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Biological meaning of Lotka-Volterra Jacobian matrices
In a book about community ecology, I learned about Lotka-Volterra models and dynamic food web models (I am not an ecologist in the first place).
In one of the chapters, a Jacobian matrix of partial derivatives of the Lotka-Volterra model at equilibrium densities is given:
\begin{bmatrix}-&-&0&0\\+&0&-&0\\0&+&0&-\\0&0&+&0\end{bmatrix}
where + and – represent positive or negative values.
This matrix is later interpreted in terms of direction of trophic links in a food web, but the reasoning allowing to jump form one to the other is not detailed.
So what is the biological meaning of these values?

The Jacobian tells how the system changes along different state variables (which can be, for instance, the concentrations of the predator and the prey).
The Jacobian matrix by itself doesn't give you a lot of intuitive information. However, the eigenvalues of the Jacobian matrix at the equilibrium point tell you the nature of the steady state. For example if all the eigenvalues are negative then the system is stable at that point and the equilibrium point is called a stable node. If some of them are positive and some are negative then the system is metastable at that point and the point is called a saddle point. If all eigenvalues are positive then the point is unstable. If the eigenvalues have an imaginary part then the system exhibits oscillations. All these properties are local i.e. they just tell you the behaviour of the system near the equilibrium point.
I hope I am clear. This is not in a strict sense, a biological question. If you want to know more then read a book on nonlinear dynamics. Non-linear dynamics and Chaos by Steven Strogatz is a good place to start.

EDIT
When the system is locally linear (linearized at a given point) then the system dynamics at that point can be described as
$$\frac{dx}{dt}=J.x$$
Where $x$ is the state vector (a vector of the variables in the system) and $J$ is the Jacobian matrix. In this situation, the signs will denote the effect of a variable on the other variable. However, I am not sure (I feel it is highly unlikely) if this can be used to make any inferences about the food web.

Then I really don't understand how negative and positive values are expressed in terms of link directions in the food web, at least according to this book...

@KermittDuss I made some additions. Please check the answer.

Loop Analysis is an approach for taking a signed digraph to qualitatively understand dynamics of a community/food web. See this website, the book chapter on Loop Analysis behind a paywall, or a very succinct description (ssec 2.2).

The matrix above depicts the signs of the partial change of a function with respect to each species. Because there are 4 rows and columns, this means there are 4 species. Each row represents a partial change in each of the 4 differential equations representing the rates of change for each species with respect to each species, which is each column. To rewrite the Jacobian for species 1–4 ($N_1, N_2, N_3, N_4)$:
$$\mathbf{J} = \left[\begin{smallmatrix}
\frac{\partial F_1}{\partial N_1} & \frac{\partial F_1}{\partial N_2} & \frac{\partial F_1}{\partial N_3} &\frac{\partial F_1}{\partial N_4} \\
\frac{\partial F_2}{\partial N_1} & \frac{\partial F_2}{\partial N_2} & \frac{\partial F_2}{\partial N_3} &\frac{\partial F_2}{\partial N_4} \\
\frac{\partial F_3}{\partial N_1} & \frac{\partial F_3}{\partial N_2} & \frac{\partial F_3}{\partial N_3} &\frac{\partial F_3}{\partial N_4} \\
\frac{\partial F_4}{\partial N_1} & \frac{\partial F_4}{\partial N_2} & \frac{\partial F_4}{\partial N_3} &\frac{\partial F_4}{\partial N_4} \\
\end{smallmatrix}\right]
$$
The signs above correspond the effect of species on each other's rates of change. For a first example, the first row and column is effect of species 1 on its own rate of change. It's negative, meaning that it's rate of change decreases with increasing density (crowding). A second example is the first row and second column—species 2 has a negative effect on the growth of species 1. In a food web context, this means that species 2 consumes species 1. A third example is the first row and third column—there is no effect of species 3 on species 1. Lastly, the second row and first column has a positive sign, meaning that species 1 has a positive effect on the growth rate of species two. In a food web context, that means that species 2 consumes species 1.
Notice that in food webs, for each positive effect, there is a corresponding negative effect and vice versa (i.e., species grow from eating another species, and species shrink from being eaten).
In sum, (1) species 1 is the only species who is affecting by crowding, (2) species 1 is consumed by species 2, (3) species 2 is consumed by species 3, (4) species 3 is consumed by species 4, and (5) no other species interact.


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My BRIG run is suspiciously quick. What is a typical length of time for a run?
I use the BRIG (BLAST Ring Image Generator) program to compare prokaryote genomes. It executes a local BLAST+ and visualizes the results as rings around the reference genome. I downloaded three genomes (~5 million to ~5.5 million base pairs long) from the NCBI to test the application with. It only took 5 to 10 minutes for BRIG to finish. In my personal experience, BLAST is never that fast. Certainly not while comparing entire genomes. I'm also quite sure my computer is not thát fast and changing BLAST parameters doesn't do much difference. The output appears to be good however.
Is my input just small, is my PC better than I know or is it something I'm not aware of?
What would be  a typical time for a run of that magnitude?

Sources:
Website BRIG
Genomes used:

Accession: BA000007.2 GI: 47118301
Accession: AE006468.2 GI: 973795115
Accession: AL513382.1 GI: 30407157

If the output looks correct and there are no errors then it could be perfectly fine. The web versions can take a lot longer because the servers are receiving so many queries.

@James That makes sense. I just got this weird feeling that something, somewhere is not right. This speed doesn't correspond with my own experience at all. I'm used to BLAST runs that take hours and even days while using grid computing. With this input I expected a run-time of at least a couple of hours because I don't have my grid anymore

source: Stack Exchange

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sort: votes


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How do tea, coffee, and beer dehydrate you?
For the long time I am trying to find out if the following is truth: They say that some beverages dehydrates. I heard that about tea (sometimes green, sometimes black, sometimes both), coffee, beer and more (for example coke).
How does hydration from these sorts of drinks compare to others (e.g. water)? Why do these drinks less efficiently hydrate?

Diuretics
These drinks contain minor diuretics. Caffeine is the diuretic found in tea and coffee. Alcohol is the diuretic in beer. Diuretic substances increase the amount of urine produced i.e causes dehydration. This is often offset by the water content of mild diuretics like tea, coffee, and alcoholic drinks.
Tea, coffee, and coke
Caffeine belongs to the xanthines, and inhibits re-absorption of Na+ by cells, and increases flow rate of filtered fluid through the kidneys. This reduces water content in your body. In other words diuretics do dehydrate you, specifically caffeine will. Coffee, coke, and tea (very low doses of caffeine) are mild diuretics.
Beer
On the other hand alcohol is an anti-diuretic hormone inhibitor that inhibits arginine vasopressin.

OK, thanks. I wonder if the benefit from amount of fluid we get from them is bigger or smaller then the handicap of dehydration.In other words it is worth to dink them if we want to have a good drinking regime?

@TedGar That's a great separate question I guess!

As a quick guess: there isn't enough caffeine in a mug of tea to dehydrate you in any noticeable way, you would have heart complications if all you drank was coffee, and the alcohol would wipe out your liver. But I imagine there is still enough liquid retained to hydrate you, but you would be drinking much more than the equivalent water.

Thank you, it seems logically. And I'll try open a new question, who knows…

There's some data to show moderate caffeine intake doesn't necessarily dehydrate you, but the parameters are undoubtedly obscured by what you're doing, and what you're drinking. In terms of alcohol, i believe it was approx 10mL urinated for every 1g ethanol, though i cant substantiate that claim with a source.

New question: http://biology.stackexchange.com/questions/28098/dehydration-from-caffeine-alcohol-and-other

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Where can I find mutation datasets for cancer?
My lab has been using TCGA data (somatic mutations and clinical data) to develop panels of genes and of mutations we expect to see in certain cancer populations. We'd like to validate our panels by checking how they hold up against other cancer datasets.
I know that one resource we can use is the International Cancer Genome Consortium but I'm wondering if members of this forum can suggest a few other places we can get both clinical and somatic mutations data for cohorts of cancer patients.

As I'm sure you're aware, there is no complete centralised database for cancer gene mutations. The most comprehensive database is the TGCA as you've already mentioned. That doesn't mean that other data isn't out there.
A broad option that might fit your needs is to query OMIM hosted by NCBI. You can search "cancer" or something more specific and then select the dbSNP tab and it will return a list of gene locations of mutations that match the query.

For a more specific search, COSMIC hosted by SANGER allows downloads of the "cancer genes" in fasta format, and various other downloads with other information are available. It's manually curated which is always a bonus, however this does mean that it's limited to just a few genes. There is also BIC. This is specifically focussed on genes related to breast cancer and is hosted by NHGRI. Again, an account is required for the download and it is limited to genes affecting breast cancers.

The cBioPortal is an extraordinarily useful centralized source of cancer datasets. As of this date, it contains data from 105 cancer genomics studies. Many of these are TCGA studies, but the list includes many others as well. Furthermore, the human interface to the data is among the best I've seen.

That's a really neat portal I was unaware of, and I'll certainly have to edit my answer now! But since the question needs a comparison dataset against TGCA, what is the use of more TGCA data?

@James : many of the studies listed there are not TCGA. In my field of head and neck cancer, there are 2 (partially overlapping) TCGA data sets and 4 other data sets. The balance differs among cancer types. The TCGA data sets, of course, are typically the largest.


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Why do horses recycle their endometrial lining while humans don't?
How does not recycling the endometrial lining of the uterus benefit humans (and other organisms that menstruate), while recycling it is beneficial to horses (and other organisms that undergo estrus cycle)?
So the question linked by user137 gave me some useful points to work from. Bear with me though, because I learned alot of new jargon just by reading it.
Helps immunity:

"forces loose not only the endometrial lining but sperm-borne pathogens contained therein."
"menstruation delivers immune cells to the uterine cavity, triggered by the mechanical pressure exerted via the shedding of endometrial lining."

Energy efficient:

its simply more energy efficient to shed. saving 6 days worth of food per 4 cycles.
for individuals/species with high fecundability shedding of the lining is less useful
larger uterus = increased likelihood of menstrual shedding (from the answer I learned humans have a larger uterus -- relative to body size -- compared with other mammals who don't shed.)

