True or false & fill in the blanks A ribosome is where amino acids are linked together by peptide bonds.
A virus is NOT considered prokaryotic because it does not have a membrane.
The nucleotide ATP is one of the most used energy molecules of a cell.
Sugar phosphates are the type of lipid moved through the blood.
A compound that lowers the pH is called an acid.
The cell wall is a carbohydrate covering of all cells.
The term cytosol is only applied to (blank) cells?
An A-U base pair is part of the (blank) found in RNA.
The major form of usable energy in animals is (what)?
A polypeptide is a subunit of a what?

This is what I said
1. True
2.True
3. True
4. False (cholesterol)
5. True less than 7 acidic
6. False
7. Don't know
8.complementary
9. ATP
10. Protein or amino acid? Don't know

1-6: OK;

prokaryotes. Cytosol is the portion of cytoplasm which is devoid of any organelles, i.e., cytoplasm = cytosol + organelles. As prokaryotes don't have any organelles in their cytoplasm, they have only cytosol. So the answer would be prokaryotes (their cytoplasm consist of cytosol only). For a special case in eukaryotes see Crags answer below.
Double strand;
Glucose? (but not ATP, fat would also be a suitable alternative specially in animal living in cold regions thanks to @CRags);
protein


Why do the major and minor groove exist in DNA? So I know that the major/minor groove arise from the offset pairing of the two strands in the helix.  All my textbook tells me is that "pitch causes the off-set pairing of DNA and this gives rise to the major and minor grooves."

I'm not too sure what this is saying.  What exactly is pitch and how does it give rise to the grooves?

Pitch is not a great word for this, as its meaning is ambiguous. It's hard to find a universal nomenclature for DNA geometry, but see the "Base pair geometry" section of this wikipedia page. The relevant property is what they call "opening".

From the biochemistry textbook by Berg:

To explain in words, if the glycosidic bonds (which attach the nucleic base to the sugar in the backbone) stuck straight out at 90 angles on both sides, then the grooves in double-stranded DNA would be symmetrical. Because the glycosidic bonds are at an angle (relative to the interface between the AT or GC pairs), one of the "faces" of the base pair is larger than the other.

Words and flat pictures, however, will never really give you a good intuitive sense of what's going on with the 3D structure of the grooves. A good modeling kit will be of great help to you.


can dissolving be endothermic process can dissolving be endothermic process. I have a container with glucose(solid state) and added water and found the container getting colder. was wondering there is no reaction(just a physical process) and why would it absorb heat.

The answer to your question in general is yes.
There are many salts and compounds that are endothermic - they cool the solution when they dissolve.  It also turns out that glucose is endothermic when it dissolves if this sheet i found is to be believed.  Its not a strong effect but you made an accurate observation!

Endothermic salts can be quite cold.  This is how home ice cream makers often work in fact - rock salt dissolves into the ice and makes it even colder than it started out to be. I believe that is how ice cream was made before refrigeration and ice storage arrived in the 19th century.


Confusion about resting membrane potential and the Na/K pump To this day, very few people and sources have been able to clear up my confusion about resting membrane potential and how it is maintained. It seems like this is one of those topics that few people are able to explain very well...

Here is what I do understand:

Chemical Gradients:

at rest, the inside of a neuron is negative and comprised mostly of Potassium (+) and negatively charged proteins (-)
at rest, the outside of a neuron is positive and comprised mostly of Sodium (+) and Chloride (-)

Electrical Gradients:

at rest, the sodium ions are attracted to the negative charge on the inside of the cell and tend to move inwards
at rest, the Potassium ions on the inside of the cell are attracted to the negatively charged chloride ions on the outside of the cell and thus move outwards

So overall, there is a net inflow of Sodium and a net outflow of Potassium. Got it, pretty simple.

However, the sodium/potassium pump is where I get lost. Why does it reverse all that just happened, and why doesn't it cancel out the resting potential if it moves K+ back inside and Na+ back outside? Isn't the voltage fluctuating because of this back and forth movement of K+ out, K+ back in, Na+ in, Na+ back out, etc.? I would imagine this would completely negate the positive/negative charge distribution, but it doesn't. Why?

Clarification: there is a net outflow of Potassium and a net inflow of Sodium. Why does the Sodium/Potassium pump intentionally reverse this by pumping out Sodium and pumping in Potassium? How does that contribute to resting potential?

The Sodium/Potassium pump maintains the overall concentrations of ions on either side of the membrane. In other words it keeps the neuron's battery charged.

Imagine the neuron like a circuit. We can imagine that the electro-chemical gradient for each ion species (Potassium, Sodium, and so on) as batteries. So When the ions flow according to their electrochemical gradient, the potassium current flows outward and sodium  current flows inward as dictated by these batteries reversal potentials [negative for potassium, positive for sodium].

However, note that this will discharge those batteries, i.e. the concentration of sodium on the outside of the cell will drop (slightly) as sodium flows inward the cell, and potassium flows outward the concentration on the inside will drop slightly. Thus the magnitude of the reversal potential of the Sodium and Potassium drops (they move closer to zero).

To counteract this discharge the Sodium/Potassium pumps expends energy in the form of ATP in order to recharge the batteries. The amount of current that the pumps moves is very small relative to the larger currents of sodium rushing in and the potassium rushing out during an Action Potential. Thus when a neuron fires there is very little overall current contribution from the pumps.

When the neuron is at rest (not firing) then the Sodium/Potassium pump is able to recharge the membrane and the current becomes important. Still this is a very slow process, relative to action potentials.

Another thing to note, even though the cell is at rest the batteries are discharging slightly. Their is a leakiness to the membrane, sodium leaks in and potassium leaks out. Thus the pump's current will counteract these leaky currents at rest, keeping the batteries charged and thus the overall net current  across the membrane at rest will be zero.

Remember though, these currents are very small currents.

EDIT: Based on Discussion with @Christiaan, I decided to post a update to clarify.

At rest potential Sodium Ion influx is much smaller than potassium ion efflux and thus can be ignored. Whether or not Sodium is ignored the above still holds true. The neuron's membrane is at rest which means the net current is equal to zero. This means that the outward potassium current is counterbalanced by the pump's current thus keeping the relative concentrations of Potassium and Sodium constant while at rest and maintaining a steady rest potential.

EDIT 2: Clarifying as per OP comment:

So during an action potential Sodium and Potassium ions move in large currents and this current flow discharges the batteries. At rest there is still current flowing (thus smaller discharging of the battery) but there is no Net current flow thus no change in voltage(thus the neuron is at rest). It is exactly counterbalanced by the sodium/potassium pumps. The reasons the pump doesn't overcharge the batteries is the constant but smaller discharge at rest. When the recharging current is equal and opposite to the discharge via the leak current, a equilibrium is reached.

However when lots of action potentials fire, the resting potential will be altered from the larger discharge rate, thus when the neuron returns to its new resting potential the leak current and pump current will not be balanced, thus the recharging pump current will be larger in magnitude and will bring resting potential back to its normal value.  (Note what constitutes large is relative between species and even neurons.)

Edit 3: Rates of Leakiness and Pump activity.

If only you could say one is stronger than the other. It depends on the conditions of the cell.

Lets focus in on potassium. The leak current for potassium is dependent on two (really three) things. The permeability (or conductance) to the membrane to potassium, and the reversal potential of potassium (which is dependant on the internal and external Concentration of Potassium. Thus varying these things will strengthen/weaken the power of the leak current.

The Sodium Potassium Pump is dependent on three things. The External Concentration of Potassium, The internal concentration of Sodium and the availability of energy (in the form of ATP).

The point where these two strengths are about the same is when there is more Potassium on the inside of the cell. That is to say pump is capable of keeping up with the leakiness of the membrane until the internal concentration of potassium reaches about $140$ $mM$ (again that just a ballpark number). If their is less Potassium in the cell then $140$ $mM$ the pump is stronger, if there is more than $140$ $mM$ the leak of potassium is stronger.


Spider identification (Caribbean) I live in the Caribbean (Puerto Rico) and found this spider in my garage. Is it venomous?

It measures about 8 inches as a whole.

It appears to be a Banana Spider:

  ... a male Heteropoda venatoria, also called a Banana Spider. The female is a more robust spider with shorter legs. This is the spider that is responsible for the rumors that tarantulas come into the U.S. with bananas because they are often spotted emerging frrom a bunch of bananas in a fruit store in the North. This Giant Crab Spider is usually the culprit. The species is found in all tropical regions, its range extending clear around the world. It is very abundant in all tropical seaport towns, being transported in trading vessels. Its chief food is cockroaches. The female carries her eggs beneath her body. According to this site it is also called the Huntsman Spider.

https://www.whatsthatbug.com/2003/11/11/banana-spider-from-peurto-rico/


Standard Free energy of hydrolysis of phosphoenolpyruvate (PEP) In ATP we have two anhydride bonds, each with a Standard Gibbs free energy of hydrolysis ~ -30 kJ / mol and one phosphoesterbond of ~ -20 kJ/ mol, if my notes are correct.

In phosphoenolpyruvate (PEP) we also have a phosphoester bond, but the Standard Gibbs free energy of hydrolysis is three times higher, at ~ -62 kJ / mol.

How does the double bond / enol form contribute to this high free energy of hydrolysis?

An answer to this is given in the online version of Berg et al.

  Why does phosphoenolpyruvate have such a high phosphoryl-transfer potential? The phosphoryl group traps the molecule in its unstable enol form. When the phosphoryl group has been donated to ATP, the enol undergoes a conversion into the more stable ketone—namely, pyruvate.

  Thus, the high phosphoryl-transfer potential of phosphoenolpyruvate arises primarily from the large driving force of the subsequent enol-ketone conversion

Note that Berg et al. use the term “high phosphoryl-transfer potential” or “high phosphoryl group-transfer potential”, as explained in sections 14.1.4 and 14.1.5. These sections are worth reading, and this terminology is worth following.


Does a woman contain all the genes needed to make a man? I know the answer of inverse is at here, but how about this question?
I also read this question, can I imply to human that a woman can also contain all the genes needed to make a man?

