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How do crickets get away with being so loud without getting eaten?
How do crickets get away with being so loud without getting eaten? There are a number of bugs that reproduce by blatantly advertising their location. For instance fireflies advertise their location with physical light and are extremely easy to catch.
How is this evolutionary selected for?

For loud calls to be stable in large-population evolutionary dynamics, the fitness benefit from the call (e.g., mate attraction) must exceed the fitness costs from the call (e.g., predator attraction).
Individual species can 'solve for' benefit > costs by any number of devious tricks. One classic trick used by noisy insects (e.g., cicadas) is 'predator saturation'. Imagine you're a predator that hunts noisy insects by following their call - any time you find one, you'll eat it - unless you're already so full that you literally can't fit any more insects down your gullet. If the noisy insects have a short breeding season, and are noisy for the whole of that season, then during the season you will very quickly fill up and be unable to eat, but you will only have eaten a tiny fraction of the insect population.
If the predators are already full, the costs of predation risk are very low. The benefits of mate attraction remain as high as ever. In that case, an insect's best strategy is to sing as loud as possible.

Periodical cicadas are a great example of a noisy prey species with a remarkable predator satiation strategy.

Do you have some citations to go with this answer? Studies which have experimentally / theoretically shown that theory explains what we might see in nature.

Your explanation of cost/benefit ratio is spot on, but I'm not sure if predators 'being full' is that applicable in nature since that would just increase the predator population. It probably has more to do with relative risk of predation (i.e. it's not that the predator is so full that it stops eating, rather, the predator is just eating your neighbor instead of you).

@etis You're right, I simplified some of the details. Predator saturation also requires that the predator population doesn't grow to the point where it can eat all of the saturating prey: predator populations must be limited by something other than peak prey abundance. Fortunately for the cicadas, there are eleven months per year where their predators aren't stuffed to the gills, and the food supply in those months are what limits the predator population.

@bshane That definitely makes sense for the cicadas that all emerge and call at the same time. Do you think it still holds for crickets that call consistently throughout much of the year?

@etis re: 'being full'; formally, I should have talked about 'prey handling rate', which incorporates the rate at which predators can find, catch, handle, and digest prey. I don't think the distinction makes much difference in practice - there's still a point at which the predators just can't keep up with the sheer volume of prey.

They don't always 'get away with it'!  A study by Pascoal et al. (2014) found that field crickets (Teleogryllus oceanicus) on Oahu and Kauai islands of Hawaii have lost the ability to produce sound after an invasive wasp that is acoustically oriented to prey was introduced to the islands within this century. There are a few mutation to the crickets' wing morphology that produces "flat wings" that cannot make sound. Ordinarily, this mutation would reduce fitness through a reduction in competition for attracting mates. However, the selection pressure from the wasp caused independent mutations for flat winds to sweep through the island to the point that the Kauai population was 96% flat wing.
This example illustrates that the deciding factor between 'getting away' with producing so much noise comes down to the selection balance of attracting more mates or attracting more predators.
Reference:
Pascoal, S., Cezard, T., Eik-Nes, A., Gharbi, K., Majewska, J., Payne, E., … Bailey, N. W. (2014). Rapid convergent evolution in wild crickets. Current Biology: CB, 24(12), 1369–1374.


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What are the chances that Tyrannosaurus Rex could roar?
Tyrannosaurus Rex is now thought to have possibly had lips. Less of chance of it roar though I was told by a friend just because there are birds doesn’t mean they can’t.
Evolution isn't linear, just because one branch of a tree could/couldn't do something, doesn't mean 70+ million years later descendants could/couldn't do it too?

there's info on that here. https://www.washingtonpost.com/news/morning-mix/wp/2016/07/12/think-dinosaurs-roared-like-in-jurassic-park-the-truth-new-research-says-is-a-bit-wimpier/?utm_term=.868191bc02b2 The thoracic musculature uses bones that describe some kind of roar power if it is present.

birds and crocs can't that's called bracketing, which is not definitive but a good indicator.

Careful now: T Rex was not a bird, it was a non-avian theropod. Birds are dinosaurs but not all dinosaurs are birds. In the same way, tigers are cats but not all cats are tigers.
The argument that T Rex could not roar is not only based on none of its closest relatives being able to as you seem to indicate. Dinosaurs (and by extension birds) are archosaurs, a clade that includes crocodilians too and crocodilians are quite a bit more close to the basal form of archosaurs than T Rex was. Crocodilians can only sort of "hiss", not roar in the colloquial sense. And birds cannot roar. This is a decent start to a thought process but this isn't really the argument for why dinosaurs likely didn't roar in the past.
Researchers who have studied the potential vocalizations of prehistoric, non-avian dinosaurs have found indications that similar closed-mouth vocalization to those found in other living archosaurs are very probable: https://news.utexas.edu/2016/07/11/dinosaurs-may-have-cooed-like-doves
Closed-mouth vocalization is not really compatible with what people typically think of as roaring. It still allows a variety of sounds that don't necessarily (though perhaps probably) somewhat resembled crocodialian or simple bird vocalizations. So no, it's not impossible that some non-avian dinosaurs could roar but the current state of our knowledge is that they very likely could not.

so you are saying they couldn't roar at all since u say they could not in the end :(

I'm not claiming that they definitely could not. I'm saying that the current scientific consensus seems to be that they probably could not.

I guess they couldn't :(

Of course you have to ask yourself, if you scale a goose honk up to t-rex size, how different is it really from a roar.

a cooing T-rex :-)

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Can someone help me identify this spider?
Can someone help me identify this spider? Saw it in Malawi; aprox. 5 to 6 cm. Seems like a Solifugae but I cannot go any further... I thank you in advance!

That is a sun spider. It is in the order Solifugae, family Solpugidae. I don't know the species. Looks like genus Zeria.

Just to make it clear - although Solifugids are arachnids, they are not spiders.  Those big heavy 'pincers' in front of the face are the useful ID factor.  They are not venomous (as far as I know), but the pincers can give you quite a nip, like a crab or lobster.

According to museum.wa.gov.au, there are four solifugid species in Malawi. Ceroma johnstonii, Ceroma zomba, Zeria niassa and Zeria paludicola.
Ceroma johnstonii has a grayish-brown tint, not the dark brown, almost black coloration (and red) of your solifugid. Ceroma zomba is only 8 mm in length, much too small even if your estimate of 50-60 mm was referring to the legspan.
Zeria niassa is only 24-28 mm in body length, significantly smaller than what you saw unless you meant legspan. Zeria paludicola is also smaller than your 50-60 mm estimate, so it must have been the legspan, not the length. The only photo I could find of any Zeria species is from eol.org and is of an unspecified species. In the photo, it has a dark brown coloration and a very faint tinge of red on the side of the abdomen.

So your image is either of Zeria niassa or Zeria paludicola.

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Does imprinting occur at different life stages?
For example, consider the offspring of a bird species. Can offspring get imprinted by other individuals of the same population at various life stages (e.g., hatchling, nestling, fledgeling, juvenile)?
If you have any literature, please send the links.


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For which taxonomic levels are xylotomical, embryological, and palynological evidence each most useful in determining species relationships?
From the 2010 USABO Semi:

In plant systematics, three
  lines of evidence may be useful in determining relationships; xylotomical (wood anatomy),
  embryological and palynological. Match these three with the level for which they are most
  useful.

The options for the levels were order, family, and genus. The answers matched xylotomy to genus, embryology to order and family, and palynological to genus, but if anybody could provide some examples to explain that would be great. Thanks!

Do you have any initial ideas yourself about the given answers, as a starting point?


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Is this Indian snake venomous?
I found this snake near a small garden.
Location: India (Hyderabad, south India)
Temperature: 38 oC
Humidity: 28%
Time: 2 hours past noon (2PM).
Similar snake was found in drainage of our locality.

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Why haven't prey evolved the ability to always outrun their predators?
I can understand why some prey can't outrun a recently evolved species. However, since cheetahs have existed for so long, why haven't its prey evolved to always outrun it, driving cheetahs to extinction. Is it because the cheetah population size is so much smaller than the population size of most of its prey species that its prey species are under very weak natural selection to outrun cheetahs? Is it that those that can run faster have more other biological costly traits?

what will stop predators to evolve to always catch their prey?

There are limits to how fast a given animal can go.  Prey also tend not to run in straight lines so there are many ways to improve via evolution.... there are no supersonic animals for instance!

For further reading check out the Red Queen Hypothesis

An alternative (facetious) question: "Why haven't they evolved wings to just fly away?" I've marked this question as a duplicate of "If a trait would be advantageous to an organism then why hasn't it evolved yet?"

What prevents predator overpopulation? explains the dynamic between preys and predators in absence of evolution. That may interest you.

Just remember, not all prey are at their peak physical fitness all the time. Just because a cheetah caught one one doesn't mean it could have caught any. In other words, perhaps all prey actually can out run a cheetah, but not when they: are sick, pregnant, juvenile, in the middle of taking a dump, half asleep, critically dehydrated, in unfamiliar territory etc... What I'm getting at is that your assumption that "caught and eaten" = "can't out run a cheetah" is not necessarily accurate

The same way, if prey "evolved" to always outrun their predators... the predators would simply start attacking their young, who can't outrun them yet. Which actually happens all the time, so prey animals "learned" to protect their young (e.g. herding). Running faster doesn't help you protect your children - and prey animals who run away while letting their children get eaten don't pass their traits on future generations.

They don't have to outrun their predators, they just have to outrun their friends!

@James Before I read your comment I was going to reply with "Of course they've evolved, we have birds don't we?", in jest of course :)

If prey were never caught by their predators then they would not have predators. The question is essentially meaningless if taken literally (e.g. "always").

predators cull the week from the herd, allowing the strong increased access to food and mates. while unfortunate for the eaten animal, it is beneficial to the long term success of the species. and that is all your genes care about.

I have decided not to vote to close: much of the material is covered in the duplicate but this question also relies heavily on co-evolutionary arms races which is not covered in the other question.

"Evolution is a journey, not a destination."  In other words, they're working on it; give them time.  (Meanwhile, they're hoping cheetah's don't evolve jetpacks.  Although I'm not, because cheetahs with jetpacks are cool.)

can't believe this question got 6 answers. People need hobbies

@aaaaaa Or some predators chasing them away from their computers.

The main thing to get is that there is no end game for evolution. (and that its not a competition) Its an ongoing process of species adapting to changing circumstances.