Miscarriage discardation?:
the comment section also had an interesting reason saying that sloughing off the lining regularly helps get rid of dead embryos.
All of this is very useful and interesting but I'm still confused as to why horses don't shed. I would think horses have low fecundability since their awkward bodies would make it hard to mate. And if shedding the lining is more energy conservant, then why don't horses? I want to know why it is evolutionarily better for horses to fully reabsorb, compared to humans?

What do you mean with help?

I don't have the source right now, but human women do reabsorb much of their uterine lining during menstruation. However, there is so much of it, and the duration of menstruation is so short, that it can't all be reabsorbed in time, so it leaks out instead. EDIT: here is a related question that might be more informative.

@JordiZambrino When I say help im assuming its better for human females to do it this way and i'm wondering why.

@user137 thanks but that source doesnt say anything about humans reabsorbing their lining . at least nothing that I could find. it really useful though thankyou

Horses do not undergo menstrual cycle; they have estrus.


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How likely is it that a person's progeny has an inheritable disorder based on this pedigree?
Case study:
A person (let's just call him "John") had 3 aunts that died back in the 1950's in early childhood due to an unknown form of neuromuscular disorder. One died at birth, one at 2 years and one at 3 years. John's father was the only surviving descendent of John's grandparents. John and his brother do not show any symptoms. John's brother has a daughter who shows no symptoms. John has two sons, one does not show any symptoms and his other son is a 4 month old who is exhibiting signs of some sort of neuromuscular problem.
John has provided me with a pedigree that he believes is correct (note, the ones with the blue square are the ones that exhibit the symptoms):

I took a bit of genetics in university, but basically I am just trying to understand the genetics here. These are my assumptions. Please correct me if any are wrong:

Since the disorder appears to prevent developing past childhood it must be autosomal recessive because everyone who exhibits symptoms is not be able to reproduce due to their early death.
Both of John's grandparents must have been carriers.
The probability of John's dad and any aunts and uncles having the disorder is 25%, and the probability of being a carrier is 50%. The 3 aunts who died must have just lucked out.
John, his dad, and his wife must all be carriers of the disorder.

However I really feel like I'm wrong about these assumptions since the math really doesn't add up. The likelihood that so many carriers for a relatively rare disorder all coming together and the fact that 3 of the 4 offspring of the grandparents died with only a 25% chance all seems improbable.
It could be that John's son doesn't have the disorder and what he has is something completely different. What do the geneticists say?

Although your question is actually about genetics (and not personal medical advice), I would still recommend that you remove personal references and make the question as general as possible.

@WYSIWYG Why exactly would you recommend removing personal references?

Things are often not as clearcut as simple mendelian inheritance suggests, and you might be interested in this wiki article on penetrance. It includes a couple of concepts you might need to consider when trying to reconstruct the pedigree.

@Mike I meant you can say that this is a case study in which an aunt of a person is affected.. and so on, instead of "my aunt" and "my son" etc.

@Mike personal medical questions are off-topic on this site, which is why you need to remove any and all personal details from these types of questions.

@fileunderwater Thank you for the information.

@MattDMo I did not realize that it was against the rules. I have removed any references.

The probability of carriers for a genetic disorder mating is higher than you think. Without knowing the specific disorder you're asking about, we can't look up prevalence rates, but as an example, about 1 in 30 caucasians carry an allele for cystic fibrosis. So any two caucasians have about a 0.1% chance of both being carriers.

Please state the condition generally or somehow so we can somehow understand. I do have access to appropriate databases but need to understand about condition. Vascular? Tissue growth? Which genes do you think? Any findings of genes?

@Masi I have a feeling it was spinal muscular atrophy, but I can't be certain.

@Mike Please, put it then Suspected Condition: Muscular atrophy. Differential Conditions: ... [here comes all other possibilities] ..., excluding life-threatening conditions first based on gene tests, imaging, history, ... Please, provide us gene tests if you have them generally. Etc evidences.

@Masi I don't have any of the information you are asking for.

This is a very rough draft about the case, not verified, and should not be used for any medical conditions. Ask your own doctor. It is just for demonstrating some Mathematics and genetic passing generally.
Condition: Muscular atrophy
Differential conditions: TODO
Support: history of genetic passing in -1 and -3 generations
Disease
Muscular atrophy as a condition jumps over a generation. The environment/living of your greatgreatgrandfathers determine your grandfathers future, as a rough estimate.
The disease's common feature is recessive autosomality.
Assumptions

Autosomal recessive disease because everyone who exhibits symptoms is not be able to reproduce due to their early death.
TODO genetic passing
What is the genetic profile? Is there any other autosomal recessive diseases in the gene map?

Proposed probabilities where the random variables $X = disease$ and $Y = carrier$ such that the subscript 0, -1, -2 and -3 is about new children's, John's, parents' and grandparents' status, respectively.
Both of John's grandparents must have been carriers
\begin{equation}
P(Y_{-3}) = 100\%
\end{equation}
The probability of John's dad and any aunts and uncles having the disorder is (TODO think this again with the correct genetic passing)
\begin{equation}
P(X_{-2}) = 25\%
\end{equation}
The probability of being a carrier is for dad, aunts and uncles (TODO think this gain with the appropriate genetic passing)
\begin{equation}
P(Y_{-1}) = 50\%
\end{equation}
Disease as a process

$X \sim P_{i}(\mu, \sigma)$, $i = -3, -1, 1, ...$  where I propose the mean $\mu$ and the variance $\sigma^2$.

To understand this better, we should know how the generation $-5$ lived.
Can you get it?
Assumptions

Assume the events of individual probabilities independent i.e. (-3) events do not affect (-1) events in the series.
...

Test if the two independent statistics $X_{-3}$ and $X_{-1}$ are from the same population.
If you assume it, put it to assumptions.
Probability Density Functions in Generations -3, -1, 1, ...
Probability density function

At $X_{-3}$, the 3 aunts of 4 died. The mean $m = 0.75$ (=3/4).
You cannot use Binomial because sampling is not with replacement, not Poisson because occurrence probability is not less than 10%, ...
...

Conditional probability and Bayes theorem

Consider the conditional probability $P(X | Y)$ that is what is the probability of getting the disease for the generation when given the carriers ...
...

You propose 25% probability for generations series $-3, -1, 1, ...$.
You can test this. Select the statistical significance $\alpha = 0.05\%$. Select the appropriate probability density function or teach neural network to it.
False assumptions

John, his dad, and his wife must all be carriers of the disorder. Why wife should be a carrier?

Literature

Blythe, Peter.  Mathematics for the international student Mathematics HL (Options). Haesa & Harris Publications. I recommend this for beginners.
TI-84 and TI-86 have good manuals about the statistics.
Some publications about teaching a neural network doing some of the genetic analysis.
...

About "why wife should be a carrier?", it seems clear that "Me"'s son must have inherited the disease gen from both parent's. If he hadn't, he wouldn't show the symptoms. Am I missing anything?

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How do you call "pocoya" bird in English?
I am translating a Spanish book and I have here a bird named in Spanish "pocoya", about which I know the following:
1) it flies at night
2) it makes sounds that allow to confuse it with an injured animal
3) it lives in Nicaragua or at least lived several centuries ago.
My own research brought me here: https://en.wikipedia.org/wiki/Pauraque and here: https://en.wikipedia.org/wiki/Ocellated_poorwill.
I don't know which one of them it could be, nor how it could be in English (the first article doesn't have an English version) when spoken (my indigenous people can't use Latin names, for sure...)
Thank you in advance for your  quick response!

I have done some reading based on your descriptors of the bird and your examples, the bird in question is a nightjar and I think they are referring to the Common Paruaque. All nightjars fit your first 2 points, the 3rd point is the only clue we can use to determine what species of nightjar you are describing. There are 11 species of nightjar is Nicaragua.
It seems the Common Pauraque (Nyctidromus albicollis) is commonly known as the "Pocoyo" in spanish, but the spelling may not been certain. Here's a quote from page 9 of an article on the birds of Nicaragua from 1957:
"The species is known in Nicaragua as “Pocoyo” (exact spelling uncertain)".
Reference.
The other bird you describe, the Ocellated Poorwill (Nyctiphrynus ocellatus) is referred to as the "Pocoyo ocelado".
The only other nightjar that might be called Pocoya is the Common Nighthawk (Chordeiles minor), but it is referred to as "Anapero".
I believe when referring to "Pocoya" it is most likely the Common Pauraque as the Ocellated Poorwill would have another descriptive word in it's name in spanish.

Les Beletskys' ecotravellers wildlife guide to Costa Rica says the Spanish name of the Pauraque is 'Tapacaminos Común', probably because it often rests at the road. They also say it is extremely common in Costa Rica and the most abundant caprimulgid of Central America.

Thank you! Yes, my doubt primarily raised from the fact that initially in the description of Nyctidromus albicollis I found that it barely flies. After that, when I discovered pocoya, I assumed pocoyo and pocoya should be two different, distinct names, and happily decided pocoyo will be Nyctiphrynus ocellatus while pocoya is Nyctidromus albicollis. https://vianica.com/sp/animales/aves/chotacabras-y-estaqueros/127


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What's this spring-like structure in the plant parenchyma cell?
I observed a transverse section of an amaranth stem in biology lesson today. When I boost the magnification to 600X, I found this spring-like structure in one of the parenchyma cells near a vascular bundle. I could only find one of these in the section. Can anyone tell what structure is it?

It looks like a part of a xylem cell (particularly vessel). Take a look at pics in wiki article. Another good example is here on pic. 36. Possibly you have dragged a part of it during cutting. So it is presumably not a part of parenchyma cell.

I came here to ask the same question. Thanks for the answer and links!


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Agglutination test of cats

Is the blood test result for the P1 cat is logical?
Because, it shows that even the card containing no antibody, has undergone aggluntination!


text:
Why does underwinding create topological strain of DNA?
I am currently studying the supercoiling of DNA. I understand why overwinding would create additional strain for two attached strands of DNA, but I really don't get why underwinding would create strain and thus supercoiling. If anything it seems that the strands would just separate and strain would be relieved from any DNA helix. If someone would care to explain, that would be great!