Edit:
I think everyone has  the ability of being a man or a woman in terms of their DNA, and that their gender is just determined by the presence of SRY.
Is my concept correct?

Human female cells contain most of the genetic information required to make a male, but they do not contain a critical component: The Y chromosome. This is a relatively small chromosome. Wikipedia claims we have identified around 200 genes on it to date, compared to estimates of 20,000 - 25,000 genes overall in the human genome.

Importantly for your question, only other males contain and make full copies of all the genes on the Y chromosome. The Y chromosome does not cross-over* with the X chromosome during meiosis when producing sperm cells, which keeps the Y genes isolated, except for rare exceptions (e.g. gene translocation). So those genes are passed down the male line only. The SRY gene is just one of the genes encoded uniquely on that chromosome, so something else is definitely missing - the question could be re-phrased "how important to being a functional male are the unique genes other than SRY unique to the Y chromosome?"

The linked question (an experiment on mice that produced XX "males" by finding an alternative trigger to the SRY gene to induce male development) demonstrates that in terms what we might consider a physical male specimen, the Y chromosome probably contains a minority of critical unique features. The mice developed into apparently complete physical males. That means genes outside of the Y chromosome cover most of the body development plan for both males and females.

However, such XX males will in most mammal species not be fully functioning males - the missing genes do make a difference. One outcome is infertility - biologically speaking, XX males do not possess a key male function, the ability to mate with a female to produce offspring. There are missing genes related to sperm production.

Human XX males - as in developmentally male - do occur naturally. This can be caused by gene translocation - specifically the SRY gene moves to the X chromosome in a sperm from the father (potentially other Y genes will move in the same event). The symptoms that present with the syndrome vary, but give some indication of which critical components are missing.

Not all animals have the same mechanism. Birds have W and Z chromosomes (with males being ZZ and females ZW). Yet other animals do not use genetic switches, but environmental ones. In those cases, the female does contain all the necessary genetic information to create a male. In cases where there is parthenogenesis (production of offspring without fertilization), then this can be fully demonstrated.

* Technically there are some small regions, about 5% of the Y chromosome, which do cross-over with X, called the pseudoautosomal regions. At the time of writing the linked article mentions 29 genes found in these regions.


Clustal Omega - convert from distance into # of substitutions I have a set of nucleotide sequences for which I have aligned using Clustal Omega. In particular, I performed a full alignment, and obtained a full distance matrix.

The distance matrix scores range between 0 and 1. I am looking to use this score to back-compute the number of different positions present in the alignment. Is this possible? If possible, I'm looking to avoid using code (my own or otherwise) to re-compute the number of positions differing between each pair of segments, and instead compute it directly from the distance score.

Here is a toy example of what I am receiving from ClustalOmega:

Sequence    1    2    3    4
1           0    0.1  0.06 0.1
2                0    0.4  0.23
3                     0    0.05
4                          0

The numbers are the "distances" as calculated by ClustalOmega. According to the README file, they are computed by the k-tuple measure. I tried parsing the original paper (published in 1983 in PNAS), but I could not figure out how k-tuple distances are computed, and I could not figure out how the distance metric (as reported like above) is computed from k-tuple distances.

I would like to convert those numbers into the number of positions that differ between each pair of sequences when the two are aligned. This includes substitutions, insertions, deletions. I am currently doing this for 520 sets of virus sequences. Is this possible?

It uses a gonet matrix to compare each of these two sequences. Since you you could have insertions and extensions as well as substitutions, it becomes a 3 parameter problem. 1*open + 6*penalty + substitution_penalty = X. X can be solved by a linear combination of substitution_penalties, extensions, and insertions. So I think this will be really really hard

with that being said. Clustal outputs the multiple sequence alignment. Why don't you just look at sequence 1 and sequence 2 and see what the insertions and substitutions are!


How quickly do estrogens break down in the environment? Of all the synthetic hormones we use, estrogens are probably the most common.  They are used for birth control as well as hormone replacement therapy.  This researcher also shows that there is plenty of it in milk because dairy cows are often pregnant while they are being milked.

Estrogen is a sturdy compound, very much like cholesterol.  I was wondering if anyone had any idea how long it would survive in the environment, given that some people are concerned about it interrupting animals life cycles.  How fast does it break down in the wild?

Months to years - although the actual duration in a specific environment depends on the nature of that environment and is tied to oxygen level. Higher oxygen, faster degradation. Less oxygen, the estrogen molecules interconvert among various closely related molecules which hampers both their detection and their degradation.

For more info, please see: Environmental science: The hidden costs of flexible fertility (Nature 485, 441 (24 May 2012))  and this Science Daily article.


If we change our breathing rate so easily, then what is the point of measuring it? When we are self-conscious of our own breathing, its rate changes very easily. Therefore, if it changes so easily, what is the point in measuring it?

Thank you for your time and effort

We may be able to voluntarily control our respiratory rate, but only for a short while. The buildup or depletion of CO2 will force us, against our will, to either speed up our respiration or slow it down. So, you can't effectively "fake" your respiratory rate for long, nor, to an astute observer, convincingly.

Normal breathing patterns are "normal" for a reason. Aberrations from normal do occur in pathological states, but they are compensatory mechanisms driven by a number of factors your blood chemistries: the pH and the intimately linked CO2/H-CO3 concentrations, etc. You can pretend any way you like: you won't be able to keep it up comfortably. Also, normal breathing isn't simply "breathe in/breathe out". It is a more complex thing characterized by an inspiratory phase of certain duration, an expiratory phase of a different relative duration, and a normal, periodic deeper breath (close to a sigh), all done physiologically and unconsciously.

With certain illnesses come certain breathing patterns. You might be able to fool one person's quick assessment, but not more than that. If the faked breathing pattern (largely unsustainable anyway) doesn't appear physiological, you will be quickly found out.

For that reason, a sustained increased or decrease in respiratory rate is indicative of particular pathologies, whereas a normal respiratory rate is a helpful sign.


Can someone identify these eggs? They were attached to a tree in a black-water inundated forest (igapó) near Manaus, Amazonas, Brazil. The photo was taken in mid June, the water level was already high, and the eggs were about one metre above the water (not sure if they had been or would be under water at some point). It's been many years now, but I think the whole group was about 5 to 10 cm long (about 2–4 inches).

That's an apple snail egg cluster. They're freshwater snails, and by placing their egg clutches above the water line they protect them from predation.

We actually have an issue with apple snails in Florida, because while the Florida applesnail Pomacea paludosa is native, three different invasive species have been introduced that are eating through native vegetation without many predators (1).

Different species produce different colors of egg mass, and a good example of the green egg masses includes Pomacea haustrum, the titan applesnail, which is present in the continental US, but actually native to Bolivia, Brazil and Peru (2, 3). Since other species also produce green eggs, it's difficult to tell exactly what snail produced those, however.


GWAS: why is replication in another cohort so crucial? Almost all the landmark GWAS (Genome-Wide Association Studies) reviews agree that, for a GWAS finding to be valid, it needs to be replicated in an independent cohort. What exactly is the rationale behind this? Is this criterion still valid even when the objective is looking for genes to do functional studies, instead of a clinical perspective of searching for susceptibility loci? Considering the difficulty in replicating some phenotypical characterizations in a large numbers of subjects, for a biologist this whole thing seems irrelevant.

Consider the following scenario: Suppose I have 5000 phenotyped individuals with a budget to genome-wide genotype them all. The phenotyping requires state-of-the art methodology with immense costs, and the cohort was phenotyped through another grant. What would be the point of dividing my cohort to two as a discovery and replication groups, other than to save money in exchange for stat power. To this, add the subsequent functional studies on the associated loci, what would the point in genotyping a few SNPs in 500 more people be? If one can indeed find that additional cohort, wouldn't it be a better option to combine any available cohorts in a meta-analysis, rather than using them for replication?

As an elaboration of my comment.

Summary: Replication is required in GWAS studies to account for non-random technical biases.

An example of such bias is, for example, a chip used for genotyping giving consistently incorrect genotypes for a locus. In this situation adding more subjects will not correct for this effect and therefore the only solution is to genotype additional subjects with another method (e.g. another chip or experimental protocol). Another source of non-random technical bias is at the phenotype measurement level. You might want, if possible, to measure the phenotype using other techniques to make sure that bias will be corrected.

A replication cohort does not need to be huge and the actual size needed will largely depend on the effect size of the SNP seen in the discovery cohort. A "power-to-detect" calculation would help in predicting the cohort size needed. For a SNP to be significant, it must pass Bonferroni correction but as you can run a statistical test at the candidate site only the correction will be usually not very astringent (i.e. you might run association tests on "only" a few dozens or hundreds SNPs).

Historically GWAS replication was also required to correct for population structure but as the tools evolved substantially (e.g. the use of principal component analysis) and the cohort sizes are now substantially bigger compared to the first GWA-studies, this is less a concern. What was required is to sample independently other subjects from either the same or a different population.

For your situation what you could do is to split your cohort into a discovery and a replication panel, genotype your subject in the replication panel using an independent technique, eventually do the same with the phenotyping and replicate you candidate SNPs. The replication panel needed is usually must smaller than the discovery cohort for the reasons stated in the previous paragraph.

For your last question about the meta-analysis. Yes this could also be a way to go but be careful that you will still need a replication cohort to validate SNPs found this way therefore resulting in the exact same problematic you described.

I hope this help!


(Updated question) Problem with Fold-change mean compared to absolute data (in qPCR) For the problem below I am aware of the statistics involved but just can't get my finger around the following:

In biology we use qPCR to measure gene expression or basically number of mRNA copies. It does this by counting how many cycles of amplification (2^) it needs to reach a threshold. So to simplify everything lets assume that 1024 copies would require 10 cycles (2^10). If there are more copies it would take less cycles to reach the threshold, therefore 2024 copies would take 9 cycles, 512 copies 11 cycles etc.. Now imagine the following scenario:

We have the following samples:

Sample 1. 1024 copies of gene A and 4096 copies of gene B
Sample 2. 1024 copies of gene A and 16384 copies of gene B

Now we want to compare sample 2 to 1, with gene B in relation to gene A:

In absolute numbers this would be:

Sample 1. 4096 / 1024 = 4x more B
Sample 2. 16384 / 1024 = 16x more B
The average amount more B = (16 + 4) / 2 = 10x more B

Now with qPCR the same samples from above would look like the following:

Sample 1. Gene A 10 cycles, Gene B 8 cycles.
Sample 2. Gene A 10 cycles, Gene B 6 cycles.