Maybe the preadator prey system is an evolutionary stable strategy. There's a biological cost for the prey running away faster because doing so burns more energy and it's not definite that it will get eaten if it doesn't. If the preadator population size is larger, the prey evolve to run away faster because they need less risk of being eaten on each chase in order to survive and reproduce and that reduces the preadator population size.

I think this might actually be an unsolved problem. None of the answers fully explain why they don't always outrun their predators. Ell's answer doesn't explain why the cheetah and gazelle system appears to be stable without gazelles evolving to be even faster at running away. Surely some people are so smart that they could actually figure out the answer to this question.

There are (at least) three important factors to consider here; evolution under selection requires genetic variation upon which to act, selection can act on covarying traits causing trade-offs, and adaptation also occurs in the predator. A lot of this is covered elsewhere on this site (including the effects of the other mechanisms of evolution), but little specific reference is made to predator-prey co-evolution.
Adaptation and genetic variance
One of the mechanisms of evolution is selection, and adaptation occurs when species evolve as a response to selection. For a response to selection to occur there must be genetic variation within the trait, such that the genes an individual carries affect the individuals fitness. For example, there may some genes which give the carrier better muscle structure for fast running, and this increases survival which, in turn, increases reproductive output. The importance of genetic variation is often overlooked, but is highlighted by the breeders equation. Genetic variance can arise by novel mutations, or can exist as standing genetic variance.
Selection on covarying traits
Selection is seldom, if ever, a univariate process. That means fitness is not determined by a single characteristic, so fitness in a prey species may be determined by the speed at which it can run, but also its metabolic rate, stamina, ability to acquire nutrients, the way it provisions nutrients for growth and repair etc.. Genetic covariance between traits (induced by linkage or pleiotropy) can impact the response to selection, because any selection acting on a covarying trait can cause affect the adaptation occurring in the focal trait (strengthening, weakening, neutralising, or even reversing the direction of response). Therefore, if running speed covaries with other traits it may be difficult for selection to increase running speed. Think about athletes, I doubt Usain Bolt could run 10,000 metres as fast as Mo Farah and vice versa, because there is a trade-off between speed and stamina.
Adaptation in other species
If selection did cause speed to increase in the prey species then that would strengthen selection for increased speed in the predator. This is called an evolutionary arms race, where the adaptive the evolution of two species interacts causing adaptation and counter-adaptation. For example, genes which allow faster running might spread through a population of gazelles (prey) because carriers are more likely to outrun the lion (or the other gazelles), but this will increase selection on lions (predator) to increase speed (or adopt other strategies) which will spread genes to make the lions faster (use other strategies); the result being adaptation and counter-adaptation between the gazelle and lion populations.

There is a little series here about Butch Brodie and his studies of coevolutionary arms races between garter snakes and toxic newts. It would be good to read on the Red Queen Hypothesis, which describes how species, under interaction with other species, must continue to evolve just to prevent extinction. Also worth noting that prey species often have more than one predator species (and predator species often have more than one prey); interaction and coevolutionary networks are complex. What may be adaptive in some interactions may also be maladaptive for other interactions (see specialist and generalist, and selection on covarying traits).

Good answer, but for readability I would restructure it and put the arms race/RQH parts at the top, since those issues are most targetted to this particular question. Genetic variation and covariation/trade offs are always an issue in evolution, but more general than the coevolution between predators and prey.

Maybe it would. I put it this way around to introduce the concept of adaptation as a response to selection first before talking about how subsequent adaptation can affect selection in other species. I also put the comment at the start regarding predator-prey co-evolution to highlight it's importance from the outset.

Assuming the animal books I read as a child didn’t lie to me, the peregrine falcon and pigeon might be a rather insightful example of an arms race, since (the book asserted) the two birds’ body shapes are similar because the shape is well-adapted to high speed, and the peregrine falcon is so fast because of its constant need to maintain a speed advantage over pigeons. (That factoid really captured my interest and has stuck with me, so here I am rather confident that if incorrect, it is the book’s fault and not my memory’s. :P)

When looking at what's evolutionarily favorable, you need to keep in mind that predator-prey relationships are rarely a simple binary.  For example, evolving speed to out-sprint the lion won't help if you're being chased by a human who will keep pursuing until you drop from exhaustion.

The snake / newt arms race was the first thing I thought of when I read the question.

I don't understand why it seems like the cheetah and gazelle system is stable and gazelles aren't evolving to run away even faster. Do you know a more detailed answer of the different reasons a prey species gets eaten by predators as often as it does? If so, can you edit your answer to explain it?

There are two reasons for this: evolutionary trade-offs and coevolution (the "Red Queen hypothesis", as mentioned in the comment above by Luigi).
Evolutionary trade-off describes situations where one trait cannot increase without a decrease in one or more others. Some hypothetical examples:

longer legs may help run faster, but past a certain point, it will increase the risk of injury, decreasing survival;
lower body weight may increase top speed, but past a certain point, it will decrease starvation tolerance;
more muscle may help acceleration but will increase energy requirements.

All changes have costs and benefits. In situations where the outcome of an event is simply "success/failure", there is therefore an evolutionary incentive to evolve to be just good enough. Once you are good enough getting better only increases the cost (I am oversimplifying this a bit).
Change in an extrinsic driver will change the balance of cost and benefit, shifting evolutionary pressure. For example, when predators are absent (island populations) birds sometimes become flightless, because one benefit of flight (escape from predators) no longer applies.
The interesting bit happens when the "extrinsic driver" is another living thing that is also capable of evolving. In this case you suddenly get an evolutionary arms race where each side is constantly subject to a selective pressure to be slightly better than the other, which is a moving target. You therefore get an arms race situation (or the extinction of one or the other side). The Red Queen hypothesis is named after a quote by the Red Queen in "Alice through the looking glass" (Carroll, 1871):

Now, here, you see, it takes all the running you can do, to keep in
  the same place.

Using the example of a lion and a gazelle: lions run fast enough to catch and eat the slowest gazelles. The remaining gazelles are on average faster, for whatever reason(s). Some of those reasons will be heritable and the next generation of gazelles will be faster. The slowest lions will starve, and some of the reasons for the remaining lions being faster will be heritable so the next generation will be a bit faster, and then you're back where you started. Rinse and repeat.
Predation obviously operates on a much faster timescale than selection, so this doesn't always occur (putting a fox in a chicken coop won't evolve fast chickens).
Coevolutionary "arms races" can be seen in predator-prey interactions, mimicry and much more (including for example the evolution of sex, but that's off-topic for this answer).

I would use the leopard as an example which actually is fully in this arms race.

To what extend would e.g. a 5% increase in the speed of all the gazelles in an area affect predation?  I would think that in many cases, the primary limiting factor on the speed of animals caught by lions is the speed of the slowest prey animal.  Once the lion has caught the slowest animal, the remaining animals will be safe from that lion for awhile.  Unless a species gets fast enough to outrun some other prey species, it's unlikely to get fast enough for all its members to outrun predators.

@supercat:  the old joke, I don't need to outrun the bear, I just need to outrun you.

Predators always have to be much better hunters than the prey - they must eat every few days after all. But they can only get so good.
Predator/prey population balance will tend to look like a competition where if the predators are too efficient they will kill off the prey.  If that happens they start to starve to death.
If the prey outrun the predators (or at least escape all the time) then the predators will starve to death.  Then they breed until there are so many that they eat all the grass/vegetation and then they die off.
While both of these have certainly happened in natural history what is more stable for predators and prey to evolve in competition with each other such that their populations look like a stable equilibrium. If not, one of the would just disappear.  Then later via migration another animal would come in to replace them.

The first paragraph sounds a little wrong and seems to contradict the so called "life-dinner principle".


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Can viruses be toxic?
Bacteria can produce toxins like endotoxins and exotoxins. In diseases like cholera or tetanus they can harm infected people due to these toxins.
Now, although viruses are much smaller and are dependent on the host cell for their production, are there DNA sequences in viruses which can produce similar toxins, or are viruses made of something that is toxic?
If not, can viruses be seen as causing an allergic reaction because like common allergies they don't harm directly, only our immune system generates the problems?

In general, DNA that encodes toxins can be incorporated in a viral genome and thus it can be expressed in the infected host inducing toxicity.
Here an example: http://www.sciencedirect.com/science/article/pii/S1438422104000542
Also, viruses can trigger allergic reactions (http://www.ncbi.nlm.nih.gov/pubmed/21980825) or promote them (http://erj.ersjournals.com/content/19/2/341).
Finally, there are some reports about viruses causing "with symptoms that mimic allergies" (https://www.youtube.com/watch?v=iDF07R1XHSk)

"The genes encoding Stx are encoded in the genome of heterogeneous lambdoid prophages (Stx-converting bacteriophages; Stx-phages)" You say in general but is Stx the only known viral toxin? If I understood the article well it comes originally from a bacteriophage but are there also viruses that could programme our own cells by producing toxins?

@Marijn Ofc. not, there are many toxic viruses, e.g. ebola has (at least one) toxin too. http://www.ncbi.nlm.nih.gov/pubmed/15596847

In addition to @alec_djinn's answer, viruses can also indirectly be toxic by causing lysis in cells that themselves have toxic components. The presence of bacterial endotoxins in poorly filtered solutions of early attempts at phage therapy is probably the canonical example of this.

Yes viruses can import toxin encoding genes, at least in humans and in plants.
With Ebola a protein called Delta-Peptide is released in large amounts by the virus genome, and it attaches to cell walls and makes them more permeable.
it does this to the cell wall, and some researches have described it as ebola toxin.

http://jvi.asm.org/content/early/2017/05/18/JVI.00438-17
https://www.sciencedaily.com/releases/2015/01/150121103304.htm
Toxin from a maize virus:
http://www.sciencedirect.com/science/article/pii/0006291X87903792
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2171720/
Conversely, plants generally use alkaloids as toxins. Alkaloids are a large family of N containing organic molecules, for example those found in Datura, Angel of Death mushroom, Cyanide, etc. and I found no evidence that viruses make us produce alkaloids. Scientists research on the anti-viral abilities of some alkaloids.
Tonins in venoms are more often protein based... Tangentially to your question, here's a page on the diversity of venom toxins for background.
https://en.wikipedia.org/wiki/Venom#Diversity

In theory, there's no reason why a virus couldn't encode bacterial toxins. In practice, that doesn't happen much because viruses have no incentive to sabotage their host cells in that manner - there's largely no fitness advantage, all it would do is make the viral genome larger and shut down the host cell preventing further replication.
Even if a virus specifically wanted to shut down its host cells, it's more efficient to spawn large numbers of copies of itself and exhaust the host cell's resources.
in short:
virus produces toxins in host cell -> host cell dies -> no replication opportunity and virus gets trapped in the cell
virus produces large numbers of copies of itself -> host cell runs out of resources and dies -> numerous replications and avoid getting trapped


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Do plant and animal bacterial pathogen differ too much?
I will be involved in a plant disease produced by a bacterial pathogen, Acidovorax citrulli. I've previously worked with animal pathogens such as Haemophilus parasuis. Are there any big differences among them?
H. parasuis and A. citrulli are 2 and 4 MB genome size. What are these 2 MB extra genome size for?