Take a look.

The double helical structure of DNA with ~10.5 bp/turn is thermodynamically favorable. Any perturbation from this results in strain. Thus, if DNA is under wound, it is favourable for it to adopt a negative supercoil to return to ~10.5 bp/turn.
That said, negative supercoiling and DNA melting are in fact in some kind of equilibrium. This is important for processes such as transcription and replication which require ssDNA.

it is favourable for it to adopt a negative supercoil to return to ~10.5 bp/turn - can you cite a reference, in support of this?

@SanjuktaGhosh Do you disagree with that statement or do you just want further reading?

I want to know if it does (decrease the bp/turn), how does it achieve it.

@SanjuktaGhosh At the end of this answer, there's a video which shows the interconversion between twist and writhe, if that's what you're asking: http://biology.stackexchange.com/a/56721/6307

No I'm not talking about that.I'm asking that how does negative supercoil decrease the length of the twists of its associated region as you mention in your answer.

Good question! I didn't know the answer either, but I think I have a good idea after thinking of DNA as a normal rope.
This answer helped me put it into perspective: https://physics.stackexchange.com/questions/30871/what-prevents-a-natural-fibers-rope-from-untwisting-when-it-is-elongated
As well as the video linked to in this answer: What is positive and negative supercoiling?
Basically, imagine you have two long strings, then you twist them around each other (DNA helix structure), each twist is called a coil.
Now tie each end to opposing hooks (imagine the hooks located on each side of a doorframe at equal height) without allowing your two strings to untwist.
Once your double stranded rope is secure (the hooks it's tied to represent a point opposite the unwinding site on the circular DNA), pull the two intwined strings further and further apart from each other at the middle of the rope. (This is what underwinding does)
Because each end is secured, it can't untwist, so it supercoils. By pulling the strings apart in the middle, you didn't untwist the coils, you just pushed them closer together, squishing them 'tighter' (stressed) on each side.


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Identification of Insect found on beach in Maharashtra
 Six legs, two antennas, Neon green colour pattern with black. Had no wings.

This appears to be a Lychee Shield Bug, Commonly found in India, formerly considered a beetle, but now classified as a True Bug.

You should add some more details, maybe with some authentic images, to support your answer.

This is a Lychee Shield Bug, Chrysocoris stolli, also known as jewel bugs or metal shield bugs. See this picture from the Wikipedia:

Some more information can be found here and here.

What's wrong with the answer?

Probably that the question was already answered, only without picture and link.

@AlexDeLarge Since I don't think the other answer is very good (neither referenced, nor has it an image) I decided to write another one. And I don't expect it to get better, as it is now four weeks old.


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What kind of fish is this?

What sort of fish is the big one in this picture? I saw it in an aquarium so I don't really know anything about its habitat.

Its a Giant Gourami, Osphronemus goramy.
The giant gourami (Osphronemus goramy) is a freshwater species  believed to be native to Southeast Asia, and has been introduced to other parts  of the world.
This species is commercially important as a food fish and an aquarium fish.

(Source: tropical-fish-keeping)
Reference: fishbase

Several smaller gouramis' are common in the aquarium trade ; this one maybe only as a special order. Interestingly one of the small ones is also called "giant" (about 4 in. long).


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What makes DNA sticky-ends sticky?
When restriction enzymes jaggedly cut double stranded DNA it results in so called sticky ends. What is the substance that makes the DNA sticky?

What are sticky ends.
There is no substance that is attached making the DNA ends "sticky". What has actually happened is an overhang of at least a few nucleotides. Blunt ends are another kind of cut, but have no overhanging residues.

Why are sticky ends sticky?
Restriction enzymes usually cut these ends deliberately so that a four nucleotides are overhanging on the 5' end of the double strand. These are complementary to other overhangs and because they are less stable than a bound double strand region, and are able to hydrogen bond easily with complementary bases, they are easier to attach with a ligase.
Below is an image of the base pairs interacting via H bonds.

The sticky ends are sticky because they have complementary bases. Typically used restriction enzymes cut the two complementary DNA strands at different spots, generating 'overhang', or sticky ends:

These overhangs allow for perfect base pairing (C with G, A with T), which is the result of hydrogen bonding. Just like water molecules show strong affinity to each other or other molecules with -OH and -H groups (e.g., alcohol), hydrogen bonds between nucleotides glues the ends together.
The principles of base-pairing has been nicely answered by @MadScientist in "Why does A pair with T and G with C?"

The "substance" is hydrogen bonds (H-bonds), or rather the potential to form them. Each of the unpaired A/T bases in the sticky ends have the potential to form 2 H-bonds with a complementary T/A, and each of the unpaired G/C bases have the potential to form 3 H-bonds with a complementary C/G.
From the perspective of a biophysicist, H-bonds are often thought of as being the strongest intermolecular interactions. I personally think that it's a little bit lazy and unphysical to see things this way, but the prevailing view in the field is that H-bonds determine specificity in all macromolecular interactions (e.g. the specificity that causes a single DNA strand to bind mostly to complementary DNA strands and poorly to random DNA strands).


text:
Henrietta Lacks and HeLa cells
Why did Henrietta Lacks die when her cells didn't die? As I understand it only the cells from her cervix were immortal so perhaps the cervical cancer took her life and the cells never died.

It's the feature of cancers. The normal cells die via apoptosis or stop to replicate, cancerous cells lose their specialization, travel in the body, and grow tumor by anarchic replication.

@Quidam This is very interesting because I have the same understanding: "cancer cells are "immortal" in the sense of permanent division". So HeLa cells are not very specific. But sometimes, Henrietta Lacks is presented as a unique discovery. Why is that? Is it because her cells were the first to be cultivated?

The cells never died in the sense that they kept replicating, individual cells still died. They were safely cultured in petri dishes before Henrietta Lacks died. The cells came from a tumor that developed from her cervix. The cervical cancer cells had developed high telomerase activity. Telomerase builds telomeres on the ends of DNA, protecting the chromosomes. In normal cells, telomeres tend to get shorter as the cells divide, eventually the DNA is damaged and the cells die. HeLa cells are protected because their telomeres are well maintained.
There was nothing special about Henrietta lacks that made her tissues immortal, so digging her up wouldn't be worth it. Her family would probably get mad too.

Yeah that makes perfect sense! I guess I took the word 'immortal' literally. Now I don't have to commit a crime. XD Thank you so very much!!! I really really appreciate it!!! Wising you a happy Thanksgiving! ;D

There has also already been some controversy over using HeLa cells. Permission to use HeLa genome was never explicitly granted by the family until the relatively recent HeLa agreement. nature.com/news/deal-done-over-hela-cell-line-1.13511 - Nature 500, 132–133 (08 August 2013) –


text:
Where should I start looking for an online gene library?
Is there an online library that includes all known genes in stored in their nucleotide form of all living organisms?
I'm presuming that such a database doesn't exist. So to kick of my search, how can I find a gene amongst all the other databases? Where is a good place to start looking for information about my gene given that it is a well studied sequence? The issue is that I have been provided with the sequence, but I just don't know what organism the sequence belongs to or what it codes for.

Databases
There are too many databases to list here, but Wikipedia has a decent list of the genome databases. For example, there are databases dedicated to genes of individual species, like Wormbase, SGDB and countless others. Alternatively, as others mention a great place to kick off your search is the NCBI.
Finding your nucleotide sequence in databases
It sounds like you already have your sequence. If you want to see if your sequence has been found elsewhere or if there are any similar sequences, you can use BLAST from NCBI. Although it is not strictly a database in itself, it looks to align your sequence to similar sequences in external NCBI databases and quantifies the sequence similarity. It will reveal the species for you to go to a more appropriate database along with a lot of other information about the gene.
There are plenty of parameters to alter to suit your specific needs, but generally, the default settings are a great place to start analysing your gene. You'll need to run a nucleotide test since you want to find the DNA sequence. The results might be difficult to interpret.

NCBI is a good option.
http://www.ncbi.nlm.nih.gov
If you're looking for a gene sequence,  you can search for the gene name in the nucleotide database. For example, here is the annotated human insulin gene;
http://www.ncbi.nlm.nih.gov/nuccore/J00265.1

SwissProt is a human-annotated database of genes/proteins with known functions.

Although this does have the gene information (or at least information on where to access information on the genes) this is a protein centric database and deals in amino acid rather than nucleotide sequences.

There is no properly annotated DNA database. Use this to find function of interest and use a tBlastn to find the gene. Alternately, BRENDA is a human-annotated enzyme database. Use tBlastn to find gene.

No, you are wrong in your assumption that there is no such library.
GenBank. One-stop shop.
Blast your sequence against it on-line. If it isn’t there you are not likely to find it.


text:
Why do slime molds pulsate when growing into their fruiting body?
An example can be seen in this Youtube video, where the slime mold pulsates as it engulfs a rock in order to form its fruiting body.
Why does this pulsing happen?

Adding to @CDB's answer:

...Saigusa speculates that it instead depends on an internal mechanism
  of some kind, perhaps involving the perpetually pulsating gelatinous
  contents of its one cell, known as cytoplasm. The slime mold's
  membrane rhythmically constricts and relaxes, keeping the cytoplasm
  within flowing. When the amoeba's membrane encounters food, it
  pulsates more quickly and expands, allowing more cytoplasm to flow
  into that region; when it stumbles onto something aversive—such as
  bright light—its palpitations slow down and cytoplasm moves elsewhere.
  Somehow, the slime mold may be keeping track of its own rhythmic
  pulsing, creating a kind of simple clock that would allow it to
  anticipate future events.

from: http://www.scientificamerican.com/article/brainless-slime-molds/
In the paper itself he says:

The model is based on physiological observations. We assume that
  multiple chemical oscillators of a series of periods underlie the
  multirhythmicity of locomotion, as multiple rhythms were observed in
  cellular activities in a Physarum plasmodium. This means that there
  are continuous frequencies of oscillation....
...Oscillators with the same biochemical identity can interact over a
  distance by chemical diffusion and active advection of protoplasmic
  streaming. These direct interactions will tend to synchronize phase,
  but it may not be enough to make a strong synchrony. In fact,
  macroscopic cellular behaviors often show fluctuating oscillatory
  variations rather than clear oscillations with a large amplitude, and
  the fluctuating oscillatory variations of different chemical
  identities display frequent switching between in-phase and
  out-of-phase relationships, although each biochemical component still
  shows the slightly oscillatory behavior. This consideration implies
  that the noise ξ should be small so that desynchronization effects are
  relatively weak.