Now using the methods standard used for qPCR data we first take the difference between Gene B and A. Followed by the mean of the difference and this is taken 2^.

Sample 1. 10 - 8 = 2 cycles
Sample 2. 10 - 6 = 4 cycles
The average amount more B = 2^((2 + 4)/2) = 8x more B

All publications / software tools etc will compute an average of 8x more B. And I am aware this originated from a log2 scale, however why does this statistically correct method differ in outcome from absolute numbers?

Update
I oversimplified my question therefore below some more details of my "problem".

Condition 1 biorep 1. 1024 copies of ref and 1024 copies of gene X
Condition 1 biorep 2. 1024 copies of ref and 1024 copies of gene X
Condition 2 biorep 1. 1024 copies of ref and 4096 copies of gene X
Condition 2 biorep 2. 1024 copies of ref and 16384 copies of gene X

So to compute in absolute numbers the average amount more of gene X in condition 2 versus 1:

We can forget the reference gene here as cDNA amounts are the same, therefore:
Condition 1 biorep 1 & 2: average (1024 + 1024) / 2 = 1024 copies
Condition 2 biorep 1 & 2: average (4096 + 16384) / 2 = 10240 copies
Condition 2 vs 1: average 10240 / 1024 = 10x more gene X in condition 2 vs 1

Now with qPCR CT values based on the numbers above:

Condition 1 biorep 1. Ref_CT 10 and GeneX_CT 10
Condition 1 biorep 2. Ref_CT 10 and GeneX_CT 10
Condition 2 biorep 1. Ref_CT 10 and GeneX_CT 8
Condition 2 biorep 1. Ref_CT 10 and GeneX_CT 6

Now using the official qPCR calculations:

Condition 1, Ref_CT mean (10 + 10) / 2 = 10
Condition 2, Ref_CT mean (10 + 10) / 2 = 10
Condition 1, GeneX_CT mean (10 + 10) / 2 = 10
Condition 2, GeneX_CT mean (8 + 6) / 2 = 7

Ref_deltaCT (10 - 10) = 0
GeneX_deltaCT (10 - 7) = 3

delta_deltaCT (3 - 0) = 3
Difference Condition 2 vs 1 = (2^3) = 8x

This equates to 8x more of Gene X on average in condition 2 compare to condition 1. Here now is the difference of 8x vs 10x. Also any program you will use to fill in these CT values it will result in a ratio of 8 compared to 10.

Is this perhaps as this method equating to 8 should only be used for technical replicates, and bioreps should use a different equation resulting into 10?

Sample 1. 4096 / 1024 = 4x more B
Sample 2. 16384 / 1024 = 16x more B
The average amount more B = (16 + 4) / 2 = 10x more B

That is not the right way to go about. You are calculating average expression of B in both samples. It does not mean there is 10x more B. There is just 4x more B in Sample-2 relative to Sample-1.
Gene-A does not change its expression between samples and can be used as a reference gene.
If you calculate by threshold cycle the fold change $ = 2^{8-6} = 4x$
See this post too.
The average is calculated between replicates, not between different experimental conditions.
Sometimes the average of two experimental samples is calculated — this is typically done in a MA-plot analysis which is done to filter out genes which show very high fold changes just because of their overall low expression (1:4 vs 100:300).
Answer to your Edit
You should not take the average (arithmetic mean) of Ct. They don't scale linearly with expression (and so is the converse).
For any non-linear function $f(x)$:
$$f(x+y) \ne f(x)+f(y)$$
$$f\left(\frac{x+y}{2}\right) \ne \frac{f(x)+f(y)}{2}$$
Furthermore, for a convex function:
$$f(E[x]) \le  E[f(x)] $$
$$ Jensen's\ inequality $$
where $E[x]$ is expected value of $x$
$a^x$ is a convex function with respect to $x$ ($a$ is any real number > 1). So you can apply Jensen's inequality to Ct values and expression.


Why does cell differentiation start with the morula? I suppose that cell differentation has to start by some external symmetry breaking. The first time there are two different types of cells is the morula with roughly 16 cells: there are some 12-15 cells forming the surface of the morula and some 1-4 cells in the interior of the morula. These are exposed to physically/chemically different local environments which might be the initial triggers of cell differentiation.

(source)

Questions:

Is this kind of argument/picture correct?
What are the significant differences in the environments of the outer and the inner blastomeres of the morula that trigger cell differentiation - and how do they do?

(Partial response) You're actually correct that inner vs. outer position is a differentiator, but there's still controversy whether position is a cause or whether differentiation actually happens sooner.

For a long time it has been believed that cells are identical within this ball at least until they take up distinct inside and outside positions, but is this true? A number of studies [2, 3, 6, 7, 8, 9] over the last 10 years involving a variety of markers such as oil-drops, dyes, fluorescent beads and proteins, together has challenged this view. These studies indicated that cells start to develop their identity earlier than expected, before taking inside or outside positions and, importantly, that these differences between cells are significant, as they bias cell fate [2, 3, 6, 7, 8, 9]. This view has not been universally held, however, because differences between the cells were not detected by other groups and so the view that cell fate choice is random was maintained [10, 11, 12]. It was also proposed that the bias in cell fate might simply result from the shape of the zona pellucida surrounding the embryo until implantation [13], an interpretation that has itself been questioned [14]. The random (stochastic) view of development became popular as it seemed to fit more comfortably with the experiments showing that early embryo cells are plastic and can adopt different fates upon transplantation.
The new contribution from Kevin Eggan’s group [1] now further challenges the view that early mouse development is stochastic.

And from a slightly more recent paper:

Drosophila has been found to have a pre-pattern in oocytes and zygotes. Several molecules that act as maternal determinants of the future body axis (for example, bicoid mRNA) are thus localized asymmetrically in both oocytes and fertilized embryos of Drosophila [6]. No such molecule has been identified in the mouse oocyte or embryo, although certain molecular and structural asymmetries have been described in unfertilized mouse oocytes. For example, Par4 protein is asymmetrically localized in mouse oocytes [7], but whether this protein is unevenly distributed among blastomeres after fertilization remains unknown. In addition, transcriptome asymmetry in terms of mRNA regionalization within mouse oocytes and zygotes has been identified, but no such asymmetry was detected between blastomeres within 2- or 3-cell-stage embryos [8]. However, several recent studies suggest molecular differences exist between blastomeres of the mouse embryo as early as the 4-cell stage. These molecular heterogeneities include the level of H3R17me2 and H3R26me2 (dimethylation of histone H3 at arginines 17 and 26, respectively) [9] and the level of Cdx2 expression [10].

Wikipedia also mentions this fact about Drosophila, so for insects at least it seems uncontroversial.


Why are pilots under the illusion of gaining altitude without doing so? We had a lecture about the balancing systems of the body (mainly the otolith organ / semilunar canals) in which a case was described where a pilot crashed into a ship. He was supposed to keep his altitude and had not been looking at his instruments, but was guiding the plane by feeling.

However, he was under the illusion that the plane was gaining altitude when it wasn't and so steered it downwards, dropping and eventually crashing into a ship which happened to be at that particular spot that moment.

Since the otolith organs detect de- and acceleration in all directions (that just comes from how the mechanism works), if the pilot was flying at steady altitude, why would they signal that he is rising?

(Will add an article later if I find one.)

See this link. It provides a great overview. The answer you want is in the otolith section. To paraphrase, it states that our otolith organs are designed to help us lean forward while running to maintain our center of gravity when in motion; however, in a plane this reflex can backfire by causing a pilot to believe he is going straight when in actuality he may be going downward.


Mesoderm vs Mesenchyme- what's the difference? My embryology textbook states that mesoderm can exist as Mesenchyme or Epithelium. I'm not sure what 'epithelium' means. Here is a quote for context:

  Somatic, splanchnic, and somite mesoderm can be temporarily an epithelium.
  The temporary epithelium transforms to a secondary mesenchyme

What does this quote mean?

Mesenchyme is the meshwork of embryonic connective tissue in the mesoderm; from it are formed the connective tissues of the body as well as blood vessels and lymph vessels.
So it's a part of mesoderm


What percentage of RNA splicing happens during transcription? Splicing can happen either during transcription, or directly afterwards.

I am reading about single-cell RNA seq, and according to this paper, they observed that 15–25% of reads contained unspliced intronic sequences.

Now assuming that the majority of reads from RNA seq will come from RNA that has finished being transcribed...

Does this suggest that 75-85% of all genes are spliced during transcription? In other words, are 80% of our genes fully mature (spliced) immediately following transcription?

I don't think it will be possible to give a conclusive answer to this question, because a) it's a matter of active research and b) the rate / percentage of transcripts that are fully spliced co-transcriptionaly is almost certainly not constant but will depend on a lot of factors & regulatory mechanisms.

Another important detail is that this analysis / paper is based on mRNA sequencing, which uses oligo-dT primers to enrich for polyadenylated mRNA molecules. However, oligo-dT primers can also bind to stretches of A's inside of RNA molecules (this process is called internal priming) and since such stretches are more common in introns compared to exons this may contribute to the abundance of intronic reads in mRNA sequencing data (I don't have a good literature source for this specific case, but it's a known 'issue' for sure).

Maybe some of these reviews are also helpful (not sure if all are freely available):

Splicing and transcription rates in living cells
Environmental influences on RNA processing
Co-transcriptional spliceosome assembly and function


Can untargeted metabolomics detect epigenomic changes such as methylation? My main focus is transcriptomics analysis and very recently I have also started working on metabolomics. From my transcriptomic data it looks like there is a gene/protein that could potentially generate epigenetic modifications. I also have untargeted metabolomics data of equivalent experimental conditions that I plan to analyse soon hoping it will complete the picture. However, I have searched for publications linking specific metabolites with hyper/hypomethylation or chromatin structure and I have only been able to find a few references (see link below) and I got the feeling that untargeted metabolomics does not seem to be an obvious technique to observe epigenetic signatures.
https://www.ncbi.nlm.nih.gov/pubmed/30125527

What metabolites would be regulated under epigenetic circumstances?
Does anybody have any experience or know of any particular study that looks into this relationship between untargeted metabolomics and epigenetic modifications? Thank you very much for your help!