What kind of differences are you expecting? Related species can have unrelated hosts. It is not very uncommon. For example Erwinia is a plant pathogen that belongs to Enterobacteriaciae which also includes Shigella, Salmonella and Escherichia. There are several Pseudomonas species that infect plants.

@WYSIWYG. I'm not looking for a special type of difference, just asking for the most obvious ones. Maybe the differ at gene level, some kind of protein or transporter. Any paper studying all this would be also useful, thanks.

you really have to narrow down your question.


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What's the composition of Actinobacteria's hyphae?
I'd like to know which chemical compounds form hyphae in Actinobacteria. Is it the same structure of the cell wall?
Thank you

Can you specify this a bit more? You want to know the single building blocks of the hyphae?

I understood that cells grow in tubular structures that form the hyphae, but i'd like to know how cells build this structure. Which are the chemical compounds that cells secrete to bulid the hyphae?
Is it clear?


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What is the name of the property of viruses that can go dormant in the host for 30 years?
The Varicella zoster virus causes chickenpox in children and shingles in adults.
It appears after the initial infection, it can go dormant in the nerve, and reactivate itself decades later.
My question is: What is the name of the property of viruses that can go dormant in the host for 30 years?

What do you mean with property? The place, where these viruses hide?

As far as I know dormancy in viruses like the above stated chicken pox virus is known as virus latency which wikipedia defines as:

The ability of a pathogenic virus to lie dormant (latent) within a cell, denoted as the lysogenic part of the viral life cycle.


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Where do mushrooms get their energy from?
I'm wondering where field mushrooms get their energy from.
I've heard that they can easily grow on soil in a dark room. So, it seems to me that there wouldn't be any photosynthesizing plants from which they could get energy. Also, as far as I know, they don't have seeds from which they could directly get energy initially.
So, I have two questions:

Where do mushrooms get their initial energy from? (The spores, if that is the right term)
Where do they get their energy from in later stages? (If there is a difference at all)

Plant-physiology is an incorrect tag because fungi aren't plants.

The difference between plants is also related to your question because plants get their energy directly from light and fungi from organic material.

Mushrooms are the fruiting bodies of fungi. Fungi get their energy by decomposing dead or decaying organic material, such as fallen leaves or dung.
Some background: spores of fungi germinate forming mycelia consisting of threadlike hyphae. When the hyphae of different fungi meet, they may have sex and form mushrooms. The mushrooms produce the spores. See https://en.wikipedia.org/wiki/Fungus.
So, each of these stages get their energy ultimately from decomposition, although the mushrooms get their energy from the mycelium. Spores rely on their internal energy storage to germinate and start decomposing. Even though spores are tiny, the have energy stored, like all cells do.

Why don't you add a link for further reading?

The Wikipedia pages on this are OK, but not really an authoritative source.

@Daan in that case, maybe alternative sources?

Add them still. Thez are accepted as sources for general topics and really helpful for further reading, especially for laymen.

Daan is right here, but there is a lack of information and someone asked for links to read more.
It's the recycling system and decomposition that are the keys to the mushroom's energy.
They simply break down organic things and absorb energy through mycelium.
Here is the full informative article on this: Where do mushrooms get their energy from?

Research mushroom " metabolism/enzymes/catabolism/respiration/glycolysis" to read nice texts of concise info for that topic.
Mushrooms use enzymes to break down cellulose and substrates into smaller substances and eventually they use CO2 for respiration, glycolysis, and ATP production.
https://books.google.fr/books?id=xmB_DYPp9LIC&pg=PA49&lpg=PA49&dq=mushroom+metabolism&source=bl&ots=mEkG_WGfaY&sig=9XAXzpPgSMHkRg_8kPjE1LIYatQ&hl=en&sa=X&ved=2ahUKEwjfwJvjmLLdAhXjx4UKHUiiA_UQ6AEwA3oECAkQAQ#v=onepage&q=mushroom%20metabolism&f=false
Cellulose is not that different from sugar and mushrooms get sugar from it using cellulase and lignase enzymes, although some mushrooms dont have cellulase. https://www.google.fr/url?sa=t&source=web&rct=j&url=https://www.researchgate.net/post/What_are_the_nutrients_required_for_the_growth_of_mushrooms_like_oyster_and_shiitake/amp&ved=2ahUKEwj4pLC3m7LdAhWRyIUKHf27DD0QFjACegQICBAB&usg=AOvVaw2b-TTVDZHQBcS8l-TMYmz0&ampcf=1
Its the digestion process is probably a complex physical absorption by the hyphae, so research hyphae structrures, they must be cool.
https://www.ck12.org/biology/fungi-nutrition/lesson/How-Fungi-Eat-BIO/


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Mangroves and desalination of sea water
I am not an expert but I guess that mangroves (or some other plants that thrive in sea water) perform some kind of desalination to extract fresh water from sea water.
Is this true? If yes, What biological mechanisms are used to remove salt from sea water?
I am interested in any research about biological desalination.

This paper might be of interest to you: https://advances.sciencemag.org/content/6/8/eaax5253.
The researchers created a synthetic mangrove that actually performs desalination, using the principles of natural mangroves.
The introduction has a good overview of the main ways mangroves desalinate saline water, namely:

Physical blockage by suberin within cells walls
Selective permeability of cell membranes in root
Negative pressure caused by evaporation that acts as hydraulic pressure to cause take-up of water by roots

All these combine to turn the mangrove into a kind of natural RO (reverse osmosis) machine.

There has been a lot of research in this field which asserts that mangroves desalinate sea water.
Scholander (1968) concludes that this process in mangroves use an ultrafiltration mechanism in the roots of the plant where membranes extract freshwater which is taken up the plant.

 Scholander, P.F., 1968. How mangroves desalinate seawater. Physiologia plantarum, 21(1), pp.251-261.


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How do fish tolerate pH changes in water?
I want to know how aquatic animals behave as a natural indicator of the acidity in lakes and rivers.
How do they tolerate these pH change?

By tolerate do you mean the mechanisms that fish have to mitigate the harmful effects of the pH change?

Often, in terms of a water body becoming acidified, it depends on the rate of acidification.  Fish and other aquatic species, such as invertebrates, are fairly resilient to miniscule changes, but they also have a threshold at which not a lot of them, adapted or no, can survive.
From the U.S. Environmental Protection Agency (http://www.epa.gov/acidrain/effects/surface_water.html):

Acid rain causes a cascade of effects that harm or kill individual fish, reduce fish population numbers, completely eliminate fish species from a waterbody, and decrease biodiversity.  Low pH [...] is directly toxic to fish. In addition, low pH and increased aluminum levels cause chronic stress that may not kill individual fish, but leads to lower body weight and smaller size and makes fish less able to compete for food and habitat.
Some types of plants and animals are able to tolerate acidic waters. Others, however, are acid-sensitive and will be lost as the pH declines.

Commonly, benthic invertebrates (including insects, crustacean and molluscs) are used as indicators for ecosystem health.  Invertebrates that need a high amount of calcium, such as crayfish (for their exoskeleton), are typically not found even in slightly acidified lakes.  Other invertebrates can be used as indicator species because they respond to changes in water conditions, such as pH.

A good example of this is the acid rain that occurred in Sudbury, Ontario, Canada as a result of sulfur dioxide emissions from mining activities, which were especially high in the 1970s.  This affected the lakes in the area not only from acid rain, but the runoff as well as there were no trees left.  The pH was so low that it effectively made all lakes in the area sterile. Since then, a lot of effort has been put into bringing back the native aquatic species, such as liming the lakes and restocking them with species such as Brook Trout (Salvelinus fontinalis).  More information can be found here:
http://link.springer.com/article/10.1007%2FBF00160348
Therefore, I do not know that aquatic animals necessarily behave a certain way as a natural indicator of acidity, however it is more of their presence or absence that biologists use to determine acidity and the overall ecosystem health in lakes and rivers.

Commonly, benthic invertebrates are used as indicators for ecosystem health. Invertebrates that need a high amount of calcium, such as crayfish are typically not found even in slightly acidified waters. Other invertebrates can be used for indicator species as they respond to changes in water conditions, such as pH.

This doesn't answer the question as it speaks of fish as indicator organisms not how they tolerate pH changes in water

This actually does attempt to answer the first part of the question, which is how acquatic animals behave as natural indicators of acidity. The answer here states that benthic invertebrates are not found in acidic water. Thus their absence may indicate acidity.


text:
Plant growth in blue light
For the past two weeks, I have been in a group of 3 studying how different lights affect plant growth. So we growth two chickpeas plants and put one in white light and the other in blue light.
These are the results:
Days    Blue light    White light
           (cm)          (cm)
__________________________________
 1          6.6           8.2
 2          8.5           9.9
 3         11.0          11.6
 6         15.8          16.0
 7         17.2          17.6
 8         18.0          18.2
 9         19.6          18.7

The blue-light plant didn't really branch out a lot whereas the white-light plant branched out a lot.
My question is:
What caused the white light plant to not grow as fast like blue;
Why did the white light plant branch out?
What I read about the second question:
Experiments with blue light resulted in plants that are wider than usual. This can be explained by reference to the fact that more flowering buds (more branches) could form by reason of diminished apical dominance at the growth point.
http://www.canna.com.au/influence_of_colours
I don't understand why the blue lights plant did not branch out a lot like the white light ones?