From: Saigusa, Tetsu, et al. "Amoebae anticipate periodic events." Physical Review Letters 100.1 (2008): 018101.

Very interesting find! +1 and bravo

What you have observed is called shuttle streaming. This is how Physarum polycephalum (I assume this is the species of slime mold in the video) and many other slime molds move.
I found this here;

The movement of P. polycephalum is termed shuttle streaming. Shuttle streaming is characterized by the rhythmic back-and-forth flow of the protoplasm; the time interval is approximately two minutes. The forces of the streaming vary for each type of microplasmodium.
The force in amoeboid microplasmodia is generated by contraction and relaxation of a membranous layer probably consisting of actin (type of filament associated with contraction). The filament layer creates a pressure gradient, over which the protoplasm flows within limits of the cell periphery.
The force behind streaming in the dumbbell-shaped microplasmodia is generated by volume changes in both the periphery of the cell and in the invagination system of the cell membrane.

+1 for identifying the name of the behaviour. But why does this happen (as in, what benefit does the fungus gain from having its protoplasm flow back and forth, instead of directly oozing along?)

@MarchHo Its not a fungus.

@MarchHo This behavior is very similar to our own circulatory system. Even when this organism is not in the act of moving, this shuttle streaming is still going on, only now it is acting more like cytoplasmic streaming, which is what most cells use to move nutrition around the cell. I.e. the main reason for this behavior is to transport nutrition, waste material, etc. wherever it needs to be.

@RoverEye Thanks for clearing that up, you got here a little sooner than I did.

@RoverEye Thanks for the correction, corrected the tag.


text:
What metabolic processes do dormant and ungerminated seeds carry out?
What metabolic processes does a dormant embryo in a seed carry out?
Seeds will not germinate, either because of a lack of favourable conditions, seed hibernation, or because of a genetically pre-determined physical or physiological mechanism preventing germination before a specific period or event. In addition to not germinating due to those factors, seeds can also experience dormancy.
With these germination preventing mechanisms in place, the seed will not germinate in the absence of specific triggers. But the seed viability period is limited in which it germinates if the trigger is available.
If any, what metabolic processes do seeds carry out in their dormant/hibernating state, on cessation of which, the seed becomes non-viable?

Does the embryo in a dessicated dormant seed respire, excrete, ingest etc, though with a reduced speed? If it does, is the depletion
  of the respiratory substrate which results in termination of seed
  viability?

hormones gibberelin and absciscic acid play antagonistic roles in seed germination.

@biogirllajja Thanks :), But I want to know what happens before germination, when the seed is just dormant., not germinating but viable.

@biogirl gibberellins actually promote germination!  To Satwik Pasani this is a very interesting question. I've done some reading on dormancy and germination in the past but I don't remember reading much about the metabolic state of the embryo in dormancy, probably because so little metabolic activity actually occurs in the seed. Some seeds can remain dormant but viable for 50+ years because they use so few resources. I'll answer if I find anything!

@CactusWoman Much appreciated. I also want to know what metabolic activity occurs therein.

@cactuswoman Hi! What I meant was that gibberellin promotes germination and absciscic acid inhibits it. So they are antagonistic to each other :)

Good question. Refer: Dalziell, E. L. & S. Tomlinson. (2017). Reduced metabolic rate indicates declining viability in seed collections: an experimental proof-of-concept. Conservation Physiology 5, cox058.


text:
Do males of all sexual species have Y chromosomes?
I know for instance some cells are sexual, so, this got me wondering, do the males of all species that have distinct sexes have Y chromosomes?

Very short answer
No, not all males of all sexual species have Y chromosomes. You might want to have a look to the Wikipedia page on sex-determination systems.
Long answer
Diversity among the species that reproduce sexually
Not all species that have sexual reproduction have sexes. Yeasts, for example, have mating types but no sex.
Diversity among the species that have sexes
Sex is determined by both genetic and environmental factors. In some species, genetic factors are more important than environmental factors in other species it is the reverse. Species which sex is mostly determined by the genetics are said to have GSD (Genetic Sex Determination). For example, humans are GSD, as the female is XX and the male is XY. The species where sex is mostly determined by the environment are called ESD (Environmental Sex Determination). For examples, crocodiles are ESD as sex is determined by temperature. It is important to understand however that there is a whole continuum between these two extremes.
Diversity among the species that are GSD
Among the species that are GSD, some have sexual chromosomes some don't. Some have one locus  (locus=position on a chromosome) that determines the sex, some have many loci (loci=plural of locus). Humans, for example, have sexual chromosomes (X and Y) and have only one locus which determines the sex. This locus is called SRY and it codes for a protein called TDF.
Now you can split GSD with sexual chromosomes into two more categories (it is a bit more complex in reality): XY and ZW. XY are those species where the male is heterogametic (XY), while the female is homogametic (XX). In ZW systems, the male is homogametic (ZZ) and the female is heterogametic (ZW). Birds and some plants have ZW systems for example, while mammals (except "basal" mammals) and Drosophila have XY system.
See also the post What determines sex in birds?
Extra Information
Dosage Compensation
In species that have sex chromosomes, there is a difference in the number of copy of genes between the sexes. In eutherian mammals, for example, females have two copies of all the genes on the X chromosomes, while males only have one copy of most of these genes (plus a few Y chromosome genes). The set of methods to deal with this issue is called Dosage Compensation and there is also an impressive diversity dosage compensations.
Comments on this diversity of sexual systems
The diversity in a sex-determination system, dosage compensation and other things related to sex are impressive. It is even more impressive when we look at how many independent origins there are. Below are some other examples.
The Amazon molly (a fish) is a species that have sexual reproduction but there are no males. The females have to seek for sperm in a sister species in order to activate the development of the eggs but the genes of the father from the sister species are not used. (see this article)
There are also hermaphrodites including sequential hermaphrodites (first male, then females or the opposite) in plants and animals. There are also species where populations are made of hermaphrodites and females and others where there are hermaphrodites and males (very uncommon).
In some species, the sex is determined by social factors. In clownfish, the sex is determined by comparing its own size with the size of the other fishers living in the same anemone.
In an ant species (or two species actually), males and females can both reproduce by parthenogenesis (some kind of cloning but with meiosis and cross-over) but they the meet they reproduce together and their offsprings are sterile workers. So males and females are just like two sister species that reproduce sexually to create an army to protect and feed them. See more information in this paper

Here is a nice figure from Bachtrog et al. 2014 that offers an idea of the diversity of sex determination system (thank to @rg225 for pointing out this figure).

Book suggestion
The Evolution of Sex-Determination is a great book that may interest you.

http://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.1001899

You should modify your wording in the beginning of the answer so that gender --> sex for an accurate terminology, see wikipedia: sex and gender distinction

Fixed! Thank you for the comment @fileunderwater.

No. There are many sex-determination systems. Mammals and fruitflies use the XX/XY sex-determination system — except for the platypus, which has 10 sex chromosomes.
ZW sex-determination system is used by birds and some reptiles. It's similar but with the male having two of the same chromosome (ZZ) and the female being the heterogametic sex (ZW). There's several other variations, such as X0 (XX for females, X for males, with no Y).
There are also animals with temperature-dependent sex determination and others use reverse their sex.

another fun fact is that the bird sex ZZ/WZ and the mammalian XY/XX evolved independatly without common origin... also the genes involved in sex determination is mostly the same but the order of the activation of genes is different. For example: birds are capable of sex reversal on stimulation/inhibition of  estrogen, unlike mammals but like reptiles...


text:
Can it be said that proteins determine phenotypic traits?
I am not ignoring the function of genes, or the gene-environment interactions. What I want to know is if behind every "observable characteristic" we can find a protein -or a group of proteins- which is responsible for that trait. The idea comes from a school curriculum, and it is expressed as follows:

In this unit the core topic is the central role of proteins as executors of fundamental biological functions and thus as responsible of an organism phenotype...

Thank you in advance.

Yes proteins are executors of our fundamental biology. But the proteome is the critical word here (takes into account spacial and temporal features of all proteins). For example if you had a perfectly functional ion channel, but with low expression, then a different phenotype would be exhibited than a perfectly functional ion channel that was expressed in higher amounts. The proteins are the same but the proteomes are different.

A general note on phenotype
I think that the meaning of phenotype has become more complicated over time compared to what it was when it was first coined. As you said, in simple words, a phenotype is an observable characteristic of an organism. However, for Mendel, an observable characteristic would have been only an obviously gross change in the morphology whereas with the current state of technology we can observe the assembly of macromolecules inside a cell. We can also study the physiology of an organism/tissue/cell in real time using various sensors. We can also observe the gene expression profile using different technologies (with different levels of sensitivity and resolution). The question now is, can you call such a characteristic (for e.g. an assembly of some complex in a cell observed by cryo-EM) a phenotype? In other words "what is an observable"?

Coming back to your question:

Can it be said that proteins determine phenotypic traits?

Yes.

Are they the sole determinants of phenotypic traits?

No. A phenotype is usually determined by many factors. Many genes are involved, which may code for proteins as well as functional non-coding RNAs. However, if you make a comparison, proteins seem to be more versatile than ncRNAs (also most of them are involved in direct action). So you may say that proteins are the primary determinants of most phenotypic traits, but I would generally advise that such generalizations should be used cautiously. I'll give a counter example in favour of RNAs. If there is a mutation in a tRNA or a rRNA, you'll see a great effect on the phenotype.