This is a fascinating question, and I spent a fair amount of time looking into it. From what I've been able to find regarding the relationship between metabolics and epigenetics, it seems that metabolites drive epigenetic changes, not the other way around.
This can be shown quite well by looking at cell differentiation and induced pluripotent stem cells. The epigenetic changes that happen in these processes happen due to the cell's environment.

However, epigenetic changes cause changes in transcription rates, so it can indirectly influence metabolics. The circadian clock uses this system (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3392647/).
Cell signaling appears to be the most significant cause of metabolic change, though. The aforementioned paper also says this:

  As most metabolites are not diffusible between mitochondria and
  cytosol/nucleus, accurate determination of the cytoplasmic pool size
  is critical to understand their effects on epigenetic signaling.
  Although attempts have been made, so far the technology to reliably
  measure metabolite concentrations in different cellular compartments
  is lacking.

Which, I'm sorry to say, leads me to believe that there are very few metabolic pathways that have known effects on epigenetic factors.
That said, there are several references in that paper which may put you on a good path forward.


What are the costs associated with carrying lots of genetic material What are the costs (if any) associated with carrying lots of genetic material (Big genome size)?

energy for copying?
raw material for copying?
space in the cell?
Maintenance cost (matter and energy)?
time to copy is a limiting factor for the minimum generation time?
Less robustness?
More likely to evolve a gene that spreads well but has a negative fitness impact on the rest of the genome (selfish gene or outlaw)?

The answer probably depends on the organism. I am interested about any information concerning uni- or multi-cellular eukaryotes, bacteria or viruses.

Do we have any knowledge about how important are these costs or is it pure guesses?

This post comes in reaction to @AlanBoyd comments on this post.

It is generally known that the smaller (or less complex) an organism is, the more "condensed" it's genome is. For example, bacteria (or some eukaryotes) have operons (http://en.wikipedia.org/wiki/Operon) or overlapping genes using different and they don't have introns, which alltogether saves a lot of space.

There are many reasons for that. Available space in the cell is definitely not one if it, however. Energy for copying and maintenance is a good point, but you have to keep in mind how evolution works. Bacteria and unicellular eukaryotes are usually adapted to a very specific environment in which they can reproduce rapidly. This means, they only need a small set of genes, specific for this environment and they have to reproduce very frequent, which means they are very prone to mistakes during DNA-copying. Such a mistake can lead to the death of the cell, which in this case equals the death of the organism.

In higher organisms however, the advantages of a bigger genome outweigh the disadvantages by far. Evolution can happen much faster because and mistake while copying does not necessarily lead to the death of the whole organism. Adaptation to a much greater variety of conditions is also necessary, e.g. when you look at plants: Their genomes are (on avarage) much bigger than the ones we mammals have, because they cannot move if the conditions around them become unpleasent. Instead, they need to find a way to adapt. This means, a big genome is in this case a fitness bonus. More interestingly, plant genoms are highly mutable (http://en.wikipedia.org/wiki/Transposable_element), which was originally thought to be a huge disadvantage.


Pigmentation in Jaundice My textbook says that the yellow appearance of a jaundiced person is due to the accumulation of bile pigments in the skin. I am unable to understand why these pigments are not deposited in a healthy person? Please help.

The yellow color comes from the accumulation of Bilirubin in the body. Bilirubin is a breakdown product of hemoglobin (contained in erythrocytes, also known as red blood cells, and responsible for the oxygen transport in the body). (This is also the reason why bruises get colored, as the blood which was released into the skin gets removed.) As erythrocytes live only for around 120 days, the hemoglobin needs to be recycled at the end of the life cycle, as free hemoglobin is a pretty problematic substance.

The recycling of the erythrocytes happens in the liver, the iron is recycled, and the hemoglobin is split in the globin (which is further broken down into the amino acids) and the heme which is oxidized by the heme oxidase to biliverdin and further by the biliverdin reductase to bilirubin.

As bilirubin is not water soluble it is bound to albumin and released into the bloodstream for the transport to the liver. In the liver this process goes on further until the bilirubin is water soluble and can be released with the bile into the intestine where it is finally excreted. See the image (from here) for an illustration:

If your liver is not working properly (for example due to an infection) the break-down process of the albumin-bound bilirubin is reduced or doesn't work and the yellow bilirubin accumulates in the body until the skin gets yellow. So this indicates a liver malfunction and is usually nothing to take easy.


Any forms of pneumonia that can be caught? I am aware of the fact that there are several different types of pneumonia.

However, I am wondering if any of these types of pneumonia are contagious from person to person.
Is this possible?

Pneumonia means inflammation of lungs- especially alveoli.
There can be many causes of it including infectious agents, autoimmune condition and  chemical irritants. Pneumonitis is a more accurate word for lung inflammation, the causes of which includes the abovementioned agents; Pneumonia in common usage refers to the condition due to infectious agents such as bacteria, viruses and fungi.

In almost all the cases the infectious agents are airborne in the form of aerosols (spread by cough) and infect the respiratory tract directly. Some cases of fungal pneumonia (Pneumocystis, Penicillium) are observed more commonly in immunocompromised individuals, such as AIDS patients, and dissemination happens via spores.

As you can intuitively figure out the infectivity is different for different pathogens.


What features cause mechano sensory adaptation? In relation to mechanoreceptors (e.g. pacinian corpuscles), what stops a constant stimulus from producing action potentials?

I understand that adaption is used to filter out stimuli that aren't changing, but what are the cellular mechanisms going on within the neurone that drive this process?

At the molecular level this is called receptor desensitization. This is the reason why for example spices (like red hot chili paper) taste more pungent the first time you put them in your mouth and less and less subsequent times (in this case the receptor is called TRPV1).

Mechanosensory perception is mediated, at least in part, by similar transient receptor potential (TRP) channels therefore mechanosensory perception is also subjected to desensitization at the molecular level. In this particular case it is specifically called homologous desensitization.

This is, in my opinion, the primarily reason why a constant stimulus will stop producing action potentials, in essence the receptor will be desensitized and does not provoke a membrane-potential change that mediates the transmission of a neuronal signal.

Footnote

Desensitization in TRP channels happens because those channels open to let $Ca^{2+}$ ions to enter the cell and after prolongated stimulation the intracellular $Ca^{2+}$ concentration will reach the same $Ca^{2+}$ level of the extracellular medium preventing more $Ca^{2+}$ ions to enter the cell.

$Ca^{2+}$ influx into the cell is what provokes a difference in membrane-potential (i.e. the cell is now electrically charged) which mediates a signal that is then transmitted to the neuronal circuitry.


What is DNA-cellulose chromatography? I am going through a paper where they have done DNA-cellulose chromatography to study the interaction between protein and DNA. They are adding the protein to the column and eluting with high salt concentration.

DNA-cellulose chromatography is used to purify proteins that bind DNA (Potuzak and Dean 1978, Abdullah et al., 1985).

The idea behind it is quite simple: you attach DNA to a cellulose matrix and keep conditions so that the DNA does not dissociate from the cellulose. This stationary phase is then used as a bait for DNA-binding proteins from the mobile phase. The purified DNA-binding proteins can subsequently be dissociated from the column with high salt concentrations.

The method was (as far as I know) first described by Litnam (1968) who used it to extract a DNA polymerase from Micrococcus luteus.


How can natural selection occur at species level whilst not occuring at the individual level? The chapter by Douglas Futuyma in 'Evolution' (Losos et al 2013, Princeton) states that natural selection can occur at the species level. Futuyma states that if natural selection occurs at the species level it does not occur at the individual level:

  Neither gene selection nor species selection has molded the advantageous characteristics of individual organisms; rather, they have affected properties at the gene level or at the species level.

But how does natural selection occuring at the species level not affect individuals? Surely any selective advantage of a particular species must occur among particular individuals of that species. For example, if Species A is selected because it is browner than Species B, this will be because individuals of Species A are browner than individuals of Species B.

I think you have misunderstood the passage. Here is a larger section (found at google books):

  Natural selection can also occur at the level of species, for certain characteristics enhance the rate of origin of new species or diminish the likelihood of species extinction. For instance, the number of species in lineages of herbivorous insects has generally increased faster than in closely related lineages that have other feeding habits. Neither gene selection nor species selection has molded the advantageous characteristics of individual organisms; rather, they have affected properties at the gene level or at the species level. But individual selection, selection among individual organisms within populations, is at the center of evolutionary theory. It is at this level that selection explains most of the adaptive features of organisms.

Going through this part-by-part; the first two sentences state that lineage/species selection can occur, in the sense that species traits can enhance the speciation rate of a lineage or decrease their risk of extinction, relative to other lineages (e.g. in herbivorous insects).

He is then saying that the traits that are the target of this selection are not traits of individuals but traits/properties of the species/lineage.

An example might help to explain the point. For instance, it has been argued that pelagic larvae in sessile ocean species will lead to higher dispersal rates, which means that species can colonize new environments, and this can lead to speciation through adaptive radiation (Jablonski & Hunt, 2006). A larger range will also correspond to lower extinction rates (everything else equal). The trait might also be fixed within a lineage (so there is no variance at the individual level within-species), and if so, this lineage as a whole could have higher speciation rates and lower extinction rates compared to a sister lineage that lacks pelagic larvae.

The individuals within species will naturally have the underlying traits (pelagic larvae), but the traits that are selected at the lineage level (extinction risk & speciation rate) are not properties of individuals but are traits of the lineage/species.

He then ends by continuing with "normal" individual selection, and states that processes at this level is responsible for most adaptive features of organisms. It should also be noted that lineage selection is still considered controversial, and it has been shown that it is inherently much weaker than selection at the individual level. Personally, I think there are some very good examples of how species/lineage selection can function, but to what extent it is an important process for species and organisms is an open empirical question. If you are interested to look further, Jablonski (2008) and Okasha (2007) are two good starting points.