Hi and welcome to Bio.SE. There are a lot of factors that need to be considered here; temperature, time exposed to light, moisture, earth/fertiliser used, size of potting etc. In order to somewhat account for the variation that will be introduced even if all those factors are controlled, you will need to repeat the experiment and see if any trends emerge. For example, could we be sure of the conclusion (blue lit plants grow more than white lit plants) if we re-ran the experiment and it showed exactly the opposite was true?

With all the research I did this is my understand of why the plant that was exposed to blue light grew taller than the plant that was exposed to white light.
The results of this experiment proves the hypothesis that the plant that was exposed to the blue light will grow taller than the  plant that was exposed to white light. Chlorophyll is a green photosynthetic pigment that is found in most plants. The chlorophylls are found around pigments in the photosystem, chlorophyll helps the plant to get the right wavelength of light. There are two types of chlorophyll a and b. Chlorophyll a absorbs red and violet wavelength best, but it absorbs very little blue light. Chlorophyll b absorbs a lot of blue light. Understanding chlorophyll  b will explain why the blue plant grew taller than the white plant. It grew taller because in both of the photosystems there were more chlorophyll b then a, therefore there was a lot of pigments that absorbed the blue light and the plant was able to use the energy to produce more ATP which in the end resulted in more growth.  There were many factors that we could not control  temperature, time exposed to light, moisture, earth/fertilizer used, size of potting. In order to get an accurate result of different light affecting the growth of plants some of these factors must be implemented.
Sources:
http://scienceline.ucsb.edu/getkey.php?key=3155
Can someone Confirm if this is right?


text:
Are Pond Algae Edible for Humans?
I've been farming freshwater fishes. After some time, i found some green algae grows there. When the algae dried, it looks like nori (which commonly used for sushi wrapping).
So, i wonder if those algae edible for human. Are the algae safe to eat?
Here's the picture:

Can you advise where you are at (not an address or anything, just what state/region/country something like that)?

I live in Indonesia

If you really would like to eat it without causing you problem, your best chance would be to eat a very small amount first, get accustomed to it and gradually increase the amount you eat. Given that the pond is relatively clean :)

Looks like blanket weed (various green algae) to me.

If the fish dont, it not nutritious. Grow cress or nutritious species.

I came across a this Wikipedia page which said blue green algae from ponds can be used as dietary supplement (in tablet form).
Many other articles on the internet like  here suggest it is included in many diets in many places across the globe.
However, without proper regulation one can include a heavy metal contaminated vegetable to their diet which is detrimental to health. Furthermore cyanobacteria are known to produce toxic substances known as microcystins which can cause damage to human organs as well.
So unless you are certain of the biochemical balance of your pond I would  recommend not integrating it in your diet. Rather you can find commercially available ones which your local regulatory authority(s) recommend for dietary purposes.

First off: Don't risk it
I'm not an ecologist but I believe the type of algae you are holding tends to be cyanobacteria.
Cyanobacteria make all kinds of toxins, check the first table in this article.
Some cyanobacteria are eaten like Arthospira (commonly called spirulina) but I would not eat any random filamentous cyanobacteria. They also tend to be quite hard to digest so at best you will have increased your dietary fibre level and at worst ... well make sure your sanitary facilities have enough capacity.


text:
Is there any virus that contains both DNA and RNA in its genome?
It is known that viruses contain DNA or RNA- either one and not both.
I came across a question: Which virus contains both DNA and RNA?

RDHV virus. http://science.opposingviews.com/can-viral-genome-made-dna-rna-22901.html First google search result.

@GerganaVandova There is RNA "contamination" in genomes of complex organisms too (http://dx.doi.org/10.1038/nmeth.3259). This is said to cause genomic instability. However, this is different from what OP is asking. I am not sure if the link you mentioned is trustworthy. I generally do not believe in science blogs. My guess is that it (if it really is true) is something like a RNA contamination in DNA because of a non-selective polymerase.

Here is the real scientific paper:https://biologydirect.biomedcentral.com/articles/10.1186/1745-6150-7-13

Here is the results summary of the study that describes the discovery of DNA:RNA hybrid virus:

Results
  Bioinformatic analysis of viral metagenomic sequences derived from a hot, acidic lake revealed a circular, putatively single-stranded DNA virus encoding a major capsid protein similar to those found only in single-stranded RNA viruses. The presence and circular configuration of the complete virus genome was confirmed by inverse PCR amplification from native DNA extracted from lake sediment. The virus genome appears to be the result of a RNA-DNA recombination event between two ostensibly unrelated virus groups. Environmental sequence databases were examined for homologous genes arranged in similar configurations and three similar putative virus genomes from marine environments were identified. This result indicates the existence of a widespread but previously undetected group of viruses.

And here is the link to the paper:
https://biologydirect.biomedcentral.com/articles/10.1186/1745-6150-7-13

Please forgive me if I'm missing something, but that group of viruses are still only DNA-containing. "...group of circovirus-like DNA genomes whose common ancestor appears to have incorporated a capsid protein (CP) gene known previously only in RNA viruses." They do not have both DNA and RNA; just very strong similarities to a group of RNA viruses. The OP asked if there were/are viruses containing both DNA and RNA. How does this definitively answer the OP's question?

@anongoodnurse. You are correct, these viruses contain only DNA as their genetic material. But they also contain this capsid protein found exclusively in RNA viruses. So technically, yes, it is a DNA virus. Evolutionary, it is probably a DNA:RNA hybrid virus.

Can modified vaccinia virus be considered as an RDHV? http://www.ncbi.nlm.nih.gov/pmc/articles/PMC189881/

Hepatitis B virus (and other hepadnaviruses) have mainly double-stranded DNA genomes, but include a short piece of RNA

Genome: The HBV virion genome is circular and approximately 3.2 kb in size and consists of DNA that is mostly double stranded. ... The other strand, the plus strand, is variable in length, but has less than unit length, and has an RNA oligonucleotide at its 5' end.

--What is HBV?

Unlike others, HBV virions contain both DNA and RNA. Moreover, some regions of the packaged genome can be single stranded, double stranded, or even triple stranded. These peculiar features are a direct result of the HBV genome replication mechanism which will be covered later in this chapter.

--Robert's HBV Page
However, this is just a short piece of RNA that's used to prime genomic replication.

Most virions have either RNA or DNA - never both. The exception to this rule is human cytomegalovirus (HCMV). In 2000, researchers reported that although HCMV contains mainly DNA, it also carries four pieces of RNA that are used to synthesize viral proteins.
Microbiology: An Introduction.
Barry L. Batzing

Can you add a link or an excerpt from the book that really says this?


text:
What do red ants secrete while marching in a line, one after the other?
Red ants often move in a group, and seem to follow a trail one after the other.
Once, I rubbed a part of the path along which they were moving and surprisingly found that the successive ants roaming around the rubbed region became confused as to where to go. It seems that the preceding ants secrete some kind of chemical (hormones, excretory wastes or body secretions) which guide the other ants to follow it. What is this secretion?

Possible duplicate of https://biology.stackexchange.com/questions/56654/how-do-ants-follow-each-other

The simple answer is that ants secrete a substance called trail pheromone as they forage for food and each ant follows the trail of trail pheromone that is laid down by the preceding ant.
The term 'trail pheromone' can be a bit indistinct, however. Rather than consisting of a single chemical, trail pheromone is composed of many different chemicals, the exact compositions of which appear to be used deliberately to deliver complex information about the details of a given foraging site.
In the linked paper, the authors suggest that the

use of several trail pheromones that differ in their persistence
  provides memory over differing time scales. In particular, a
  non-volatile pheromone can provide a longer-term memory, while a
  volatile pheromone can allow rapid choice among potential feeding
  locations by quickly ‘forgetting’ depleted locations.

This means that ants may be able to use pheromones to assemble a sort of "collective memory" for the colony, concerning the locations of food and the quantity of food found at each location.

Do all the ants marching secrete this 'trail pheromone'?

From what I've read, most ants secrete 'trail pheromone', but can vary the chemicals that are in each secretion of trail pheromone, to tailor it to their particular need.


text:
How does having spare receptors change ED50 in an irreversible agonist
Competitive antagonists increase the ED50 while the Emax remains the same. Irreversible antagonists do not change the ED50 while decreases the Emax.
Katzung pharmacology, says that the irreversible antagonist may change the ED50 when spare receptors are present. How is that? What difference would it make? Could anyone explain the change graphically?
Spare receptors are said to be present when the Kd (dissociation constant, from the drug-receptor binding curve) is more than the ED50 (from the dose-response curve). This may happen due to

prolonged effect of a drug-receptor interaction or
when the receptors are actually in excess of the drug

ED50 = effective dose at 50% of maximum effect, Kd = Dissociation constant.

Irreversible antagonism is like removing receptors.
If there are spare receptors, maximum effect, or any effect level, can be recovered with more ligand (because displacing the irreversible ligand is not necessary, when there are other sites to fill).
$$K_D = \frac{R*L}{RL}$$
A given effect level corresponds to a given $RL$, but with less receptor $R$ available, more ligand $L$ is needed. That is by definition a change in ED50.
If you have no spare receptor (or there is enough antagonist to prevent full effect even with spare receptors), then maximum effect cannot be recovered. There is a new Emax, lower than without antagonist; but without shifting the dose-response curve to the right.
Here is an example in Rang&Dale (8th ed., p. 12, fig 2.6). Curves are labelled with time of incubation with a given quantity of irreversible inhibitor, that is equivalent to varying concentration of irreversible inhibitor at steady state. First two show the situation with spare receptors, and last two show what happens when the original Emax cannot be reached because there are not enough receptors left to elicit maximum response.


text:
Are there bacteria that respire anaerobically in aerobic conditions?
There are facultative anaerobic bacteria that switch to anaerobic respiration in an anaerobic state, but are there any organisms that would still perform anaerobic respiration even when shifted to aerobic conditions? Obligate anaerobes would die when introduced to an aerobic condition right? Are there any which can survive?
This doubt came into my mind while reading the Hugh-Leifson Oxidative Fermentative test. Such a bacterium would be read false positive for oxidisers in such a case because it would ferment glucose even in aerobic conditions.

There are aerotolerant anaerobes.

Are there any organisms that would still perform anaerobic respiration even when shifted to aerobic conditions?

Yes, there are. They are called aerotolerant anaerobes as shown in this figure on tube 5. In the thioglycollate broth, growth is seen throughout the length of the tube
Legend

Obligate aerobe
Obligate anaerobe
Facultative anaerobe
Microaerophilic
Aerotolerant anaerobes

Are there any which can survive?