About the question "what is an observable?", I would agree with this: "...the term phenotype includes traits or characteristics that can be made visible by some technical procedure." (https://en.wikipedia.org/wiki/Phenotype#Difficulties_in_definition)
In the case of an tRNA/rRNA mutation, that would lead to a change in the amino acid sequence, am I wrong?

@PiQ It may not necessarily cause a change in the amino acid sequence (it could increase the error rate). It might just reduce the rate of protein synthesis.

Yep, that is correct in general. However, sometimes proteins indirectly determine phenotype. For example, the skin colour is dependent on melanin (not a protein) but the melanin producing cells work because of proteins. Further, melanin production is also controlled by proteins. Thus, skin colour is not DIRECTLY determined by proteins but because proteins produce the pigment melanin, proteins are ultimately the reason behind our skin colour phenotype.

You might modify your answer to clarify your statements "…is controlled by proteins" and "proteins produce pigments". I don't think a novice would understand them. I would say that non-protein substances responsible for a phenotype are produced in reactions that are catalysed by protein enzymes. That's why proteins determine the phenotype.

When you say "in general", is it explained in the next sentence? Or were you referring to something else?


text:
What is a cognate enhancer sequence?
What is a cognate enhancer sequence?
While reading a paper (1) presented at a journal class in graduate school, I encountered this sentence:

HIF-1 binds to its cognate enhancer sequence, the hypoxia-responsive
  element (HRE), and induces the expression of various genes related to the adaptation of cellular metabolism to hypoxia (the switch from oxidative to anoxic respiration),16 escaping from hypoxia (invasion and metastasis of cancer cells),17,18 improvements in hypoxia (angiogenesis)19,20 and the resistance
  of malignant tumors to chemo as well as radiation therapy.

(1) Is Wikipedia's definition of an enhancer correct for this case? Then does 'cognate' mean "related to, tending to be found together", whereas "sequence" means there's a chain reaction that occurs?
Y Zhu et al, "Involvement of decreased hypoxia-inducible factor 1 activity and resultant G1–S cell cycle transition in radioresistance of perinecrotic tumor cells" Oncogene (2013) 32, 2058–2068

Cognate means of common origin.
In molecular biology, cognate is used to refer to known interacting pairs of functional entities. For example, cognate receptor of a ligand means the primary (default) receptor with which this ligand interacts. Similarly, cognate sites (which also includes enhancer) of a transcription factor (TF) refers to the well known and validated binding sites of the TF.
Also see this post.

I disagree. Cognate, as used in biological science, does not mean "of common origin", it just means related. See my answer to a later question.


text:
Where does the inverse seconds unit come from in the association constant?
I'm working to determine Kd(s) kinetically by generating association and disassociation curves.  Kon (association constant, or on-rate) is in inverse seconds multiplied by inverse molar.  I get that the molar comes from concentration, but where do the seconds come from?

First order association reaction:
$$\ce{A + B <=>[k_f][k_r] AB}$$
Rate of association (units: concentration per time) = $k_f\times[A]\times[B]$
 Since [A] and [B] are concentrations and LHS is conc. per time the units of $k_f$ has to be such that it gives conc per time when multiplied by conc2 ([A] ×[B])  Which is conc-1 × time-1
Rate of dissociation (conc. per time) = $k_r\times[AB]$
 Therefore units of $k_r$ would be time-1.
Dissociation constant is actually $\dfrac{k_r}{k_f}$; Its units therefore would be conc.


text:
tandem repeat sequence; causes of contraction and/or expansion question
Question:
Which of the following events, occurring within a tandem repeat sequence, will cause an expansion or contraction of the array?
A) Endoduplication    B) homologous recombination    C) Unequal
   crossing-over   D) Error-prone DNA repair    E) Inversion
I know for a fact that upon replication, tandem repeats of DNA (specifically trinucleotide repeats) can form loops which are repaired by mismatch repair enzymes (MSH2-MSH3); and failure to correct this would lead to an expansion of the array post-replication. However, this answer was incorrect.
Could someone assist me with this question? I read up on the topic but its not clear to me why DNA repair defects do not suffice as an answer. I don't also necessarily understand the correct answer (C)
Thanks so much
-Chris

Gene-duplication would not result in contraction (only expansion). Endoduplication would affect all the genes in the chromosome. Error prone repair would cause small-indels but not expansion of the repeats. Inversion will certainly not do anything to the sequence except changing its orientation.
During unequal crossover, the chromosomes can align imperfectly because of multiple alignment sites in the repeat region, thereby leading to unequal crossover products.  Crossing over however essentially happens because of homologous recombination. Crossover is a "phenomenon" and not a "mechanism" in a true sense.

Mechanism of crossover
Reproduced from: Bugreev, Dmitry V., et al. "The resistance of DMC1 D-loops to dissociation may account for the DMC1 requirement in meiosis." Nature structural & molecular biology 18.1 (2011): 56-60.

Another thing to note is that homologous recombination in the absence of crossover can lead to expansion of repeats but not contraction (see below).


text:
Why and how is DNA synthesis so much faster then RNA synthesis in bacteria?
DNA synthesis in E. coli is 20x faster than RNA synthesis at 1000nt/s vs 50nt/s. (Mirkin'05)
I find that perplexing since DNA polymerization has better proofreading than the RNA variety, which requires extra time as you need to backtrack, excise, and replace. Also, in bacteria there's almost no splicing, so that doesn't slow you down. And the 1000nt/s is a single replication fork. We are not talking about several replisomes together clocking 1knt per second.
Is there an explanation of this or, in the absence of evidence, hypotheses?

(shamelessly unreferenced) hypothesis: DNA synthesis needs to be faster, as you need to replicate huge amounts of DNA relative to a single RNA transcript. I believe that there's only a single origin in prokaryotes (compared to many in eukaryotes), so if there's a selective advantage towards growing/dividing/replicating faster, it makes sense that there's a difference in speed

It makes sense that replication should be fast, but that in itself doesn't mean replication should be faster than transcription.

Good question. As Luigi was suggesting, I would guess it has to do with the amount of nucleic acid that must be synthesized. RNAs are tiny compared to DNA, so there is little selection pressure for speed. Also, multiple RNA polymerases can initiate simultaneously, effectively increasing the synthesis rate.

To throw in another hypothesis: note that mutations in DNA tend to occur when RNA synthesis and DNA replication meet heads-on (antisense) ( http://www.nature.com/nature/journal/v535/n7610/full/nature18316.html ) Ultimately this would suggests that - if the speed of DNA synthesis was similar to the speed of RNA synthesis - there would be more head-on encounters and mutations

I wouldn't call them hypotheses, but the question is intriguing, and, as it seems to be ignored in the literature, I'll make a couple of suggestions.

Perhaps it has something to do with recognition of termination signals in relation to selective pressure for speed in the two processes.

Perhaps if elongation of the RNA chain were any faster it wouldn't be able to respond to the rho-independent termination signals which are thought to be specific stem–loops in the DNA that cause the RNA polymerase to pause and fall off the DNA. The speeding RNA polymerase might disrupt the loops instead. The termination system for DNA replication may have evolved to be much more robust so as to be able to bring faster elongation to a stop. (Note: my suggestion of different ‘robustness’ in termination is not based on any data, it's pure speculation.)
If this were true, it would beg the question of why transcription hasn't evolved a more efficient termination system in concert with the a evolution of a smarter RNA polymerase. Perhaps the answer here is that there is no selective pressure for faster transcription — the rate is clearly sufficient to supply the needs of the cell — whereas the rate of DNA replication determines the time between cell divisions and thus the rate of growth, which is subject to selective pressure.

Perhaps it has something to do with error frequency in relation to selective pressure for speed in the two processes.

First I'll make it clear that I think the proofreading argument in the question is a bit of a red herring. If the rate replication is 20x as fast as transcription, the occasional backtracking will not have much effect on the overall difference. However errors and proofreading could be involved in a different explanation.
RNA transcription does not have proof-reading. The length of RNA transcripts is such that the cell can tolerate the errors that occur. However if the speed transcription were increased it is reasonable to expect an increase in error frequency, which might be detrimental. The current rate of transcription may be a trade-off between efficiency and accuracy. Of course one can imagine a proof-reading system for transcription evolving if it were necessary, but, as discussed above, if the rate of transcription is adequate there would seem to be no selective pressure to produce.

Processivity may be an additional factor. I am not sure about the processivity of RNAP, though.

@Jagoe — No need to apologize. The source you cite was not known to me and is very pertinent to this kind of question. Like many others, I had thought transcription and translation were coupled in prokaryotes. Selective use of images perhaps. (But I wish they wouldn't keep referring to The Central Dogma all the time.)

This is because of the fact that DNA polymerase does the fast process that is 1000 nu/sec as compared to the RNA polymerase that 1000-2000nu/min because this process is done without discrimination and also DNA pol has exonuclease activity

Welcome to Bio. Could you expand your comment into a full answer by adding references and additional background to it? You might wish to go through the help center on answering questions. There it will become apparent that the SE network is not the place to answer posts with one-liners. -1


text:
Can/Do any spiders "release" their own web in the presence of a threat?
Preface
We live in the north eastern US and have a spider that has setup shop next to our front door.  I've lived in this area my whole life and she's the largest spider I've seen.
We're too interested and afraid to do anything but let her be, so we've been watching her for the last couple of months.
The "Event"
My wife almost bumped into her web while we were looking for our cat tonight. (I mean she was really close). The spider was hanging around in the center of the web at the time.  A short while later my wife saw the spider scurrying furiously and then she crawled back into her hiding spot behind the shutter.  Next time I looked over, her web was completely gone - neither of us think we got close to it again during that short time.
I'd also like to point out that it was a bit gusty tonight, a rain storm was probably about an hour away.
We are wondering if something happened to her web, or if she took it down intentionally.  If she did, is this behavior common in spiders?
Other Information

She's got a blackish/yellowish bulbous body with the same color striped legs
She's about the size of a ping pong ball (including legs)
She hides during the day behind the shutter, but always comes out when the sun starts setting.
Unfortunately I have no pictures of her that aren't the underside, she never comes around the front of her web.
She builds a "classic" looking web, a hair longer than a foot in diameter with a couple of longer guy lines out to the door and the stoop. There are never any messages written in it.
She either never catches anything, takes her food back into her little den, or eats very quickly because I've never seen anything wrapped up in her web.
Our cat found his way home a couple of hours later

Photo

Thanks!