Why are hybrids infertile? Let's take a quote from Wikipedia about zebroids.

  Donkeys are closely related to zebras and both animals belong to the horse family. These zebra donkey hybrids are very rare. In South Africa, they occur where zebras and donkeys are found in proximity to each other. Like mules, however, they are generally genetically unable to breed, due to an odd number of chromosomes disrupting meiosis.

First, if I understand meiosis, the resulting cells don't actually end up with half the number of chromosomes, but closer to a full set of halves of chromosomes. How is the meiotic process disrupted?

Then,

  A donkey has 62 chromosomes; the zebra has between 32 and 46 chromosomes.

Apparently this difference doesn't obstruct producing (infertile) offspring. How comes the process of recombination of such vastly different number of chromosomes in gametes is viable? What happens to chromosomes that don't find their 'pair'?

And then,

  Horses have 64 chromosomes, while most zebroids end up with 54 chromosomes.

54 is an even number. How comes zebroids can't just normally produce fertile offspring with other zebroids of the same number of chromosomes?

A critical step in meiosis is the formation of tetrads. In diploid organisms like donkeys, they have a paternal version and a maternal version of each chromosome. Two chromosomes 2, for instance. During prophase 1, these two "matching" or homologous chromosomes form a tetrad and cross over, swapping alelles. There is no recombination and no tetrad formation in mitosis, which is used for growth and daily living.

  How is the meiotic process disrupted?

In a hybrid, there are no matching maternal and paternal chromosomes. In the zebroid testes or ovary, a lonely donkey chromosome 2 is wandering around, looking for another donkey chromosome 2, and there isn't a homologous chromosome. This mucks up Prophase 1, and the first division pulls crazy numbers of chromosomes to each daughter cell, and the gametes from this division are likely full of extra chromosomes and missing some critical ones.

  Apparently this difference doesn't obstruct producing (infertile) offspring. How comes the process of recombination of such vastly
  different number of chromosomes in gametes is viable?

An embryo needs a solid set of genes to grow up, but chromosomes don't have to be homologous for mitosis, and organisms use mitosis for growth and living, not meiosis. As long as the crazy mis-matched chromosomes in a zebroid have everything needed for a healthy organism, the hybrid will be healthy. It isn't until the zebroid starts to make gametes via meiosis that a problem occurs, as the homologues ONLY form tetrads in making eggs and sperm. The inability to recombine only occurs in the making of gametes.

  54 is an even number. How comes zebroids can't just normally produce
  fertile offspring with other zebroids of the same number of
  chromosomes?

Because even chromosome number doesn't help if they are not each homologous with another chromosome.


Do chromosomes line up as pairs in mitosis or meiosis? Here is a question from the book SAT II Success Biology E/M (where the SAT is the exam taken by the American high school students):

  Homologous chromosomes line up in pairs in
  (A) metaphase of mitosis.
  (B) metaphase I.
  (C) metaphase II.
  (D) interphase.
  (E) prophase of
  mitosis.

In my opinion, we can definitely eliminate D and E since in both mitosis and meiosis, chromosomes line up during the metaphase.
Then, I would choose the answer choice B because as far as I know, after prophase I -- when the chromosomes are in pairs during crossing-over -- the chromosomes are still in pairs and become separated into the different ends of the cell during anaphase. In mitosis and metaphase II, however, they align along the "equator" of the cell, forming a line of single chromosomes.
However, I am confused here because of my book. Here is its explanation for this question:

  The correct answer is (B). In meiosis, the homologous pairs line up as
  individuals in meiosis I in preparation for final segregation in
  meiosis II. Meiosis simply needs to ensure the pairs end up in
  opposite daughter cells in meiosis I. It is in mitosis that the
  homologous pairs line up as pairs, and interphase, of course, is not a
  phase where the chromosomes even appear.

You can see that even though the first line indicates that the answer actually is B, the phrase that's in the cursive contradicts that statement.
I suspect there is a mistake either in the bold or the cursive statement. Could you help me here?

You are correct.  The books explanation is mistaken, and badly written ("the pairs line up as individuals"???)

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

  In metaphase I of meiosis I, the pairs of homologous chromosomes, also
  known as bivalents or tetrads, line up in a random order along the
  metaphase plate.

https://www.khanacademy.org/science/biology/cellular-molecular-biology/meiosis/a/phases-of-meiosis

  So, during metaphase I, homologue pairs—not individual
  chromosomes—line up at the metaphase plate for separation.


Where did the term "vegetative nervous system" come from? I am interested in the origin of the name. I am aware that Reil coined the term in the 1800s, but want to know why did he choose the term vegetative. I have not been able to find an answer to this question. Today it is called the autonomic nervous system.

"Vegetative" doesn't only mean related to plants, but has other less common meanings.

  4 a (1) :  growing or having the power of growing (2) :  of, relating to, or engaged in nutritive and growth functions as contrasted with reproductive functions a vegetative nucleus
  b :  promoting plant growth the vegetative properties of soil
  c :  of, relating to, or involving propagation by nonsexual processes or methods
  Merriam-Webster

So the word "vegetative" refers to the growth/nutrition functions of the autonomic nervous system. The short answer is that he chose that word because, particularly at the time he chose it, that was an appropriate word to use to refer to the regulation of things like digestion. Since the autonomic nervous system has other functions, such as in sexual arousal, and because the term vegetative has other meanings, the term "autonomic" has completely replaced vegetative in this context.


Lab technique to distinguish between single stranded and double stranded DNA? What lab techniques exist to differentiate between single-strand and double-stranded DNA?

Single and double stranded DNA have different electrophoretic mobilities, ssDNA will move faster on an agarose gel, so if you know the length of your DNA and it moves further than you expect
 relative to a dsDNA ladder it's probably ssDNA. The hyperchromic effect means that ssDNA also absorbs more strongly than dsDNA, so you can heat up your DNA and if the absorbance changes it was dsDNA and if it doesnt then its ssDNA (you should take an aliquot for this so that you have the rest of your sample in tact). You could also take an aliquot and add a single stranded exonuclease and run the products on a gel together with the DNA before the digestion, if nothing is present after in the digested well then you had ssDNA if there is still a band after then you had dsDNA (i don't think this method is really used as you could just run it on a gel which is simpler and you lose less sample, but it should still work).


What is the difference between scale vs cataphyll? What is the difference between scale and cataphyll in botany - aren't these the same type of organ?
E.g. do cycad cones have scales or cataphylls? Pine cones have scales, I understand the compound nature of pine cones - does that make them scales?
On fern petioles/stipes there are often scale-like organs I've seen called scales (though they are not very scale-like).

According to "Plant Identification Terminology: An Illustrated Glossary" (Harris & Harris, 2001):
Scale:

Any thin, flat, scarious structure

Note: "Scarious" = Thin, dry, and membranous in texture; not green

Cataphyll:

Brown or colorless scale-like structures believed to be modified leaves

So "scale" is going to be used more broadly, while a "cataphyll" (though scale-like) is more specifically always some type of modified leaf.
According to Wikipedia:

Cataphylls include bracts, bracteoles, and bud scales, as well as any small leaves that resemble scales, which are known as scale leaves.

You can find good illustrations of cataphyll examples here.


What prevents predator overpopulation? I've often heard that a population, human or otherwise, will continue to grow as long as there is food available (assuming nothing else is killing them off).  It makes sense: if you have food you can live, and if nothing is hunting you you'll survive to reproduce.

I recently designed a piece of software to simulate an ecosystem, with groups of creatures of different species eating and hunting and reproducing alongside each other.  It was very simplified (each animal had simple attack/defense/speed/stealth values, etc), but something became rapidly apparent: in every simulation the predators overwhelmed the prey, reproducing until their numbers could not be sustained by the herbivores, and leading to an inevitable die-off of both groups.  I could delay the die-off by adjusting different values and initial population counts, but it would always happen eventually.  The predators would eat and breed and eat and breed until the entire system collapsed.

At first I thought it was just the product of my over-simplified system, but it got me thinking: what prevents predators from overpopulating in real life?

It seems like the natural tendency would be for (for example) the sharks to continue breeding and eating until all the fish are gone, or the wolves to eat all the deer, etc.  Obviously some predators have predators of their own, but that's just putting off the question: if the hyenas don't overpopulate because the lions eat them, then what's keeping the lions from overpopulating?  I can't come up with anything that would prevent the apex predators from growing too numerous, then fighting each other over a dwindling prey population, then dying off entirely when there was no more food to find.

Do predator populations self-regulate to prevent putting undo stress on their prey populations?  Or is there some other mechanism to keep the predator hierarchy from becoming top-heavy?

No, I don't think auto-regulation explain much in the population sizes of predators. Group selection may explain such auto-regulation but I don't think it is of any considerable importance for this discussion.

The short answer is, as @shigeta said

  [predators] tend to starve to death as they are too many!

To have a better understanding of what @shigeta said, you'll be interested in understanding various model of prey-predator or of consumer-resource interactions. For example the famous Lotka-Volterra equations describe the population dynamics of two co-existing species where one is the prey and the other is a predator. Let's first define some variables…

$x$ : Number of preys
$y$ : number of predators
$t$ : time
$\alpha$, $\beta$, $\xi$ and $\gamma$ are parameters describing how one species influence the population size of the other one.

The Lotka-Voltera equations are:

$$\frac{dx}{dt} = x(\alpha - \beta y)$$
$$\frac{dy}{dt} = -y(\gamma - \xi x)$$

You can show that for some parameters the matrix for these equations have a complex eigenvalue meaning that the long term behavior of this system is cyclic (periodic behavior). If you simulate such systems you'll see that the population sizes of the two species fluctuate like this:

where the blue line represents the predators and the red line represents the preys.

Representing the same data in phase space, meaning with the population size of the two species on axes $x$ and $y$ you get:

where the arrows shows the direction toward which the system moves. If the population size of the predators ($y$) reaches 0 (extinction), then $\frac{dx}{dt} = x(\alpha - \beta y)\space$ becomes $\frac{dx}{dt} = x\alpha \space$ (which general solution is $x_t = e^{\alpha t}x_0$) and therefore the populations of preys will grow exponentially. If the population size of preys ($x$) reaches 0 (extinction), then $\frac{dy}{dt} = -y(\gamma - \xi x)\space$ becomes $\frac{dy}{dt} = -y\gamma \space$, and therefore the population of predators will decrease exponentially.