Obligate anaerobes wouldn't survive in aerobic conditions. Hence they are named so.

Such a bacterium would be read false positive for oxidizers in such a case because it would ferment glucose even in aerobic conditions.

The thioglycollate broth shown here is used to differentiate bacteria into the above said criteria. The Hugh-Liefson test does'nt do that. You can not conclude that a bacteria is aerobic or anaerobic using that test. The H-L test, is interpreted in two ways.

Fermentative - When both the closed tube and open tube show a colour change
Oxidative - Colour change only in the open tube

In short, the words aerobic/anaerobic are not used to interpret the H-L test. But we can draw parallels.

Obligate aerobe - Open tube (+), Closed tube (-) - Oxidative
Obligate anaerobe- Open tube (+ at bottom), Closed tube (+) - Fermentative
Facultative anaerobe- Open tube (+), Closed tube (+) - Fermentative
Microaerophilic- Open tube (+), Closed tube (-) - Oxidative
Aerotolerant anaerobes- Open tube (+), Closed tube (+) - Fermentative

Yes, for example bacteria that perform lactic acid fermentation are anaerobic but aerotolerant.

Welcome to BiologySE! do you think you could put some references into your answer? we always appreciate cited references - and it will increase the value of your answer (by allowing others to read more if interested).

Sorry, I'm new here. Which kind of reference would you prefer? you can find infos about lactic acid bacteria and their fermentation in Brock "biology of microorganisms"'s book.


text:
What is the rationale behind IgM being the default antibody?
I know that the$\ C _\mu $ gene appears first in line for class switching and hence the IgM is the default antibody. But what is the rationale for it being so? There must be some advantage (evolutionary?) of having the IgM first in line over the IgG or so on.
The IgM is different from the IgG in being a cluster of five, better agglutination, having more avidity, and more cross reactivity (correct me if any of these is wrong). How do these properties help in containing the infection only for the very first time? Or, why is the IgG is not good for the initial response?

The answer is that the Cµ-C∆ locus is expressed in the precursor B-Cells. It is only after the B-cell has produced a functional B-cell receptor and has receive the proper stimulation from cytokines do you get transcription through the other constant chain loci, which then allows class switch recombination to occur.

When the Naive B cell gets activated and begins to secrete antibodies the affinity of the antibodies is low, as it hasn't yet gone through several cycles of affinity maturation. The increased avidity of the IgM balances the decreased affinity of these initial antibodies. If IgG were released at this stage, the body would have a much lower immune reaction to the antigen.
However after affinity maturation, the IgG has sufficient avidity and affinity to mount a stronger immune reaction than the initial IgM antibodies. If the body still produced IgM after affinity maturation, there would likely be a significant amount of crosslinking. This could potentially cause aggregates to form in the blood/lymph which could cause occlusions.
Edits:

If the affinity of the antigen-binding sites in an IgG and an IgM molecule is the same, the IgM molecule (with 10 binding sites) will have a much greater avidity for a multivalent antigen than an IgG molecule (which has two binding sites). This difference in avidity, often 10^4-fold or more, is important because antibodies produced early in an immune response usually have much lower affinities than those produced later. Because of its high total avidity, IgM—the major Ig class produced early in immune responses—can function effectively even when each of its binding sites has only a low affinity.

Molecular Biology of the Cell
The claim on aggregation after affinity maturation is speculation based on the crosslinking that occurs with IgA antibodies (e.g. Phlegm) when there are only two high-affinity Ig molecules joined together rather than five.

Thanks! Could you add a reference for your answer. I'd then mark it answered. :)

I do not really think this answers the question of Why IgM is the default antibody.

You are sort of explaining the rational behind Somatic Hypermutation, but not that well... The correct way to answer the question is to leave out the variable chain discussion altogether and explain the myeloid developmental program with regard to the Heavy-Chain Constant region and then discuss Class Switch Recombination in mature B cells.

Well, it answers my doubts! I know the heavy chain order in the gene. I wanted to know why it is that way. @AMR

@Polisetty The avidity / affinity of the variable regions of the light and heavy chains of the immunoglobulin provides no insight into the order of the constant region of the heavy chain. Deficiencies, such as Hyper-IgM syndrome are related to defects in cell signaling. That alone should tell you that the reason for IgM being first is the result of the developmental state of the cell and the signals that it receives, which in turn control the Transcription Factors that bind to the locus and express Cµ instead of the other loci. You can also have SIgM disorders, which you can look up.


text:
Why is it always Sodium that we talk of in blood pressure?
Why is that we emphasize so much on sodium in blood pressure? I understand that it is a major extracellular ion, but, it also is tightly regulated. So when something is that tightly regulated, won't small concentrations of the potassium matter? And what about the chloride and bicarb? They are all there in the blood in comparable quantities but we never talk of their osmotic importance. Sodium retention and blood pressure - why not chloride retention?
Is it not required (like calculating sodium includes them too)?
or is it that they actually don't matter?
Also aldosterone, we conserve the sodium but aren't we pushing out potassium? Potassium also is an ion with oncotic activity right? Why is Natriuresis so important why not say, Chloriuresis?
So all in all, why does sodium steal the limelight?

The key is in fluid compartments and osmotic activity. For the purposes of this discussion, let us say that there are two fluid compartments the ExtraCellular Fluid (ECF) and IntraCellular Fluid (ICF). Only the ECF contributes to blood volume and blood pressure.
Na is not only the major ECF ion, but it is also confined there. The ICF concentration of Na is much lower than in the ECF, and it is continuously, invariably and actively kept out of the ICF. In other words, the vast majority of ingested Na ends up in the ECF, and drag the associated amount of water (ie volume, thereby increasing blood pressure). It is the opposite for K, which is mainly in the ICF. As for Cl, it is more or less equal in the ICF and ECF, and is allowed to move freely between them, meaning that you need to ingest twice as much as a given amount of Na for a similar effect on volume distribution. Bicarb is a minor ion, and moves freely between compartments. These are the reasons why, clinically, if someone is hypovolemic (ie dehydrated, losing blood) they are given a sodium based fluid or a protein based fluid (colloid), because both will drag volume and stay in the ECF.
As for the other part of your question, isn't it tightly regulated? Yes, but extra sodium takes some time to get excreted (much less than 1% of sodium that goes through the kidneys is excreted). In other words, any extra sodium (i.e. extra volume as we have established) will stay there for some time, and if you are continually having high sodium meals, every day, you will walk around with extra sodium most of the time. Therefore, your blood pressure will be higher than it would be, if your diet was lower in sodium.
So, no, sodium is not stealing the spotlight from anyone when it comes to ECF. But the other ions have their glory under other spotlights.


text:
Wouldn't a non-poisonous variety of a mutant plant be at selective advantage?
I don't know much of evolutionary biology, but when someone asked, this seemed very much plausible to me.
Say there's a mutant plant, that produces much lesser toxin than its usual counterparts (same species). Then, wouldn't this plant be at a selective advantage over the others, since the predators (here, herbivores) wouldn't consume it assuming it to be poisonous. But sowly, as these mutants increase in number, the herbivores too realize and start feasting on them. Again selecting out ones with more toxin. Ultimately reaching some kind of equilibrium (?)
Is this phenomenon(?) called something? Is it similar to the selection that occurs in the  sickle cell trait? Are there real examples with plants with toxins showing this?

By "sickle cell thing", do you mean sickle-cell anemia?

@Harris Weinstein yup. Will edit it to be a bit more formal there.

Your question is very sensible; we would indeed expect this kind of negative frequency-dependent selection: i.e., if toxin-producing plants are common, non-toxin-producing plants should gain an advantage because they don't pay the costs of producing toxins but they do (or may) gain an advantage from herbivore deterrence. (Conversely, if toxin-producing plants are rare, they could gain an individual-level benefit by being the only ones in the population to deter herbivores.)
As of 2007, however, it seems that the empirical evidence for this phenomenon was pretty weak. In the following, "resistant genotypes" means genotypes that have some kind of anti-herbivore trait (typically production of secondary compounds that deter herbivory) [emphasis added]:

... Only a few studies have examined the role of frequency-dependent selection on plant defenses against herbivory (i.e., Berenbaum & Zangerl 1998, Roy 1998, Siemens & Roy 2005). ...  No study has manipulated the frequency of resistant/tolerant host genotypes explicitly to examine if the evolution of plant defensive strategies is subject to frequency-dependent selection. However, some studies tested some of the predictions of the frequency-dependence selection hypothesis (Berenbaum & Zangerl 1998, Roy 1998).
The study by Berenbaum and Zangerl (1998) found that in Pastinaca sativa, the range of variation in the level of a resistance component (coumarin) against its consumer Depressaria pastinacella did not change from 1873 to present, suggesting a cyclical dynamic promoted by frequency-dependent selection. In a reciprocal transplant experiment Roy (1998) did not find evidence that common hosts are eaten more and have lower fitness than rare hosts.  In a recent paper, Siemens and Roy (2005) evaluated the following: (a) if the amount of damage experienced by the most common host genotype was higher than that expected by its frequency, and the amount of damage experienced by the most rare host genotypes was lower than that expected by its frequency (assortative damage hypothesis); (b) if the most common host
genotype had higher levels of damage and lower average fitness compared with the more rare host genotypes; and (c) if the amount of damage correlated positively with the frequency of the most common host genotype. ... Unfortunately, their results provide little support for the hypothesis of frequency-dependent selection acting on plant defenses against herbivory.
... Although two studies have explored the potential for
frequency-dependent selection on plant resistance, no study has yet
examined this possibility on plant tolerance. Before
frequency-dependent selection can be put aside as an explanation of
the maintenance of variation on tolerance and resistance, explicit
experimental tests of the hypothesis are required.