Do you wish to get your spider identified? I ask it because it is nowhere mentioned in your question and it has a tag species-identification.If you intend us to do so maybe you should add that part too. Welcome to BioSE. :)

@SanjuktaGhosh Thanks for the welcome! And sorry for the ambiguity - I was mostly interested in the web tear down, but I was not sure if it was specific to the spider species or not so I included as much info as I could.  I am not aware of the species so I figured if anyone identified it it would be a bonus :)

Building a web costs a lot of energy. From Wikipedia: "It is common for spiders to eat their own web daily to recoup some of the energy used in spinning. The silk proteins are thus recycled." https://en.m.wikipedia.org/wiki/Spider_web

Interesting! I had no idea

This is an older question, but just for the information, here are a couple of points that might be helpful:

Some (not all) spiders do tear their webs down and 'recycle' the silk when the web has been damaged to the point of being unsuitable as a snare.  I don't know if any spiders simply cut the web loose and let it fall if they're disturbed, but I would doubt it - perhaps the gusty wind did something?
You were right - it is a 'she'; a female Araneid of some sort, to be more precise - the candy-striped legs and orbweb tell you what she is, and the large abdomen and general size tell you she's a female.  From the photo I can't hazard a guess* as to which spider, or group of spiders, within that general category she might be, but she is an orbweaver of some kind.  You didn't ask, but since all known orbweavers are completely harmless to people, she is too.
Some of the larger orbweavers in this group can get quite large and spin very large webs.  The largest I ever had made an orb about 3' across on a structure which stretched from the eaves to the ground, or about 10' top to bottom.  Her abdomen was maybe a bit large than an inch across, and with legs included, she would have been rather larger than a pingpong ball.  I used to feed her various things I found, and I discovered that she would happily eat small toads as well as large insects.

I include a link to one of the orbweavers which have that red tarsus - unfortunately, there are more than just one orbweaver with that feature, but if I was pressed to offer an ID, I'd go with this one provisionally:  Neoscona crucifera.  These Barn Spiders (and there are at least two spiders known by that name..) can get quite large, and make a reasonable fit with your photo.  The reddish color on the tarsi is fairly dull, not a bright red, so I lean away from N. domiciliorum and other orbweavers that might turn up in your area, although of course I'm not a fanatic about it..
https://bugguide.net/node/view/28154
*well, I guess I wasn't completely honest here..


text:
Laurus Nobilis parasite identification
In north Italy were I live I have two plants of laurus at the two sides of a garden. One of them has some sort of parasite on its leaves.

Someone know something about it? Leaves are covered with something like an oil.

Looks like some sort of scale insect. You should add where you're located, that might be helpful.

As @picapica has pointed out, I presume these are scale insects, the first instar of Japanese wax scale, Ceroplastes japonicus.
Laurus sp. is a host of this hemiptera in Italy.
Here is an image showing the second instar from Italy:

These are the adult females :


text:
Structure of proteins
Regarding the secondary structure of proteins, I know that there are 3 main types. The beta sheet formation is made up of beta strands stabilized by hydrogen bonds to form an anti parallel or a parallel structure. I learned that these beta strands are a zigzag sequence of amino acids, but what traits of beta strands differentiate it from the primary structure? Or are the beta strands just primary structures that link together to make beta sheets?

Primary structure when talking about proteins refers only to the aminoacid sequence, it does not refer to any spacial/3D structures like beta strands..

This is a little confused. Secondary structure usually refers to helices and sheets. Sheets are made up of strands that can be either parallel or anti-parallel.

As @gilleain said secondary structure is the Beta pleated sheet and not the Beta strands.

primary structure
focus = peptide bonds (because these link the amino acids
The sequence of amino acids, for example AGGVHIL..

secondary structure
focus = H-bonds between the parts of the backbone
 There are several different types of secondary structure (α-helices, β-sheets, etc.). However the most import thing to remember is that the secondary structure refers to the the patterns of hydrogen bonds formed between amine hydrogen and carbonyl oxygen atoms contained in the backbone peptide bonds of the protein

your confusion
You are partly correct from a very simple perspective you can see the secondary structure of β-Sheets just as connected primary structures. However when talking about a piece of secondary structure you have to take the hydrogen bonding into consideration as this is what connects your primary structure parts (β-strands) to form a β-sheet.


text:
Excluding the Exon, What Does the Rest of the Genome Do?
The exon is the portion of the genome that encodes protein synthesis, if I understand correctly.
But, this exon is apparently less than 5% of the genome.
So, what does the rest of the genome do?

that's the trillion-dollar question

The exome represents about 1.5% of the human genome, not 5%

A few percent codes for RNA, like microRNA, long non coding RNA, shRNA ect. These RNA while not translated into protein do have a function.
Some RNA are ribozymes, catalytically active in their own right, but they do work with proteins. An example of such complex is the ribosome, where the catalytic peptidyl transferase activity that links amino acids together is performed by the ribosomal RNA
https://en.wikipedia.org/wiki/Ribosome
Then there are miRNA, that control gene expression by RNA mediated silencing.
https://en.wikipedia.org/wiki/RNA_silencing
Then there lncRNA... these long RNA can regulate gene activity by binding to transcription factors. So a cell can maintain a high concentration of transcription factor in an inactive state that can rapidly go into use once a signal is received. This is rather recent discovery.
About 45% of the human genome is composed of what is essentially viral parasites. While some of these viral genomes are full functional and encode endogenous viruses (this is why there is come concern about xeno tissue transplant). Most of these viral parasites have degraded somewhat, having accumulated mutations that either render unable to leave the cell, but still able to replicate and multiple in the genome (we call them transposable elements), or are completely inactive (repeat elements).
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4124830/
Examples are
Alu element make up 10.7% of the human genome. It is rather old parasite... youngest expansion is about 30 million years old. Mostly inactive, although some Alu elements are still active.
https://en.wikipedia.org/wiki/Alu_element
Line repeats. ~17% of the human genome.
Some DNA is structural. The centromeric repeat array which may be several Mb long per chromosome (exact length is unknown due to variation between people and difficulty to clone and maintain for analysis). Here the DNA serves as a pad over which the kinetochore forms. This DNA tend to be transcriptionally quiet, few if any genes.
And there are pseudo genes... genes that are no longer active due to mutations.


text:
Is this a saltwater millipede?
I spotted this millipede-like creature in Hervey Bay, Australia at low tide, just kind of hanging out at the bottom of a small saltwater tidepool.

It's several inches long, composed of a large number of segments, each of which appears to sport a pair of legs.
Hard to tell from the photos, but the creature is aquatic and in both instances was observed moving around under about an inch or so of water.  No specimens, alive or dead, were observed outside of the water.
They leave obvious trails behind them in the sand at the bottom of the tidepool as they move across it, and I assume they have some ability to burrow into the sand as I saw far more trails than I did creatures.
What are these things?

Could be a Eunicid Polychaete worm. From the species present in Australia (from this site), this seems like Marphysa

I agree, it looks like a polychaete worm. These have a pair of legs on each body segment (which explains one of their common names, bristle worm) and can be found in shallow waters and soft sediments.

This is indeed a polychaete worm, and likely a member of the beachworm family Onuphidae.
From the Marine Education Society of Australasia  :

Polychaetes are particularly common on and in muddy and sandy shores. Their most obvious feature are the pairs of parapodia appendages. One pair comes from each body segment. These parapodia are used for crawling and swimming. "Para" means "like", and "podia", "pod" or "ped" means "legs". These parapodia are often tipped with hardened spine-like setae or dorsal cirri.

You can find some good informaiton on beach worms here, and information on the distribution, abundance and
population dynamics of various species here.
I'm sure a quick message to Dr. Pat Hutchings, the Austrtalian Museum's polychate expert, would prove to be be your best chance to get a species identification.
For those interested in additional polychaete identification, you can download a digital ID key.


text:
Has anyone tried to prepare chemically competent Mycobacteria?
Bacterial species like E. coli are easy to transform using a variety of methods, including both chemical transformation and electroporation. Chemical transformation is especially nice to use as it can be done in high throughput. I'd like to start working with Mycobacterium smegmatis, though, and have only been able to find electroporation-based transformation methods like the one described here. Can chemically-competent mycobacteria be prepared? If so, are they just very inefficient? Is it worth testing some E. coli-specific methods with mycobacteria?

There was no link to the paper. So I added one.

Mycobacteria are very different from E. coli. I would be rather surprised if you could adapt the methods without a lot of customization. What's wrong with electroporation?


text:
what are the best books for the IIT-JAM biological sciences exam?
I'm from India and i'm preparing for a competitive exam called the Joint Admissions Test for a Masters admission.
I need help in finding books to read from for these chapters:
General Biology: Taxonomy and physiology, Pro-and eukaryotic organism; cell organelles and their function; multicellular Organization; energy transformations; internal transport systems of plants; respiration; regulation of body fluids and excretory mechanisms; cellular reproduction; Mendelian genetics and heredity; biology and populations and communities; evolution; genesis and diversity of organism; animal behaviour, plant and animal diseases.
Basics of Biochemistry, Biophysics, Molecular Biology: Buffers; trace elements in biological systems; enzymes and proteins; vitamins; biological oxidations, carbohydrates and lipids and their metabolisms; digestion and absorption; detoxifying mechanisms; plant and animal hormones and their action, nervous system, nucleic acids, nature of gene and its function, Genetic code, synthesis of nucleic acids and proteins. Enzyme mechanisms and kinetics, nucleic acid metabolism, photo synthesis.
Structure of Biomolecules: intra and intermolecular forces; thermodynamics and kinetics of biological systems, principles of x-ray diffraction, IR and UV spectroscopy and hydrodynamic techniques.
Microbiology, Cell Biology and Immunology: Classes of micro-organisms and their characterization, nutrient requirement for growth; laboratory techniques in microbiology, pathogenic micro-organisms and disease; applied microbiology; viruses, Microbial genetics. Innate and adaptive immunity, antigen antibodies.Cell theory; Cell architecture; methods of cell fractionation; cell division; types of chromosome structure; biochemical genetics- inborn errors of metabolisms; viruses and fungi; principles of processes of development.
PS. I've studied biology only until high school.