Following this model, your question is actually: Why are the parameters $\alpha$, $\beta$, $\xi$ and $\gamma$ not "set" in a way that predators cause the extinction of preys (and therefore their own extinction)? One might equivalently ask the opposite question? Why don't preys evolve in order to escape predators so that the population of predators crushes?

As showed, you don't need a complex model to allow the co-existence of predators and preys. You could describe your model a bit more accurately in another post and ask why in your model the preys always get extinct. But there are tons of possibilities to render your model more realistic such as adding spatial heterogeneities (places to hide for example as suggested by @AudriusMeškauskas). One can also consider other trophic levels, stochastic effects, varying selection pressure through time (and other types of balancing selection), age, sex or health-specific mortality rate due to predation (e.g. predators may target preferentially young ones or diseased ones), several competing species, etc..

I would also like to talk about other things that might be of interest in your model (two of them need you to allow evolutionary processes in your model):

1) lineage selection: predators that eat too much end up disappearing because they caused their preys to get extinct. This hypothesis has nothing to do with some kind of auto-regulation for the good of species. Of course you'd need several species of predators and preys in your model. This kind of hypothesis are usually considered as very unlikely to have any explanatory power.

2) Life-dinner principle. While the wolf runs for its dinner, the rabbit runs for its life. Therefore, there is higher selection pressure on the rabbits which yield the rabbits to run in average slightly faster than wolves. This evolutionary process protects the rabbits from extinction.

3) You may consider..

more than one species of preys or predators
environmental heterogeneity
partial overlapping of distribution ranges between predators and preys
When one species is absent, the model behave just like an exponential model. You might want to make a model of logistic growth for each species by including $K_x$ and $K_y$ the carrying capacity for each species.
Adding a predator (or parasite) to the predator species of interest

... and you might get very different results.


How fast is the blood flow in various vessels? How fast is the blood flow in different blood vessels, such as the aorta and capillaries?

In the middle cerebral artery blood flow at rest is 73.7 cm/s. After a period of 3 minutes of hyperventilation, blood flow in the same artery decreases to 37.6 cm/s. This is published work.

Vena cava measures: Peak velocities during ventricular systole ranged from 30 to 45 cm/sec in the inferior, and from 10 to 35 cm/sec in the superior, vena cava, also published.


What is the evolutionary advantage of regret? Some motivational speakers may say that regrets are only useful to learn something from.

What are the other advantages?

Very interesting question.

First I'd like to highlight that this question relates to a very hypothetical field of evolutionary biology which is evolutionary psychology. This wikipedia article on evolutionary approaches to depression might be of interest as well. One sentence says: "Feelings of regret associated with depression also cause individuals to reflect and analyze past events in order to determine why they happened and how they could have been prevented". It basically says the same thing than you said in your question.

What other advantages might "regrets" have? Before trying to answer it, I'd like to ask : is it necessary that it has advantages? A behavior or a feeling might as well be a by-product of selection for big brains. It might therefore not be selected for but it exists only because there is not much selection against this by-product trait.

Our brain are often considered to have evolved for social purposes. I would hypothesize that if someone express "regrets", he might benefit from other's care and pity. And the best way to express "regrets" is to feel the "regrets". Robert Trivers would maybe say that in order to fool someone else (make someone else think we regret) the best thing to do is to fool ourself (make ourself feel "regrets"). See his book, the folly of fools.


What is "transcribed strand" This is an excerpt from a paper:

  T>C mutations at NpTpN trinucleotides, also found in hepatocellular carcinomas, shows strong transcriptional strand bias with more T>C mutations on the transcribed than untranscribed strands

What exactly is meant by "transcribed" strand: the sense strand or the template strand ?

I tried looking up for it but couldn't find any definition.

In my opinion they should mean the template strand, and they probably do. Perhaps if we had a link to the paper we could have examined the language more closely.

Here is a paper which uses the term in that sense:

  Mugal, CF et al. (2008) Transcription-Induced Mutational Strand Bias and Its Effect on Substitution Rates in Human Genes. Molecular Biology and Evolution 26,131-142

In the abstract (which I have linked to) the authors make a clear reference to the transcribed strand in contrast to the coding strand (i.e. the strand of DNA with the same sequence as the RNA transcript):

  All three [mutational rates] considered are found to be on average higher on the coding strand and lower on the transcribed strand...

There are also definitions confirming this at this Wikipedia page.


Aneuploidy in meiosis I am quite confused about nondisjuction in anaphase II. If the double chromosome is not segregated, isn't it double. On pictures they are drawn as single but I don't understand why, and if they are double do they duplicate themselves in the S phase?

What is confusing me in picture above is cell (n+1) , why are all chromosomes single? I thought, after end of division in the third cell (labeled as n+1) there should be 3 chromosomes with single chromatid,  and 1 chromosome with 2 chromatid joined at centromeric region, as it is drawn in picture above that show nondisjunction in cell during anaphase ii . When and how do these 2 chromatids get physically separated?

From Study.com >>

On the off chance that nondisjunction happens amid anaphase II of meiosis II, it implies that no less than one set of sister chromatids did not isolate.

In this situation, two cells will have the typical haploid number of chromosomes. Additionally, one cell will have an additional chromosome (n + 1) and one will miss a chromosome (n - 1) due to the nondisjunction of the chromosomes.

Here is a picture reference taken from Google.ca >>

In the image provided in the question, the chromosomes are not indicated clear and concisely, so it is very hard to follow through the logic of segregation of the daughter cells to (n + 1) and (n - 1) chromosomes.

As you can see from the updated image reference in the answer, we can notice that the cell that underwent nondisjunction in anaphase 2 gives rise to 2 daughter cells, in which, one cell receives the non-segregated chromosome plus one copy of a sister chromatid which makes it (n + 1) and the other daughter cell receives one segregated sister chromatid ONLY which makes it (n - 1).

On an additional note, from Biology Exams 4 U >>

  Fusion of n+1 gamete with normal gamete (n) = 2n + 1 or Trisomic.

  Fusion of n-1 gamete with normal gamete (n) = 2n - 1 or Monosomic.

  In short, Nondisjuntion in meiosis II leads to trisomy (2n+1) or
  Monosomy (2n-1).


Health benefits & enzymes different between Thermophilic and Mesophilic Probiotic cultures? Is there a difference between the Enzymes produced by Thermophilic vs Mesophilic Probiotic cultures ? are there any other differences in health benefits between the two types of cultures ?

Thermophilic and mesophilic enzymes differ in the optimal working temperature, due to a structural adaptation: thermophilic enzymes have more stiff surface-exposed loops than their mesophilic orthologs. Human is mesophile, which means that mesophilic enzymes, no matter whether human or bacterial, will work in human more efficiently.

Bjelic, Brandsdal, and Aqvist (2008) Cold adaptation of enzyme reaction rates. Biochemistry 47: 10049-10057; emphasis mine:

  [P]sychrophilic, mesophilic, and hyperthermophilic citrate synthases
  ... have increasingly stronger electrostatic stabilization of the
  transition state, while the energetic penalty in terms of internal
  protein interactions follows the reverse order with the cold-adapted
  enzyme having the most favorable energy term. The lower activation
  enthalpy and more negative activation entropy observed for
  cold-adapted enzymes are found to be associated with a decreased
  protein stiffness. The origin of this effect is, however, not
  localized to the active site but to other regions of the protein
  structure.

https://www.ncbi.nlm.nih.gov/pubmed/18759500

Aqvist (2017) Cold adaptation of triosephosphate isomerase. Biochemistry 56: 4169-4176; emphasis mine:

  The results show that the enzyme from the psychrophilic bacterium
  Vibrio marinus indeed displays the characteristic shift in
  enthalpy-entropy balance, compared to that of the yeast ortholog. The
  origin of this effect is found to be located in a few surface-exposed
  protein loops that show differential mobilities in the two enzymes.
  Key mutations render these loops more mobile in the cold-adapted
  triosephosphate isomerase, which explains both the reduced activation
  enthalpy contribution from the protein surface and the lower
  thermostability.

https://www.ncbi.nlm.nih.gov/pubmed/28731682


Are there any DNA viruses with junk DNA in them? I know mimiviruses and pandoraviruses have orphan DNA - DNA that is not found in other species - but this is DNA that codes for proteins. I am not able to find out if they contain junk DNA. By junk I mean DNA that does not have ANY function at all. Sort of like the junk DNA in the human genome put there by retroviruses, DNA that just sits there, doing nothing, just going along for the ride.

Viruses typically don't have junk DNA-so to speak because of their tiny size. When the particles (of virus) are so small, there really isn't any space for "junk" or extra DNA.
That being said, while viral DNA replication, there may be some errors that may make the virus DNA unable to code for proteins or "junk". While this is an interesting proposition, the mutations that occur in almost cases do not make non functional proteins but mutated proteins which make the viruses more virulent (more true in case of RNA viruses...which mutate a lot faster).
Regarding virus infecting virus, putting its own code it "kind of happens" but not as you would expect. I am listing 2 such examples here-

There are some viruses called satellite viruses and viroids which depend on "donor" larger viruses for some of the proteins they need for replication. This means a satellite virus can survive in a host only if the donor virus is present.

In animals like pigs, when different strains of Influenza virus infect together, while virus assembly genetic material (RNA) of one strain can enter into the other....creating completely novel strain.

Hope that answers your question. Please feel free to ask for clarification. Thank you and have a nice day.


What gaseous substances do humans emit? Other than CO₂ and Methane what other gases do humans produce or emit?
For example, does  skin decomposition, or aerobic respiration emit any special gases that people don't normally realize or know about.
I ask because of a discovery I made during research is that while being poisonous to the central nervous system, methanol is a natural endogenous compound found in normal, healthy human individuals.
One study found a mean of 4.5 ppm in the exhaled breath of the subjects. https://iopscience.iop.org/article/10.1088/0967-3334/27/7/007

The gases NO, H₂S, CO even have a function in the human body!

