected lines of the reference GTF.


Help identify this small spiney praying mantis? Trying to identify this praying mantis for a short film. It's found on the wild cosmos flower. It's found when the flower is in bloom at this time of year (February) in Harare, Zimbabwe.

This appears to be a species of Sub-Saharan flower mantis in the genus Pseudocreobotra.

Specifically, it resembles the spiny flower mantis Pseudocreobotra wahlbergi.

 © 2013-2018 carlarush

The species gets its name from the spiny structures on its abdomen. According to Wikipedia, the color is variable:

  being typically greenish, but it can equally be yellowish, pinkish or reddish

According to here, you can determine the sex of your specimen by counting the "abdominal appendages" (i.e., spikes):

  females have just 5 abdominal-appendages on the underside, however males have 6

 © 2004 Steffi Schuttauf

This might also be P. ocellata, which would be able to be distinguished from P. wahlbergi based on its smaller adult size [source].