This question is just too broad. Also, asking for examination tips is tantamount to homework. Book recommendation questions should be precise else they would be considered opinion-based. I'm sure there are plenty of websites that provide reading materials and recommend references for examinations like this. Unfortunately, this site is not one of them.


text:
Why are so many spermatozoa produced when only one of them fertilises the ovum?
During fertilisation only one sperm can fertilise the ovum. So why so many millions of sperms are produced?? Isn't this a waste of energy?

Short answer : Sexual selection with sperm competition
However this answer will vary depending on which species you are referring to. When female mates with multiple males (like in many insects), sperm competition increases male's chances of getting his genes forwarded to next generation. When there is not much rival competition with other males (like in humans) this has correlation with mate guarding behavior and quality of sperm.


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Dwell time equations for ATP-sythase?
I have read that every 120 degree rotation of the F1 complex of ATP-synthase can be split into a 30 degree rotation and a 90 degree rotation. In between these two are dwell times, the one before the 90 degree rotation been called the ATP-binding dwell time and the one after been called the interim dwell time and that both of these fall of exponentially. I cannot, however, find a derivation of the probability density function of these dwell times, or there exact form. If anyone knows such a derivation or where to find one this would be much appreciated.

Are you asking for the mathematical model or the experimental measurements ?

@WYSIWYG The mathematical model

Usually, the dwell time between independent reactions is exponentially distributed. You can have a look at this paper for a biophysics based mathematical model.

@WYSIWYG I am pretty sure that one depends on the concentration of atp present though

The rate of binding depends on the concentration of ADP (the substrate) but not the rate of conversion to ATP.

@WYSIWYG sorry I was thinking of ATP-hydrolysis (which I think the F1 complex can do). I think the relationship is along the lines of $p\propto ce^{-kct}$ for the binding site dwell time (where $c$ is the concentration of AD(T)P), but I have no idea how to derive it.

That is based on a simple first order kinetics... The dwell time distribution can be derived from the probabilistic  "master equation" for the reaction.. Your distributions of reaction probabilities can be modelled by Poisson distribution and conversely the dwell times would follow exponential distribution..

ATP Binding dwell time
Here is a very dodgy derivation of the binding dwell time (note I am the OP). For this we have $$E+S\rightarrow ES$$
Where $E$ is the enzyme and $S$ is the substrate (keeping this general). We can write our rate equation as:
$$rate=k[E][S]$$
But we can also write the rate as:
$$rate=-\frac{d[E]}{dt}$$
so that:
$$\frac{d[E]}{dt}=-k[E][S]$$
Now here is the bit that I think is a bit dodgy, we are going to assume that $[S]$ is approximately constant. So that:
$$[E]=Ae^{-k[S]t}$$
We can take $n=[E]V$ to represent the number of enzymes left, where $V$ is the volume, then letting $n_0=VA=constant$:
$$n=n_0e^{-k[S]t}$$
The probability of been within the time $t$ is then given by:
$$F(t)=1-e^{-k[S]t}$$
Which is our commutative distribution function. Differentiating this gives our probability density function:
$$f(t)=k[S]e^{-k[s]t}$$
Interim dwell time
The interim dwell time (also called the catalytic dwell time) involves two steps[7]:
1. The cleavage of the enzyme bound ATP.
2. The release of the hydrolysed products.
Each of which is going to follow the distribution (analogous to the above) of:
$$p_i(t)=k_i e^{-k_i t_i}$$
For $i=1,2$ respectively. The joint probability distribution is found by the convolution of these two [8]:
$$p_T(t)=\int^{\tau}_0 p_1(t) p_2(\tau-t)dt$$
Which gives:
$$p_T(t)=\frac{k_1 k_2}{k_1-k_2} (e^{-k_2 \tau}-e^{-k_1\tau})$$
Edit
Although starting from deterministic equations (which actually doesn't really matter), this method does hold and is simple. The type of reaction is called a pseudo-1st-order reaction (or 2nd order class 2) which explains my approximation for $[S]$ been constant. See [9] and [10]
Sources for additional info

https://youtu.be/X_YXTWU2maY?list=PLbKSbFnKYVY3j6ubaW1zgTXj5C4443v8s
http://www.nature.com/articles/srep08773
http://www.ks.uiuc.edu/Research/atp_hydrolysis/
http://www.pnas.org/content/85/17/6314.full.pdf
https://books.google.co.uk/books?id=uIxwICNmLKEC&pg=PA199&lpg=PA199&dq=catalytic+dwell+time+distribution+%5Batp%5D&source=bl&ots=u8oBcVNCDc&sig=PKvdVAwT0WxdqTuVwMxhU3RfSwM&hl=en&sa=X&ved=0CCAQ6AEwADgKahUKEwiGhKDalufHAhXkadsKHc54ADs#v=onepage&q=catalytic%20dwell%20time%20distribution%20%5Batp%5D&f=false
http://crystal.harvard.edu/PDFs/floyd_biophysj.2010.pdf
http://www.ncbi.nlm.nih.gov/pubmed/16258036
http://crystal.harvard.edu/PDFs/floyd_biophysj.2010.pdf
http://glutxi.umassmed.edu/grad/GradKinetics.pdf
http://chemwiki.ucdavis.edu/Physical_Chemistry/Kinetics/Reaction_Rates/Second-Order_Reactions/Pseudo-1st-order_reactions

You cannot obtain probability distributions from these deterministic equations.

@WYSIWYG Please can you explain, the equation $n=n_0 e^{-k[s]t}$ is equivalent to that for nuclear decay, which gives an equivalent probability density to that I have given.

It will not give you probability distribution because this rate is based on deterministic mass action kinetics.. You have to represent your equations in terms of probability instead of reaction rates to obtain those equations... Have a look at chemical master equations

@WYSIWYG I asked (and then when I came up with an answer, answered) the following question on Chemistry.SE I think my answers  provides a replacement for the first part of the derivation using the master equation: http://chemistry.stackexchange.com/questions/37074/master-equation-for-catylist-and-substrate-binding

check my answer on Chemistry.


text:
What are the advantages of sexual reproduction over asexual reproduction?
What are the advantages of sexual reproduction over asexual reproduction?
How does variation influence ecological and evolutionary success?

The question is unclear. You might want to rephrase. As you say, sexual reproduction is good for life because it's a method of reproduction, which allows for survival, which life requires by definition. But that's just tautological. Do you mean to ask what the benefits of sexual reproduction are over asexual methods for an organism in an ecological/evolutionary context? Or would you like to know the biological, cellular and molecular mechanisms which occur exclusively in sexually-reproducing species that allow for variation? Please clarify.

I meant to know the benefits of sexual reproduction over asexual reproduction

Genetic variation -- a variation in alleles to enable organisms to avoid passing on mutations/traits that reduce fitness and possibly create new combinations of alleles that lead to traits that actually increase fitness. You might also want to take a look at population genetics and microevolution to see how this plays out at a larger scale.

Please consider using a search engine for these kinds of questions. This question has been addressed nauseatingly often. PS: The main advantage of sexual reproduction is the introduction of a LOT of genetic variation which is not achieved through budding/regeneration/fragmentation (asexual reproduction). Variation is fundamental to evolution and as such has a protective, prophylactic effect against parasites and disease. Unique offspring are produced each time. The downside is that it's more energy-costly, takes a lot of time, requires two organisms (parents) and produces fewer offspring.

@SPr I was just wondering what else was it good for rather than the points you mentioned. The points you mentioned are addressed often to this question. I was wondering if there were any other reason. All the websites I entered , ultimately only mentioned that it's good for production of complex organisms, makes lot of variation which helps both adapt and speciate. Not anything else.

You are misunderstanding the core advantage. Sexual reproduction is not "good for production of complex organisms" - this is a misunderstanding. It's an effective strategy to introduce genetic variation between individuals of a species. It occurs in many simple organisms too. Variation is very, very important in evolution. A lineage with steadily high levels of variation between successive generations can escape diseases, be resistant to parasites, is protected from major genetic mutation events, and has the additional benefits of sexual selection. These all lower the chances of extinction!

One question at a time please.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


text:
Do carrier proteins constantly open and close or do they only work when a substance binds to them?

What causes carrier proteins to change shape ?
Do they need energy to change shape? If that is true, how are they involved in Facilitated diffusion ?
By changing shape, do we always mean opens from one side and closes from another ? (they all work by changing shape right ?)
once they transport a molecule from inside to outside, do they return to their original shape instantly or do they need to transport a substance from inside to the outside to return to their original shape ?
and finally, are all co-transport proteins carrier proteins ?


text:
Why do people in the scientific community use terminology such as renal, hepatic, cardiac instead of kidney, liver and heart?
Are there differences between renal, hepatic, cardiac and kidney, liver and heart? Is the "jargon" used more commonly because of tradition, or is there some definitive biological basis to it?

The former words have latin roots, and historically latin was the language of science. Therefore, nomenclature in different scientific fields are often based on latin roots.

I disagree with Chris. Questions on technical terminology are a perfect fit here. For example, what if the reason behind the terminology is based on historical events. Doesn't the history of biology still matter on this forum?

Also, note the answer provided by "fileunderwater". His answer makes note of the fact that there exists a specific and technical difference between the terms. If I ask why a Histone scaffold is not called a Solenoid, that is a valid question with a basis formed by the terminology set by the scientific community. In other words, it's not a matter of "english language and usage". They have essentially asked whether or not there is a difference between the renal system and the kidney.

@fileunderwater the jargon is consisted of both Latin and Greek.

Medicine is not my field, but I want to point out two things:

The former words have latin (or greek) roots, and historically latin was the international language of science. Therefore, nomenclature in different scientific fields are often based on latin.
The former words describe tissues and the related functions/processes (e.g. renal = kidney + related tissues + processes carried out by the renal system), while the latter are names of organs. Therefore, the former words are more suitable and precise when you want to describe these processes. For instance (as far as I know), Hepatic disease can be be caused by problems outside of the liver as such, e.g. blockage in the hepatic vein.