Nitric oxide is produced in endothel and neurons as messenger, and in macrophages as cause of nitrosative stress for imprisoned bacteria. Hydrogen sulfide is produced in cysteine catabolism and functions as messenger (only recently discovered). Carbon monoxide appears to act as messenger, too.

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

http://en.wikipedia.org/wiki/Hydrogen_sulfide#Function_in_the_body

Wu, L; Wang, R (December 2005). "Carbon Monoxide: Endogenous Production, Physiological Functions, and Pharmacological Applications". Pharmacol Rev 57 (4): 585–630. doi:10.1124/pr.57.4.3. PMID 16382109


Are rods/cones rejuvenated periodically? Pretty much what the title states.

Some cells/structures in the human body undergo rejuvenation periodically by flushing away older cells and growth of new ones.
E.g Skin, Blood

Does this (for want of a better word) 'rejuvenation' apply to Rods/Cones within the eye too? If so, how are the old cells flushed out - or do the old cells become part of the local humour?

The answer can be found in the excellent lecture from 1983 The Life History of Retinal Cells which also has gorgeous microscope fotos. The renewal time of rod outer membrane proteins is less than two weeks. Cells stay indefinitely, as I understand, but are periodically rebuilt in a logistical nightmare/wonder.


Non-nucleated cell-like population with RNA We're working on invertebrate hemolymph (blood) and we have found with flow cytometry (staining with DRAQ5) a cell-like population without nucleus but it has RNA production.

Does anyone any experience with something similar? May anyone recommend any publication with something like that?

More information:

1) We don't know the real population size because we have identified it by flow cytometry, future experiments we wish to use TEM to characterize it better.

2) We know that this "population" produces RNA because we have extracted total RNA using low input RNA kit and run the result in Bioanalyzer.

3) We "know"/suspected this population doesn't have cell-nucleus because DRAQ5 is a DNA staining and this population is DRAQ5-. We wish study that by confocal microscopy ASAP.

Maybe you are seeing extracellular vesicles1?

At least might be worth checking out since extracellular vesicles containing RNA have been reported within the hemolymph of mosquitos2.

References:
1: Van der Pol, E., Böing, A. N., Harrison, P., Sturk, A., & Nieuwland, R. (2012). Classification, functions, and clinical relevance of extracellular vesicles. Pharmacological reviews, 64(3), 676-705.
2: Severo, M. S., Landry, J. J., Lindquist, R. L., Goosmann, C., Brinkmann, V., Collier, P., ... & Levashina, E. A. (2018). Unbiased classification of mosquito blood cells by single-cell genomics and high-content imaging. Proceedings of the National Academy of Sciences, 115(32), E7568-E7577.


Is the genetic term "polycistronic" still used in modern biology? Is the term "cistronic", meaning an ORF on a mRNA, still commonly used in modern genetics? I´ve seen "polycistronic" being applied to prokaryotic mRNA in old textbooks, but I´ve rarely stumbled upon this in recent papers, except for research focusing on plasmid engineering.

Yes, it's still used.

If you search Pubmed for "polycistronic", it offers you a chart showing the counts of the term by year (top right). Downloading the CSV and making a chart shows that it's never been a very common term, but it's still used. I suspect, but don't have time to check, that if you were to divide the use of the term by the number of published papers by year its use-per-paper would be pretty much a flat line.

Edit, re-reading the question, it may be about "cistronic" as opposed to "polycistronic". "Cistronic" is also still used, but not nearly as often as "polycistronic" -- 13 times in 2018 to "polycistronic's" 81.


Phylogeny: Hybridization between different species sharing same genus? I am doing a cross-breeding project with Capsicum chinense x Capsicum baccatum. I'm planning to breed them until 6-8 gen.

My question: What will the completed breed be classified as? Would it be a new species or will it be considered as a strain of chinense or baccatum? Thanks.

Hybrids are not considered named species of either of their progenitors, but classified as hybrids of both. So they would be called Capsicum chinense x baccatum.


Question about different gametes that can be produced I have a question from a past exam that asks the following:

"For the organism of genotype AABbCcDDEe (homozygous for 2 genes, heterozygous for 3 genes), how many different types of gametes will be made if the C gene and the E gene are linked on the same chromosome while the remaining genes are all on different chromosomes?"

However, I have no answer key, and these answers are the choices:

A. 2

B. 3

C. 4

D. 8

E. 9

Here's my approach to the question:

We have 5 traits, and each trait consists of 2 alleles. To make functional gametes, each gamete must receive one of each allele so that it can survive. Clearly, for AA and DD, there's only one choice: A, and D.

However, for Bb, Cc, and Ee, things are a little different.

C and E are linked on the same chromosome. c and e are on different chromosomes. Therefore, a gamete can have either CE, or c and e. Similarly, a gamete can have either B or b.

Therefore, shouldn't we be able to create 4 different types of gametes?:

ABCDE, ABcDe, AbCDE, AbcDe

So wouldn't the answer be C. 4?

Please show me any mistakes I might be making, or any gaps in my understanding. This would be very much appreciated.

Thank you!

You are correct

Assuming that by linked, the question assumes perfect linkage (no cross-over ever happen), then your answer is correct! Good job!

Comments

Here are a few comments though...

  We have 5 traits, and each trait consists of 2 alleles.

There are 5 loci. A locus does not necessarily match to a single trait and a single trait does not necessarily match to a single locus. Actually, it is very very rarely (if ever) the case.

  To make functional gametes, each gamete must receive one of each allele so that it can survive.

This is not necessarily true. A "normal meiosis" (not leading to variation in copy number) may create a non-viable genotype and a "abnormal meiosis" (leading to variation in copy number) may create a viable genotype. But, it is true that we will only assume "normal meiosis" for this answer.


What are these shrimp-like insects in my cat's water bowl that appear overnight Our family has 2 cats and a dog.  We keep food and water bowls outside for them.  We clean and refill the water bowls every day.  Almost every morning, the water bowl is teeming with small aquatic insects of some kind, which look and act like little shrimp.  I would guess them to be 5 to 8 mm in length, on average.

What are these, and where are they coming from?  They appear to be aquatic, since they survive and swim in the water for hours -- but how do they get there?

We live in central Florida, USA.

They are probably some species of amphipod.

According to that link, two species common to Florida are Talitroides topitotum and Talitroides allaudi, though there are dozens of species in the US alone. In some areas, amphipods may be known commonly as "scuds."

These guys like to live in fairly wet places, depending on species - on the beach, in decomposing mulch/leaf litter/grass. They seem to be finicky with moisture: they tend to seek drier areas when it rains, often bringing them onto sidewalks or indoors, then they get dry and look for moisture. I'm guessing this is how they end up in your cat bowl: you certainly are not the first one to observe this.

https://www.whatsthatbug.com/2004/11/10/lawn-shrimp-3/

I'm not sure at all about the precise species...the species most commonly encountered by people on the sidewalks and such don't seem like they would survive long truly immersed in water since they avoid rain, but I wasn't able to find anything definitive on that - maybe their behavior is to avoid very wet but they can still survive immersed for awhile.


Do we have fundamental conflict in biology? As saying "fundamental conflict", I mean something like two (or more) widely accepted results from different areas (or scales) can not exist logically together. In physics, there have been three conflicts1. I wonder if in biology, do we have such conflicts? And how biologists resolved that?

1  One of them is the conflict between Einstein's general relativism and quantum mechanics. String theory, if it is proved to be true, will reconcile this (read more). But it can also be like the controversy of the property of light. Some said it was particle, some said it was wave. Modern physics says it is both.

Peto's Paradox is a great one. This addresses the disconnect in cancer incidence with cell number in an organism. It goes something like this:

Assume current oncogenesis theory to be correct in that mutation acquisition is the rate limiting step in creating a cancer, such that you need ~5 specific mutations in a single cell for that cell to be fully transformed into a cancerous cell. This then being the case, it is so rare that any cell can acquire all necessary mutations that in humans we don't see cancer incidence appreciably increase until the 5th decade of life.

Now, let's assume man has an average weight of 50kg and a blue whale has an average weight of 130000kg, with roughly equivalent lifespans. Assuming average cell weights are the same in both organisms, there are 2500X more cells in a blue whale than a human.

If linear mutation rate is the rate limiting step in cancer then increasing cell numbers is akin to increasing the number of times you flip a coin to try and get heads, which means there is a 2500X greater chance of getting all ~5 necessary mutations in a single blue whale cell than in a single human cell. If human cancer incidence starts to spike at 50 years, this means blue whale cancer incidence should spike after 7 days and blue whales should largely be eliminated by cancers within the first month of life.

Hopefully makes you question a bit what is causing cancer.
Make sense?


Are there any proteins assembled from non-adjacent parts of the genome? Many proteins are assembled from multiple exons with the introns between adjacent exons being spliced out. But are there any proteins that have unrelated to them exons in the middle of their sequence?

I think the equivalent question would be: are there any protein-coding genes (in any species) that are broken in two or more parts by another protein-coding gene(s)?

I think that you are talking about trans-splicing. This does indeed happen. It is fairly common in protist organisms, though in humans it is quite rare. For more information about how this process works, including mechanisms in vertebrate organisms, see this paper.

Here is one model from that last paper for how it works:


Are there specific conditions that allow humans to see ultraviolet wavelengths It is fairly common knowledge that the lens in its normal state absorbs ultraviolet (UV) radiation.  An interesting notion has come up from time to time in my reading that suggests there are a small number of conditions that result in humans being able to 'see' ultraviolet.

What conditions may cause this?  Also, those affected, would they 'see' it has a different shade of violet?

You will be interested in Aphakia, which is the lack of an eye lens usually through surgery but sometimes from birth.  These individuals supposedly see UV as a whitish-blue or whitish-violet:

  This appears to be because the three types of colour receptor (red, green and blue) have similar sensitivity to ultraviolet, so it comes out as a mixture of all three - basically white, but slightly blue because the blue sensors are somewhat better at picking up UV.1


Unwanted E. coli product in plasmid product Using a TOPO XL Cloning kit, our lab took some amplified human DNA, inserted it into the vector, and attempted to clone it in E. coli. However, upon sequencing the purified plasmid product, the sequence we got back was E. coli rather the human we had amplified. The primers sat down in the plasmid as intended, just the sequence between the primers appears to be from E. coli (as implied by BLASTing it against a human, getting no results, and then blasting it against E. coli and getting a hit).