(I haven't followed up the more recent literature to see if there is more recent evidence ...)
There is a related phenomenon that's much better documented: toxin-producing bacteria produce antibiotics to kill other bacteria of their own and other species, to minimize competition for resources. In "rock-paper-scissors" systems (2), cheaters (bacteria that are resistant to toxin but don't produce it themselves) invade toxin producers; then non-resistant bacteria invade the cheaters (because there's no toxin being produced any more); then toxin producers reinvade (because nobody's resistant any more, so there is once again an advantage to producing toxin).
I would say that the connection between this type of frequency-dependent selection and the selection that maintains polymorphism for the sickle-cell allele is loose. Sickle-cell is usually cited as an example of heterozygote advantage. It is loosely speaking a form of negative frequency-dependent selection at the level of alleles rather than genotypes; a gamete carrying a sickle-cell allele is more likely to end up in a heterozygote (and thus gain an advantage via malaria resistance) when it's rare and more likely to end up in a homozygote (and lose fitness due to sickle-cell disease) when it's common. It's also theoretically possible (although I haven't seen it discussed, and I would guess that it's not very important in practice) that increasing frequency of sickle-cell heterozygotes could also feed back at the population level to reduce the incidence of malaria, lower the advantage of resistance, and hence generate a more analogous form of negative frequency dependent selection.

Núñez-Farfán et al. "The Evolution of Resistance and Tolerance to Herbivores", Annual Review of Ecology, Evolution, and Systematics, Vol. 38 (2007), pp. 541-566 http://www.jstor.org/stable/30033871
Kirkup and Riley, "Antibiotic-mediated antagonism leads to a bacterial game of rock–paper–scissors in vivo", Nature 428, 412-414 (25 March 2004) .

This is called mimicry:

In evolutionary biology, mimicry is a similarity of one organism, usually an animal, to another that has evolved because the resemblance is selectively favoured by the behaviour of a shared signal receiver that can respond to both.

and yes, plants can do it, in multiple ways.

In evolutionary biology, mimicry in plants are several forms of mimicry, such as Bakerian mimicry, Dodsonian mimicry and Vavilovian mimicry, of other organisms by plants, most commonly flowers.

I don't have any particular knowledge of the equilibrium cycle you mentioned, though it seems hypothetically possible (no comment on the likelihood of it). If the cost saved from not producing the toxin is more advantageous than having the toxin itself, the new strain might have an advantage.

But isnt mimicry with two different species?

Ah, I missed the part about it being one species. Conceptually, I wouldn't say it's a huge distinction, though, since it's one organism deceiving others into thinking it's a more dangerous organism. I'll look into if there's a more specific term for the same-species case, though.


text:
Derivation for drug half life
The formula in textbooks for $t_{\frac{1}{2}}$ of a drug following first order elimination is generally given as $$t_{\frac{1}{2}}= \frac {\ln(2).V_d}{Cl}$$where $V_d$ is the volume of distribution and $Cl$ is the clearance.
Shown below is my attempt to derive the formula but I don't know where I'm going wrong.
Assuming first order kinetics of elimination, the rate of elimination ($R$) would be proportional to the plasma concentration ($Cp$)
$$ R = Cp . k$$
Where $k$ is the rate constant.
For calculation of $t_{\frac{1}{2}}$, since this is a first order elimination, $$ t_{\frac{1}{2}} = \ln(2)/k$$
Substituting,
$$ t_{\frac{1}{2}} = \frac{\ln(2).Cp}{R}$$
Since $ Cl = R/Cp$, substituting would give,
$$ t_{\frac{1}{2}} = \ln(2)/Cl$$
Since both the formulae don't match (this one doesn't have a $V_d$ term at all!), where have I gone wrong? Also then how is $Cl$ different from $k$?
According to the correct formula, $k=Cl/V_d$. How is that so?
EDIT
Volume of distribution is the apparent volume of blood the drug takes up and is given by $$V_d = \frac {Dose}{Pc}$$
Clearance is the volume of blood that has been cleared of the drug in unit time and is given by $ Cl = R/Cp$
Correct me if the basic definitions themselves are wrong.

Should this be asked in chemistry?

Can you define the terms, "distribution volume" and "clearance"? The problem certainly has to do with the way you have defined these terms.

$Cl = R/Cp$ seems incorrect. Cl unit is $volume \cdot time^{-1}$, R is $weight \cdot volume^{-1} \cdot time^{-1}$ , Cp is $weight \cdot volume^{-1}$. R/Cp is $time^{-1}$ which is imcompatible with Cl.

Well, $Cl = R/Cp$ is correct, but $R$ is not $Cp \cdot k$.
Given $X(t)$, the actual quantity (ie weight or moles) of drug in the system, $R$ should have the dimension of $\frac{dX(t)}{dt}$, that is $weight \cdot time^{-1}$ or $mole \cdot time^{-1}$ because the base definition of clearance is given by $$- \frac{dX(t)}{dt} = Cl \cdot C(t)$$.
The volume of distribution $Vd$ comes into play when converting from $X(t)$ to $C(t)$. Following the same steps as you did :
$$ R = \frac{dX(t)}{dt} = \frac{dC(t)}{dt} * Vd = C_p  \cdot k \cdot V_d$$
because (due to 1st order kinetics)
$$\frac{dC(t)}{dt} = Cp \cdot k$$

Substituting,
  $$ t_{\frac{1}{2}} = \frac{\ln(2)}{k}$$
  $$ t_{\frac{1}{2}} = \frac{\ln(2) \cdot C_p \cdot V_d}{R}$$
  Since $ Cl = \frac{R}{Cp}$, substituting would give,
  $$ t_{\frac{1}{2}} = \ln(2) \cdot \frac{1}{Cl}  \cdot V_d$$
  $$ Cl = \ln(2) \cdot \frac{1}{t_{\frac{1}{2}}}  \cdot V_d$$
  $$ Cl = k  \cdot V_d$$
  $$ k = \frac{Cl}{V_d}$$


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How do CD 8+ Tc cells reach the site of tumors?
In normal humoral immunity, dendritic cells present antigens to the Th cells by arriving at the Lymph node. This is fine. But consider a tumor cell. How does the Tc cell sitting in the lymph node know that there is problem out there? Consider there is a single cell which has undergone mutations and is expressing altered proteins. This wouldn't cause much inflammation to attract the Tc cell there.
So, is there continuous surveillance by the Tc cells? Where exactly do the Tc cells reside? Do they roam around like Th cells? How about the NK cells? do they too roam around in the tissues?
Cases of viral and intracellular pathogens, there may be some inflammation which draws the Tc cells there. Maybe. This can not be in tumors. So how do the Tc cells reach there?

T cells are not only present in the circulation, they are also present in the tissues.

I'd read through Trafficking of T Cells into Tumors.

Depending on tumor type, there can be plenty of inflammation inside it.

I do not remember enough details to share a mechanistic insight.
However, chemotaxis is a likely answer, which basically means moving along concentration gradient of certain ligand of interest.
Also relevant to your question: a hypothesis called 'immune surveillance' gaining support over the past few years.
http://www.biolegend.com/cancerimmunoediting

So if immunosurveillance is actually occurring, in the case of humoral immunity, why do the dendritic cells have to travel all the way to the lymph node? If there is surveillance, the Th cells themselves will be at the site. Doesn't movement of both Th and Dendritic cell reduce the probability of contact?


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What makes worms' eggs float or sink?
In parasitology, while examining the stool sample, one important thing you do is test whether the eggs float on water or sink. We never did that since our coursework limits itself to microscopic examination, but we still are expected to remember examples of eggs under each
category.
So my question is, what makes flotation such an important criterion? And how is it done? How do you know if the eggs are floating or not? Does it depend on from where you take the sample (as in, add the stool sample to water and then either take from top or bottom)?
Another interesting thing we are expected to remember is that the fertilized eggs of Ascaris float while unfertilized ones sink. What's the basic funda behind all this? What's in fertilization that changes the buoyancy?

Are you sure you've got the test right? From a quick search online it sounds like the test for fertilised Ascaris eggs is done with zinc sulphide solution rather than water, so the density is different. Furthermore, it sounds like with zinc sulphide it's the unfertilised eggs which sink, not the fertilised ones (http://www.med-chem.com/para-site.php?url=org/ascalumb).

@arboviral sorry! Ya, its the other way round. Edited :)

Okay, I found the last part of your question the most interesting and can't give a full answer to that, but I just noticed I can answer the rest so here goes.
How it works (the simple version)
It works on the principles of buoyancy. The eggs and oocysts are less dense (lighter) than the fecal flotation solution and, consequently, they float on the very surface of it. The feces themselves are more dense (heavier) than the fecal float solution and, as a result, they sink to the bottom of the solution, out of the way. Commonly used flotation solutions include sodium nitrate, Sheather's sugar solution, zinc sulfate solution, sodium chloride solution and potassium iodide solution.
The eggs of some important parasites (for example. Schistosoma species and Fasciola hepatica) are more readily diagnosed by fecal sedimentation (sediment) tests because their eggs tend to sink in flotation media.
What makes it so important?
Some parasite eggs float and some don't. Faecal flotation is a simple, rapid and helpful diagnostic that narrows down the agent causing the clinical signs in the animal.
How it's done
Use a "Fecalyser", a commonly used test kit for faecal floats. The best stool samples to get are those that are fresh - straight out of the animal within the last 30 minutes where possible. Detailed walkthrough of the protocol here and video tutorial here.
Why is there a difference in the buoyancy of fertilised versus unfertilised eggs?
No idea, sorry.  Similar effects are seen in some insect eggs - Stomoxys eggs which sink mostly hatch, while floaters don't hatch. The fact that Anopheles eggs have floats and Culex lay egg rafts implies to me that their viable eggs would otherwise tend to sink too (this could be to do with oxygenation levels being higher at the surface, but I'm speculating here). During embryonation, a serosal cuticle forms which makes the eggs highly desiccation-resistant; non-viable eggs dry out. However, according to some sources online it sounds like for parasite eggs it's the unfertilised eggs which sink, not the fertilised ones.

Thanks! Now I get it! This method can be used only for eggs that float, eggs that don't, simply sink along with the debris and are not picked up on the slide/cover slip, so we just can't see them! (At least using this method) I had thought that a sample is taken from both the meniscus and the sunken part, but I guess only the meniscus is used. Thanks :)

Glad to help! There is something called a sedimentation test or sediment test for eggs that sink; I've added a couple of lines to the answer mentioning them.

@Polisetty Any chance you could accept this if you're happy with it? :)

Waiting for the why part..

I'm at a meeting of (mostly) parasitologists this week, so I'm trying to get an answer to this for you...

Whoa! That'd be great!! :D

Nobody knew. Although someone did point out that potentially a more interesting question is why Ascaris would lay any unfertilized eggs...

Whoa! That's an altogether new and amazing question! Sometimes it amazes me on how we fail to question such stuff, which is right in front of our eyes!