Users more knowledgeable in medicine are welcome to fill in or correct me if I'm mistaken.


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Difference between protozoa, protists, protoctista?
Are protozoa, protists, protoctista different classes of organisms or simply different names for the same?

These terms are all somewhat obsolete as taxonomic terms, but they may still be used to describe certain groups of organisms.
The term "protist" is used informally in two different ways.  One usage refers to the paraphyletic group consisting of all eukaryotes other than the animals, plants, and fungi.  The other usage is to refer to those eukaryotes that exist as independent cells or, if colonial, do not form colonies with differentiated tissues.
The term "protozoa" is used informally to refer to the "animal-like" protists, i.e. those that are non-photosynthetic and motile.
Wikipedia gives a good summary of how these terms were used historically.

Protozoa as of 2017 is how Microbiologists define one of the six categories of microorganisms.
Microbiologists classify microorganisms into:
Bacteria, archaea, fungi, PROTOZOA, algae, and small muticellular animals
Then you have how Biologists categorize things, and they classify not into 6 groups but into three groups --> Bacteria, Archaea, and Eukaryote
Then you have the further refining that Biologists use which is Kingdom-  which is Bacteria, Archaea, Fungi, Protista (old name for this kindom USED TO BE protozoa), Plantae and Animalia
SO in 2017 , if someone says protozoa, they are no longer talking a kingdom they are talking about a microbiological category for a microbe. If they do say protista, this is the correct kingdom terminology for the protists... which make up the category !
Reference
Bauman, Microbiology with Diseases by Taxonomy, 4th ed. (2014)

Welcome to Biology. Thanks for your interesting answer. Could you possibly add sources to allow other users to background read on your answer?

microbiology with diseases by taxonomy fourth edition by robert bauman

Thanks. I edited your answer and I will delete this comment string shortly. +1

According to Wikipedia Protist and Protoctista are equivalent. "The term protozoa is used to refer to heterotrophic species of protists that do not form filaments." - from the same wiki.


text:
Can the dead be brought back to life by viruses?
Zombies have been a part of popular culture for decades. The living dead rising up to take over the world is a terrifying concept, worthy of Hollywood blockbusters and television hits. Some of those zombie fiction stories are based on infection by viruses or other organisms.
Is it possible to bring dead tissues back to life by virus infection?

You must tell facts from fiction; viruses need living cells to replicate because they do not have the molecular machinery at hand to generate energy and construct building blocks essential to life. So no, viruses cannot bring back the dead or revitalize dead cells.
One thing that comes close to it are the so-called zombie ants. These ants have been infected by a parasitic fungus that can take over the ant's nervous system (Fig. 1).

Fig. 1. Zombie ant found in Brazil, infested with the fungus Ophyocordiceps. Source: National Geopgrahic.
These fungi eventually kill their hosts, but before doing so they temporarily take over their nervous system. In the case of Ophyocordiceps unilateralis (Evans, 2011), the spores lodge themselves into the ant's head through an exposed part of the ant’s exoskeleton. The fungus then infiltrates and targets the ant’s brain, taking control of the ant. Then it makes the ant leave its colony and head for a leaf that provides the ideal conditions for the fungus to grow. The ant crawls under the leaf and goes into a “death grip”—biting down hard on the leaf's major veins. This allows the fungus to slowly feed on it. When the fungus finishes growing, it eventually kills the ant and releases its spores (Source: Smithsonian).
The interesting thing is that the zombie ant not only provides shade and humidity when hanging under the leaf, it is also positioned directly on top of the ant’s colony, so when the spores burst out they fall on other ants and begin the cycle all over again. There are hundreds of mind-controlling fungi like this one, but the chances of this type of parasitoid fungus evolving to target humans as hosts are unlikely (Source: Smithsonian).
Reference
- Evans, Commun Integr Biol (2011); 4(5): 598–602

@MichaelT - organisms infecting the nervous system in general can cause erratic behaviors. They don't control the brain though.

I remember an old BBC documentary-series (1980s?) - I think with David Attenborough - where in an episode, they followed one fungus-infected ant until it's death.  Then there was an episode of X-Files (the original series), where an alien fungus did attack humans and made them seek out other humans - before a mushroom exploded from their chest to spread spores...

Ahh yes...  https://www.youtube.com/watch?v=XuKjBIBBAL8

You have to wonder how a fungus could compel an ant to do something like this. Minor behavior changes? Sure. I guess it could just stimulate an area of the brain making the ant go into a rage or make it docile or something. This is a very specific set of "instructions" that it seems to be able to feed into the ant's brain though. Considering I'm sure all ant's nervous systems develop partly as a result of their environment, how could it reliably control a new ant? It's amazing.

It should be noted that wide range of parasites do influence behaviours of host. Toxoplasma gondi is one of them. However, it should be emphasized that this wide range of parasites does not influence hosts with wide range of behaviour, but one type of behaviour (per parasite). Relatively complex behaviours are possible because one signal (e.g. hormone) can start cascade reaction or influence multiple receptors, thus causing itself complex behaviour. Example might be adrenalin.

Mammals are not immune:
http://phenomena.nationalgeographic.com/2013/04/26/mind-bending-parasite-permanently-quells-cat-fear-in-mice/
There is a parasite that causes mice to no longer fear cats - so the cat can ingest it where it can then reproduce.

Certain parasites including bacteria and worms have been linked to causing obesity by releasing hormones or disrupting our digestive system to make us want to eat more. While not all obesity are caused by parasites, parasites can cause enough behaviour change to cause obesity.

@Carcingenate I asked somebody who researches these ants and fungi that exact question once. From what I remember, she said that ants can't control their body temperature directly to attack an infection, so instead they move to a sunny place to induce a fever. I'm not sure about the clamping reflex.

I recall a snail also which gets controlled, and directed to the tree canopy, where birds then eat it and re-distribute the parasite

Note: This answer is a complement to @AliceD's answer, and is partly reusing stuff from this related answer.

Since you are specifically asking about viruses, I thought that it might be interesting to mention that similar behaviour changes as those mentioned for fungi can also be caused by viruses. See e.g. this quote from Roy et al. (2006):

In many cases the final interactions, or endgames, between a host and pathogen involve complex behavioral modifications such as the infected insect seeking an elevated position where wind currents can effectively disseminate conidia. Elevation seeking by insects at late stages of infection is a common phenomenon that was recognized by early insect pathologists who noted that diseased lepidopteran larvae, such as Lymantria monacha (the nun moth), infected with baculoviruses migrated to the tops of trees where they died (94). This host-altered behavior was named “Wipfelkrankheit” or “Wipfelsucht” (meaning tree top disease in German) for viral diseases (41) and “summit disease” for fungal diseases (24, 57, 106).

Overall, lots of information about the behavioural modifications of hosts caused by fungi and viruses can be found in Roy et al. (2006).
One example of a such a virus that modifies the behaviour of insects is Lymantria dispar multicapsid nuclear polyhedrosis virus, which infects larvae of the moth Lymantria dispar and causes them to climb to high locations (tops of trees) before they die. In another interesting example a parasitic wasp might use a viral infection to control the behaviour of its host, so that the the host beetle is paralysed and is "guarding" the larvae and pupa after the parasitic larvae has emerged from the beetle (see Dheilly et al, 2015 and a popular account in Science).

(Dinocampus coccinellae "guarding" wasp pupa, from http://www.naturespot.org.uk)
References:

Roy et al. 2006. Bizzare Interactions and Endgames: Entomopathogenic Fungi and Their Arthropod Hosts. Annual Review of Entomology 51(1) (pdf)
Dheilly et al. 2015. Who is the puppet master? Replication of a parasitic wasp-associated virus correlates with host behaviour manipulation. Proceedings B 282(1803).
Wasp virus turns ladybugs into zombie babysitters, Science

Even the rabies virus is a good example in case of animals.

@WYSIWYG Rabies is very likely a major source for various “people turning into monsters” folklore, like zombies or werewolves. (“Zombie,” of course, was originally a very specific term for a particular thing in Haitian folklore which does not match up well to rabies, but the broader popular concept certainly gets many nods from the disease.)

@KRyan: Not likely. Rabies is also called "Hydrophobia", furthermore Rabies has quite destructive effect on nervous system. Werewolves are not "rabid", werewolves are people who transform into wolves (or other way around) and there is a LOT about people-turning-into-animals and animals-turning-into-people in every mythology of every nation/ethnics/tribe.

@WYSIWYG Agreed, and there are probably also many unstudied exampes of how viruses can affect human and non-human behaviour.

Stretching the limits of what is known a bit, there is an interesting example of a phage (virus that infects bacteria) infecting a photosynthetic bacterium in the ocean that deserves mentioning.  What is amazing here is that the phage has certain genes that are required for photosynthesis within its genome.  Why does it have these?  The phage extends the life of its host in order to maximize its replication.  It has been shown that while the host metabolism is all but shut down, phage genes for photosynthesis are still being expressed at high levels, giving the phage 'bonus time' to replicate.  Ok so the virus in question here is the reason for the death of the host in the first place.  Also, the host is not exactly living normally during this 'bonus level' of life, as the phage is only trying to produce more of itself.
One can imagine however, that in single celled organisms (for simplicity), a lysogenic phage (one that sits in the genome of its host and waits for the proper conditions to jump out and replicate), could theoretically bring back the organism from death, if it encodes the precise biochemical pathway that was shut down in the first place.  Think of a cell that has lost some necessary gene that is essential to its survival in a given environment.  This new mutation (perhaps because of UV light) would surely kill this cell.  If the cellular components necessary for survival remain intact, and a phage encoding this biochemical pathway (this gene) and the components to express it (yes viruses have many of these genes too), it is conceivable that this cell could return to a metabolically normal state, ie living.  This is just a thought experiment....
Ref:
http://www.cell.com/trends/microbiology/fulltext/S0966-842X(10)00196-4