The root cause turned out to be a lying spec. Using a different one, it was revealed that there was next to no template DNA in the initial amplification. No DNA, no good plasmids.


is ventricular depolarisation same as depolarisation during nerve impulse conduction? Does the change in membrane charge accumulation occur in a similar way in heart and nerves cells?

Depolarisation of nerve (here Purkinje fibres) causes Action Potential (bcoz of opening of voltage gated Na channels) which causes opening of Ca++ channels in membrane of heart muscle- results in ventricular contraction
So ventricular depolarisation is actually action potential in heart muscle of ventricles
So both terms are related
Ventricular depolarisation is a consequence of nerve impulse(depolarisation of nerve here Purkinje fibres )
Thnks
Ps: read bracket portion separately


Can plants suffer from CO2 poisoning? Is there a point where too much CO2 is bad for a plant? Basically when there is too much CO2 in the air can a plant get sick?

Since plants photosynthesize and need CO2 to generate glucose and store starch, and since chemical reactions are pushed toward their end product when the reagent concentrations are increased, one would expect that more CO2 would be better, at least lead to increased growth and survival rates.

Is there a ceiling where CO2 gets toxic?

Short answer
It has been shown that plants may already suffer from doubling the atmospheric CO2 concentration from 340 to 610 ppm, something that might happen during the next hundred years or so based on current emissions.

Background
A popular science website tells us that an excess of carbon dioxide (CO2) reduces the rate of transpiration of some plants. This is so because the stomata, which are the openings of the leaves (Mansfield & Majernik, 1970) and used for exchanging gases as well as water vapor (transpiration) will close when there is too much CO2 in the air, or other polutants such as SO2. As transpiration drops, the water flow from the soil to the leaves also drops, causing a runoff of water.This in turn stalls nutrient uptake. Indeed, doubling the present-day CO2 concentration to 610 ppm does not necessarily lead to increased growth and may in fact inhibit growth due to excess starch formation in the leaves, indicating it's simply stored as backup energy, nothing else (Coviella & Trumble, 1999). It is believed that plants might be near their saturation point and cannot eliminate CO2 faster than they are doing right now.

Somehow plants also become more susceptible to insect foraging when CO2 concentration increases.

Note however, that CO2 tolerances are species dependent. Most research in this arena has focused on common crops. CO2 tolerance in for example cotton plants is low, and starch buildup has been observed in the entire plant, but especially in the root systems and the stem (Hendrix et al., 1994). Other species, such as wheat and rice are less prone to effects of elevated CO2 (source: Nature).

References
- Coviella & Trumble,  Conservation Biology (1999); 13(4): 700–12
- Hendrix et al., Agricult Forest Meteorol (18994); 70(1–4): 153-62
- Mansfield & Majernik, Environmental Pollution (1970); 1(2): 149-54

Source
- Earth untouched


Does a mutation in the sense strand of a particular gene affect the polypeptide formed? Recently, I came across this picture which represents the DNA sense strand of a gene.

The ‘Altered’ picture shows a (frameshift) mutation in the nucleotide sequence in which a T base is deleted.

The sense strand is not transcribed — the anti-sense strand is transcribed. So why is there a change in the amino acids of the translation product when a mutation occurs in the sense strand, if the sense strand does not produce amino acids? Does a mutation in the sense strand change the nucleotide sequence of the transcribed sense strand?

We’re doing it for the children!

The basic misconception in this question is that the important effects of mutations are seen in the cell that undergoes mutation. This is not the case. So focusing on the whether the strand that receives a mutation is the non-transcribed, sense, strand or the transcribed (anti-sense) strand is of little relevance.

  What is important is whether or not the mutation is passed on to the progeny.

Don’t we have a life too?

Why isn’t it important? Consider a mutation occurring in a single E. coli cell in a population of millions of E. coli, or a single muscle cell in a human muscle. Even if there is a mutation in the strand that is transcribed into mRNA and translated into protein, the change in that one cell will not have a significant effect on the overall population.

The birds and the bees

The way in which a mutation — on sense or anti-sense strand — can affect a population of bacterial cells or whole tissue in an organism is:

(For bacteria or in tumour cells) if the mutation is passed on to some of progeny, which then have a selective advantage so that they can outgrow the wild-type population
(For normal tissues in animals) if the mutation is passed on to the progeny through the germ line so that it is present in all (e.g. muscle) cells

Still harking on about sex (Yawn)

The key point is easier to explain with bacteria. Consider a simplistic situation in which a mutation occurs on one strand (and is not corrected by the DNA-repair mechanisms). Before the cells divide into two daughter cells the double-stranded DNA replicates — each strand is the template for a complementary strand in a daughter double-stranded DNA. One cell will have the daughter dsDNA (double-stranded DNA) copied from the unmutated strand and the other will have the daughter dsDNA copied from the mutated strand.

  In the case of the dsDNA copied from the mutated strand, both
  strands will clearly carry the mutation, so it is irrelevant whether
  the mutated strand in the parent was sense or anti-sense.

If the mutation is advantageous these cells will grow and divide and out-compete the other bacteria in the population.

A similar explanation holds for tumour cells in a differentiated animal tissue.

In the case of germ-line cells in animal tissues the situation is slightly different — the mutation either will be present or absent in both strands of the dsDNA in the fertilized egg, and so will affect all of the cells in the tissues of the progeny in which it is expressed.


Why isolated, recombinant plasmid DNA without any restriction is often detected in agarose gel electrophoresis as three DNA bands? I don't understand why three bands are found without any restriction digest. Please answer me as soon as possible.

These are the three forms of the plasmid: supercoiled (smallest 3D-structure, runs fastest), linear (runs in the middle) and relaxed, nicked plasmid (runs highest). You can have another fourth band, which is the circular single stranded plasmid (runs faster than the supercoiled version). See the following figure (from this article, which I recommend reading):


PTMs of proteins via mass spec? I understand that mass spec is widely used to study PTMs like glycosylation of proteins, but how can mass spec determine correct PTM structure of say glycosylation if two glycan structures have the same mass but different arrangement (i.e. isobaric)? Also, how can mass spec determine the difference between structural isomers?

I am not a MassSpec expert but this is what I understand from my spectroscopy basics:

In tandem MS (MS-MS), the ionized analyte generally undergoes or made to undergo fragmentation (breaking up into smaller ions). Fragmentation allows you to study finer details. It is also essential for de-novo peptide sequencing. Different fragmentation techniques, such as Collision Induced Dissociation (CID) or Photofragmentation, yield different kinds of secondary ions.

You can intuitively understand that Fragmentation of structural isomers will yield different kinds of secondary ions (using the same fragmentation technique). The choice of fragmentation technique depends on the molecular nature of the analyte. In the article that I mentioned previously, they use laser induced photofragmentation to dissociate glycan-ions.

Even small molecules, which had been classically studied by MassSpec, undergo isomerization after ionization in order to stabilize the ion. Reactions such as reverse-Diels-Adler can also happen. The pattern of reactions would differ between structural isomers. For basics you can refer to a book on Spectroscopic techniques by Silverstein


What is the most basic organism to respond to Classical conditioning (capable of learning)? I have been doing some reading of Classical conditioning which is considered to be an indication of animal's ability to learn...

Before this I considered insects to be machine like - devoid of any sort of 'thinking' just doing things that evolution 'made' them to do to survive...

However I have found that cockroaches and even fruit flies could be conditionally trained...

Which made me wonder What would be the least complex species that respond to classical conditioning?

I have also read this question about single-celled organisms capable of learning and I don't think that this 'cuts it'... this is nothing more than chemical response... however classical conditioning is different and in my opinion certainly does indicate ability to learn...

Very simple nervous systems are capable of learning  C. elegans, with only 302 neurons, is reportedly capable of both learning and memory.  There is a fairly large literature on the subject, as C. elegans is a popular research subject - a Google Scholar search gives about 40K hits, e.g. http://learnmem.cshlp.org/content/17/4/191.long

We have to remember that small is not necessarily primitive: the C. elegans nervous system (like every other one in existence today) has been optimized by millions of generations of evolution to do what C. elegans needs in order to survive.

Actual evidence of learning in nervous systems in the distant past is rare.  It's behavior, and behavior doesn't fossilize well :-)  Actual nervous systems apparently don't fossilize all that well, either.  The earliest well-preserved example I could find was this http://www.cam.ac.uk/research/news/520-million-year-old-fossilised-nervous-system-is-most-detailed-example-yet-found from 520 million years ago.  But since learning would give a creature a survival advantage, I'd guess that it evolved fairly early.


What is the biological advantage of bilaterity? I was wondering why there were so many bilateral species (under the bilateria clade) in comparison with the cnidaria clade. I have two or so questions:

Am I (or are we) unaware of the diversity and population of the cnidaria clade, so I can't say that bilaterity seems to be prefered by the natural selection?
Is bilaterity an advantage only on earth and not in water (where I think most of the cnidaria clade is (jellyfishes)).
If the answer to the last question is true, why is bilaterity an advantage on earth and less an advantage in water, and why is the contrary true for "unilaterality" (I don't know what is the word to describes the cnidaria clade).

Thanks!

Bilateria, as a clade (all animals, excluding sponges, cnidaria, comb-jellies, and placozoans) is monophyletic, and as such, originated from a single species that was bilaterally symmetrical. Sometimes the explanation for a particular trait involves ancestry, and if an innovation is advantageous, it tends to spread. Along with this group came advances in the central nervous system, and digestive systems. It is advantageous to put senses up front, in the head, with the mouth. Having a tube-like digestive system, with a mouth at one end, a gut in the middle, and an anus at the other end, turned out to be efficient. Cnidaria (and other non-bilaterians) are not nearly as diverse as bilaterians, and most bilaterians are marine. So the bilateral advantage holds both in water, and on land.