Agreed! This has turned out to be a particularly interesting question, by the way - thanks for asking it.


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Is the amount of blood same in the pulmonary and systemic foetal circulation?
We learn that the stroke volume is the same for the right and left side of the heart. So the amount of blood in either circulations should also be the same. (is it? I myself doubt this statement. As in, does it need to?)There's also a list of adaptations in the pulmonary vasculature that accommodates the huge volume of blood. But that's the adult. What about the foetus?
My doubt is that, in the presence of a patent ductus arteriosus in the foetal circulation, doesn't this distribution change? This shunting of blood into the systemic circulation would result in a low pulmonary venous return and hence, a low left ventricular stroke volume. So in the foetus, both blood distribution (in the two circulations) and also the stroke volumes (of either side of the foetal heart) should be differrent. Is this so?
This actually concerns me because the DA joins after the initial three branches (left brachiocephalic and the carotids). So, wouldn't such a shunting drastically reduce blood flow/perfusion to the brain? As in there would be decreased flow to the carotids when compared to the adults.
Finally, what are the consequences of the differential blood volumes in the two circulations and differential stroke volumes of the two ventricles due to a patent ductus arteriosus in a foetus? (If happens)


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How is the acetone method different from QB buffer for extraction of plant protein?
I primarily work on animal tissue but I thought of running an SDS-PAGE for plant tissue just for fun. I searched for some protein extraction protocols online and I don't know which one to choose. One is the acetone trichloroacetic acid method where you use the precipitate (?) and chlorophyll stays in the supertanant while the other is a QB (full form?) extraction buffer which is similar to what we use in animal tissue (with a bit of DTT and PVP). Here, we use the supertanant after centrifugal ion and the chlorophyll stays in the loading sample(?). At least, this is what I gather. What are the functional differences and when to use which technique?
Since I'm planning to run a gel, which one would be the better technique?
Please correct me if wrong I'm new to this field
Protocols attached.

I can't find the mention of QB buffer in any of the linked protocols. BTW, acetone is used to remove lipids.

The extraction buffer itself is called the QB buffer I guess @WYSIWYG


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Why do I drop my pen in a drowsy lecture?
I know that there is loss of muscle tone during REM sleep. Is this loss in muscle tone the reason I generally drop my pen in a sleepy lecture? But we were taught that sleep has 4 stages and REM sleep occurs after the 4 stages, ~90mins(?) post sleep. So technically, it should be that I'd be dropping my pen after 90mins of sleep. Though this is not the case. The pen drops generally when I'm at verge of sleeping.
I realise that there also is muscle atonia during other stages of sleep but, there is this famous story of Salvador Dali and the way he slept. He had a key in his hand and kept a tin plate beneath, as soon as he reached REm (dream) sleep, the key would fall and he'd wake up to draw stuff that he saw in his dream.
Why did Dali's key drop at REM sleep but my pen, way before that?

Is "dropping the pen" just a figure of speech?

@wysiwyg No! I mean, the pen falls from my hand, only to wake me up from sleep

I meant to ask if your question has something specific about the pen. What if you don't hold a pen while you go off to sleep during your lectures?


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What decides the nocturnal periodicity of microfilariae?
Microfilariae, which are the larvae of filarial worms show a nocturnal periodicity of entering into blood in south Asia and China. This coincides with the biting habits of its vector.
The same very species in Malaysia, the larvae are present throughout the day and night but peak at specific time points (subperiodic). The vector there hase different feeding habits.
This understandably is beneficial to the worm.
What are the cues that the worm uses to understand day and night?
Reversing the sleep wake cycle also apparently reverses the periodicity of the larvae from nocturnal to diurnal.

The circadian clock is one of the primary drivers for most day-night cycles. Additional factor entrain the clock. This would be one place to start.

@WYSIWYG the problem here is that the microfilariae, figure out the 'absolute' night and not relative to the hosts sleeping habits. Isn't the circadian rhythm relative?

Circadian clock is an endogenous clock. It can operate without stimulation by light. However, light exposure regulates circadian clock so that it can adjust to the natural light-dark i.e. day-night cycles. Host/vector sleeping habits are also affected by circadian clock. When you say that reversal of sleep wake cycles affects the worms then it is likely that they are controlled by some molecules produced by host. Cortisol would be my wild wild guess.


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What decides whether an ulcer/chancre is painful or painless?
In sexually transmitted infections, it is important to differentiate a painful ulcer from a painless one. This is because painless ulcers are seen in the chancre of primary syphilis while painful tender ones are seen in Herpes and though rare, in chancroid (H. ducreyi).
I can guess that it must be due to peripheral nerves, but how does this happen?

My hat's off to you. Not only have I never wondered about this, but having consulted Cecil's, Harrison's, several neurology texts, and other scholarly sources, not a single source addresses this.

It is small things like these that we generally ignore.. Thanks :') @anongoodnurse


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Why is polyploidy much more common in plants than in animals?
There are very few animals with polyploidy like salamanders. Why is it that polyploidy is so uncommon in animals? On the other hand there are numerous examples of polyploid plants. If ut something to do with the gene dosage, how does it not affect plants?

I would suspect that the commonness of alternation of generation and haplondiplontie in plants to be related to change in ploidy level.

Polyploidy is common in plants than in animals because in animals sex determination mechanism involves number and type sex chromosomes. Polyploidy will interfere with this mechanism and hence it is seen rarely in animals. I believe its probably because an animal progeny with multiple sex chromosomes won't be able to reproduce more of its kind unless it can also reproduce asexually (which is seen in plants as mentioned below).
Plants, on the other hand do not have any such sex determination (based on number or type of chromosomes) and majority of them can also reproduce vegetatively. This vegetative propagation enables multiplication of polyploid plants. Sexual reproduction will result in loss of desired polyploidy as per the principle of segregation. However, if a polyploid plant can produce a viable progeny sexually, it might have a different ploidy than its polyploid parent which won't happen if the parent reproduces asexually. Hence, polyploid plants can be classified as sterile and fertile polyploids (the reference will give a detailed account on this mechanism).
Refer the section of Polyploidy (page 115, Chapter 6) of this book (Principles of Genetics, Snustad and Simons, 6th edition)
When it comes to gene dosage, animals do show gene compensation of X-linked genes by various methods. Example- formation of Barr Body in human females (Note that this has nothing to do with polyploidy, but happens since females have one X chromosome more than males). Whereas gene dosage in polyploid palnts has been exploited for improved agricultural yields as they have shown better productivity than their diploid couterparts.

Are there really more asexually reproducing plants than asexually reproducing animals? Can you back up the claim with a reference? Also, sex does not involve gender and gender does not involve sex chromosomes. Intuitively, I would think of the absence of gene dosage in plants (assuming this is true, reference would be needed) as preventing events of ploidy change, so your hypothesis is unclear to me.

@Remi.b I have tried explaining that why I think the sex determination mechanism has a role in this. I suggest to go through the reference once. It's really helpful and elaborate.

@AlwaysConfused Yes, you are right. These polyploids fall in the category of fertile polyploids. The reference gives an account on their propagation.


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Why do bacteria produce H₂O₂?
I recently read up that people with NADPH oxidase deficiency (Chronic granulomatous disease CGD) have a tendency to be infected by Catalase positive organisms. NADPH oxidase helps produce the $H_2O_2$ via superoxide that is required by other enzymes to kill the bacteria.
Case 1: In the phagoloysozome, when there is a deficiency of NADPH oxidase, catalase positives can clear off the $H_2O_2$ they produce, thereby stopping production of free radicals via Fenton and myeloperoxidase. The bacteria survives and hence causes symptomatic infection in CGD patients.
Case 2: On the other hand, since catalase negative organisms can't clear off the $H_2O_2$ they produce, they remain susceptible to the free radicals produced by other enzymes like Myeloperoxidase and Fenton reaction, which would still kill the bacteria. In short, the bacteria 'lend' the $H_2O_2$ which feeds into these reactions leading to its own death. Hence, CGD patients can fight off catalase negative organisms.
My question is, why do the bacteria produce $H_2O_2$ in the first place? Is it produced only by aerobic organisms? If so, why would there be organisms that produce $H_2O_2$ and still not have a catalase (as had happened in case 2)? Isn't $H_2O_2$ is harmful even in the absence of free radical producing enzymes since the Fenton reaction is a non-enzymatic reaction?

It is a by-product of oxygenic respiration which is basically toxic to the cell but it is also used by some organisms (I know of eukaryotes) for defence and some catabolic processes. Peroxidases can also clear H₂O₂. Also, catalase is present in almost all aerotolerant and aerobic organisms. Can you cite a counterexample?

@WYSIWYG yeah, catalase is present in aerobic/ facultative anaerobes. I get that. Why are catalase negatives also producing H2O2 then? Shouldn't they be able to handle it when they are producing it? As mentioned, catalase negatives can be killed even in CGD individuals.

Can you cite an example of a Catalase negative organism that produces H₂O₂?

@WYSIWYG I don't know. Well, that's what I find weird. In CGD patients, catalase negative organisms can be killed in the phagolysosome because, they 'lend' H2O2 which they are unable to clear off (unlike catalase positive organisms), to the downstream enzymes that can lyse the bacteria. This is why I posted this funda on top coz the confusion arose from this itself. The source is from a standard Hematology text, which I will quote once I get hold of it.

why does the bacteria produce H2O2 in the first place?
It is produced by all organisms as a byproduct of respiration. See this wikipedia article:

All living cells produce reactive oxygen species (ROS) as a byproduct of metabolism. ROS are reduced oxygen intermediates that include the superoxide radical ($O_2^•$) and the hydroxyl radical ($OH^•$), as well as the non-radical species hydrogen peroxide ($H_2O_2$)....The superoxide anion is formed directly from the one-electron reduction of molecular oxygen. Hydrogen peroxide is then formed from the disproportionation of the superoxide anion. This reaction occurs very quickly in seawater. Next, the reduction of hydrogen peroxide yields the hydroxyl radical, $H_2O_2 \xrightleftharpoons 2OH^•$, which can then get reduced to the hydroxyl ion and water.

 Source
But, it has some useful functions too! One of those, as you mention, is in immunity through NADPH oxidase, but there are some more! From the same above wikipedia article:

These ROS are important in the normal functioning of cells, playing a role in signal transduction and the expression of transcription factors.

For this line, wikipedia cites 3-4 articles, one of which is this:

The OxyR transcription factor is sensitive to oxidation and activates the expression of antioxidant genes in response to hydrogen peroxide in Escherichia coli. Genetic and biochemical studies revealed that OxyR is activated through the formation of a disulfide bond and is deactivated by enzymatic reduction with glutaredoxin 1 (Grx1). The gene encoding Grx1 is regulated by OxyR, thus providing a mechanism for autoregulation.

It is not produced by obligate anaerobic bacteria and that is why they are very sensitive to oxygen. See this article:

Obligate anaerobes are microorganisms killed by normal atmospheric concentrations of oxygen (20.95% $O_2$)...Because molecular oxygen contains two unpaired electrons in its outer orbital, it is readily reduced to superoxide ($O_2^−$) and hydrogen peroxide ($H_2O_2$) within cells. Aerobic organisms produce superoxide dismutase and catalase to detoxify these products, but obligate anaerobes produce these enzymes in very small quantities, or not at all.

If so, why would there be organisms that produce H2O2 and still not have a catalase (when the bacteria is outside, not in the phagosome)?
Logically, no. Producing $H_2O_2$ but not being able to handle it would be like suicide for any organism. Also, I could not find any example of bacteria which lack catalase but still produce hydrogen peroxide. However, if you talk about spontaneous formation of $H_2O_2$ from $O_2$ or spontaneous conversion of $H_2O_2$ to $OH^-$ or $H_2O$, then there could be many examples.
Isn't H2O2 is harmful even in the absence of free radical producing enzymes since the fenton reaction is a non-enzymatic reaction?
I think you have used some inappropriate words here; you probably mean free radical metabolizing enzymes (like catalase or superoxide dismutase) instead of free radical producing enzymes. And you probably want to say that $H_2O_2$ can also affect bacteria through fenton's reaction even in the presence of such enzymes (correct me if I'm wrong here).
You are partially correct. It should damage the bacteria, but, as you know, bacteria are ever-evolving and have already found a way to counteract this. First, lets see how fenton's reaction works. See this:

After addition of the iron and the hydrogen peroxide, they are going to react together to generate some hydroxyl radicals as it shows in the following equations:
$Fe^{2+} + H_2O_2 \rightarrow Fe^{3+} + OH^• + OH^-$
$Fe^{3+} + H_2O_2 \rightarrow Fe^{2+} + OOH^• + H^+$
The typical range for the iron dose is 1 part of Fe per 5-25 parts of H2O2.
After that the hydroxyl radicals are going to react with the pollutants to oxidize its. Actually the hydroxyl radicals can react according 4 kinds of reactions with the pollutants:
Addition: $OH^• + C_6H_6 \rightarrow (OH)C_6H_6$
Hydrogen Abstraction: $OH^• + CH_3OH \rightarrow CH_2OH^• + H_2O$
Electron Transfer: $OH^• + [Fe(CN)_6]^{4-} \rightarrow [Fe(CN)_6]^{3-} + OH^-$
Radical Interaction: $OH^• + OH^• \rightarrow H_2O_2$
During the Fenton's reaction all the parameters are adjusted to promote the two first kind of reaction between the pollutant and the hydroxyl radicals.

Now, lets see how the bacteria tackles this. See this:

While E. coli Dps can store iron, it prefers to use $H_2O_2$ rather than $O_2$ as an oxidant (Zhao et al., 2002). This suggests that the primary role of Dps in E. coli is to protect DNA against the potential damage of hydroxyl radical produced by the Fenton reaction, rather than an iron storage function. Although an iron storage Dps-like ferritin was found in the gram-negative bacterium Listeria innocua (Bozzi et al., 1997), recent studies have shown that it is indeed a Dps protein, which attenuates the production of hydroxyl radical by Fenton chemistry: DNA cleavage assays showed that the protein, while not binding to DNA itself, protects it against the deleterious combination of $Fe^{2+}$ and $H_2O_2$ (Su et al., 2005). It seems likely that the principle role of this family of proteins is a DNA protecting anti-redox agent (Chiancone et al., 2004).

EDIT: Now, as you asked in comments:
how catalase negative organisms manage with the H2o2 they produce
read the following paragraph from this article (emphasis mine):

Under different growth conditions we found that both L. plantarum ATCC 8014 and a catalase-positive strain, T-1403-5, were capable of utilizing $0_2$, particularly during the late stages of growth. This suggested the need for enzymes which would protect the lactobacilli
  from $H_20_2$ and $0_2$ which might be formed. Superoxide dismutase was present at low but constant levels in both catalase-positive and catalase-negative strains. NADH peroxidase was present in strain 8014 and this enzyme increased in specific activity as the cells aged and entered the period of increased $0_2$ uptake. The presence of this enzyme should protect the organism against toxic effects of $H_20_2$ in the absence of catalase production. In strain T-1403-5 this role can be performed by the very active atypical catalase, although this strain may also possess the peroxidase. When growth rates of the catalase-negative and catalase-positive strains were compared, the rates of the catalase-negative strains were greater than that of the catalase-positive strain. Therefore, it did not appear that the possession of catalase conferred any advantage on strain T-1403-5.

Or see another article on Streptococcus pneumoniae:

Aerobic growth of Streptococcus pneumoniae results in production of amounts of hydrogen peroxide ($H_20_2$) that may exceed 1 mM in the surrounding media...The mechanisms allowing S. pneumoniae, a catalase-deficient species, to survive endogenously generated concentrations of $H_20_2$ that are sufficient to kill other bacterial species is unknown. In the present study, pyruvate oxidase (SpxB), the enzyme responsible for endogenous $H_20_2$ production, was required for survival during exposure to high levels (20 mM) of exogenously added $H_20_2$...Thus, SpxB is required for resistance to the toxic by-product of its own activity. Although $H_20_2$-dependent hydroxyl radical production and the intracellular concentration of free iron were similar to that of Escherichia coli, killing by $H_20_2$ was unaffected by iron chelators, suggesting that S. pneumoniae has a novel mechanism to avoid the toxic effects of the Fenton reaction.

From the same article's Discussion heading (there are actually many points, so I recommend you read them yourself too, I'll add main points here):

The role of SpxB expression in resistance to killing by $H_20_2$ was confirmed by the demonstration that spxB mutants, which produces no detectable $H_20_2$, had a significant decrease in $H_20_2$ resistance and by demonstrating that complementation of the spxB gene fully restored both $H_20_2$ production both $H_20_2$ resistance. These results showed that SpxB expression is required for wild-type levels of resistance to $H_20_2$ rather than merely correlating with it.
when cultures of both strains were shifted from anaerobic to aerobic conditions with or without chloramphenicol, a protein synthesis inhibitor, $H_20_2$ resistance was not affected. This confirmed that de novo protein synthesis is not involved in the increase of $H_20_2$ resistance observed during aerobic growth, suggesting that an inducible response is not involved.
Furthermore, the addition of pyruvate to either mutant or wild-type cultures slightly decreased $H_20_2$-mediated killing, arguing that increased killing of spxB mutants is not due to toxic by-products resulting from the reaction of excess pyruvate and $H_20_2$. Together, this suggested that a product of SpxB activity other than $H_20_2$ acts to increase resistance
Furthermore, the ability of DF to eliminate the EPR signal caused by $OH^·$ in S. pneumoniae suggests that the inability of this iron chelator to increase $H_20_2$ resistance in S. pneumoniae is not merely due to a lack of permeability.

In the end, what I'd conclude is that different bacteria adopt different mechanisms to tackle this problem, and many of those mechanisms aren't known yet. So, there's no definite or exact answer to this question.
References:

ROS production in marine microalgae
NADPH oxidase
Activation of the OxyR Transcription factor by Reversible Disulfide Bond formation
Obligate Anaerobe
Catalase
Superoxide Dismutase
Iron Metabolism: From Molecular Mechanisms to Clinical Consequences - Robert Crichton
Oxygen metabolism of catalase-negative and catalase-positive strains of Lactobacillus plantarum.
Factors Contributing to Hydrogen Peroxide Resistance in Streptococcus pneumoniae Include Pyruvate Oxidase (SpxB) and Avoidance of the Toxic Effects of the Fenton Reaction

I'm sorry you're getting me wrong. I'll try editing my question a bit. Maybe the way I've asked it is causing some confusion. Thanks

So is there anything you still want to know? (I don't find any new question in it)

The main thing I would like to know how catalase negative organisms manage with the H2o2 they produce. The whole CGD thing I wrote is just to 'prove' that catalse negatives also produce H2O2.

Hey! I've come back to this answer after a long time. It finally says that there are mechanisms by which catalase negatives can handle the peroxide. Then the obvious question would be, why would CGD patients be susceptible to them? Wouldn't these bacteria survive by clearing of the peroxide with that mechanism.


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After getting fully vaccinated for HBV why does the antiHBs titer last for so long?
When a newborn child is fully vaccinated with HBV and let's assume he's responsive, his antiHBs titers will be high. But since the antigenic stimulus is withdrawn, shouldn't the titre fall to nill in some time? Rather, the titers stay significant for around 40 more years. (>10 IU/L is significant)
So, how are there circulating antibodies for so long if there is no more antigenic stimulus?
I understand that memory cells have large half lives but what is producing the antibodies is the plasma cells which have very short half lives.
So how do the antibodies persist for so long?

There is such a thing as memory plasma cells, discovered only relatively recently. Here is a review from 2010 discussing them, here is another review from 2012, and here is a pre-publication manuscript of an upcoming review in Leukemia (I apologize if any are behind paywalls, let me know if you can't access any of them).

Thanks!! Great! I also read up that the anamnestic response stays longer than the long lived/memory plasma cells. So are there other vaccines too where a continuous titre is maintained?

@Polisetty check out page 2 of this PDF from the Immunisation Advisory Centre of New Zealand out of the University of Auckland. It's a table of the average duration of response to a number of common vaccines.


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Difference between Fragmentation and Budding
I have heard about two terms stating similar things - Fission and Fragmentation . I know Amoeba undergoes fission and Fragmentation is done by spirogyra. So what's the main difference between them?

Welcome to Bio. Could you add context to your question? Are you talking about cellular processes?

Yes, i am talking about asexual reproduction.

As far as I remember yeast undergoes budding (in fact even hydra does). Have never heard of amoebae budding. Wasn't the amoeba thing plain old binary fission?

I am sorry for the mistake. See the edit