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How does heart beat faster while doing a strenuous task?
I know that when we do tasks which require extra physical effort (like running etc.), our heart beats faster.
I also know that the reason behind this is that these jobs require more energy than usual and, hence, require more oxygen for breaking down food. And, since, oxygen is transported throughout body by blood (by forming compound with Haemoglobin (present in RBCs), called Oxyhaemoglobin), the heart needs to beat faster to pump more blood.
However, I am not aware of how does the heart automatically start beating faster.

Is there any involvement of the Nervous System?
Does the heart have some sort of special mechanism that activates when the body performs a strenuous job?

What research have you done before asking it here?

I am sure that there are many ways that your body can regulate heart rate, but I am going to cover this topic briefly from the perspective of $\ce{CO2}$/$\ce{O2}$ concentrations, and pH.
The medulla oblongata
The medulla oblongata is part of the central nervous system, and makes up the lower portion of the brain stem. It is responsible for performing autonomic functions, including the regulation of heart rate through chemoreceptors. The medulla oblongata receives its blood supply from the vertebral artery and makes both afferent and efferent connections with the vagus nerve.
Chemoreceptors
There are two main types of chemoreceptors in your cells that are responsible for regulating heart rate.

Central chemoreceptors

These are located in the medulla oblongata, and are responsible for measuring the concentration of $\ce{H+}$ ions (ie. pH). When the pH is low, neural cells with these receptors will signal the release of norepinephrine and epinephrine.

Peripheral chemoreceptors

These are located in the carotid and aortic bodies and measure the concentration of $\ce{O2}$. The receptor cells of these structures make connection with afferent nerves, to send a signal to the central nervous system in times of hypoxemia.
$\ce{CO2}$/$\ce{O2}$ Exchange
Blood is the tissue responsible for distributing chemicals around your body. It is therefore also involved in the $\ce{CO2}$/$\ce{O2}$ exchange between tissues. Blood cells use hemoglobin as as a carrier molecule for this exchange.
When $\ce{O2}$ is delivered to tissues, it will be processed by the mitochondria of the cells to synthesise ATP, and $\ce{CO2}$ as a biproduct. ATP is also responsible for muscle contractions, and so, with exercise comes an increased utilisation of ATP. With ATP stores running low, your cells will begin to use more $\ce{O2}$, and therefore, they will produce more $\ce{CO2}$.
$\ce{CO2}$ and Acidity
So, I kinda lied when I said hemoglobin is the carrier of $\ce{CO2}$. This is mostly true, but $\ce{CO2}/$$\ce{O2}$ is also somewhat soluble in blood, and this accounts for changes in blood-pH.
$\ce{CO2 + H2O}$ $\ce{<=>}$ $\ce{H2CO3}$ $\ce{<=>}$ $\ce{HCO3- + H+}$
The above equilibrium is catalysed by carbonic anhydrase, and accounts for a decrease in pH levels.
Signalling in response to pH
So your exercising, your body is using lots of $\ce{O2}$ to produce ATP. Your $\ce{CO2}$ levels have increased, and your internal pH has dropped. Now what?
Well, as I'm sure you have guessed, your nervous system takes over.
The central chemoreceptors of the medulla oblongata send an impulse to  the adrenal glands in response to the decreased pH. This signals the release of the hormones epinephrine and norepinephrine in to the bloodstream. The release of epinephrine and norepinephrine is regulated by the sympathetic nervous system. This accelerates the heart rate by binding β-receptors in your heart tissue. Efferent nerve connections from the vagus nerve also participate in this process (I think).
For mechanisms on heart contration, see here; everything following "excitation contraction coupling" is probably the most relevant.

I think this answer is good and very extensive. However, I didn't immediately see the (important) aspect that all these measures are transfered to the heart via the sympathetic nervous system. Since the OP specifically asked for involvement of the NS I suggest adding a disclaimer stating this involvement to the top of your answer.

I am guessing from neural cells and @Nicolai 's comment that the involvement of the Nervous System is there. Am I right?

@Nicolai Thank you for your suggestion. I have edited my question. Does this seem better? And yes Arjun, of course! But, I think it is more interesting to know what it is exactly that elicits the nervous system's involvement in a function.

@Arjun Yes, I think this way it's much clearer where the different receptors are and how the signal is transferred to the heart

Whenever we think about our body changes, we have to think what come first, what is cause and what is effect. How the heart automatically start beating faster?

In short, whenever there is role of controlling mechanism, neural and humoral used to get involve. Paraventricular nucleus of hypothalamus controlling the medulla autonomic nervous system. While resting vagal tone is inhibited, sympathetic predominates leading to positive chronotropic and inotropic effect. Emotional and other factor also involve. Even anticipatory effort can have the effect. Humoral is through hypothalamo-hypophisial-adrenal medullary axis.

Thank you for your answer and welcome to Biology.SE. Could you back up your answer with references? Thank you!

Whenever we think about our body changes, we have to think what come first, what is cause and what is effect. How the heart automatically start beating faster? For this question, blood gas changes come later which is the effect of physical activity that will regulate heart rate further. All the senses visual, auditory, touch etc even the act of thinking physical activity will increase heart rate. Our body has extensive feedback system, in preparation for body need. So many references are there. I used to refer Ganong physiology review.


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What kind of bug or insect is this?
One of my friends has seen this insect-like species in water in the mountainous area in Iran (near Qom).

Where (what country / region) was is found?

@Remi.b Iran. near Qom.

Looks like some species of tadpole shrimp. I couldn't tell you what species. There's really no other basis for identification other than these are extremely unique. As you can imagine, they're endemic to a variety of wetland environments. The take home point, however, is it's a crustacean rather than an insect.

what information can be derived when  this crustacean is seen somewhere ?

@M.H I'm not too sure. As you can see, my best candidate for the species happens to distribute over multiple continents and countries.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


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What species are these baby birds?
I'm trying to save these baby birds' lives, and I need to know their species so that I can know how/what to feed them. Please help me ASAP .

A couple of questions; where did you find them, in what condition? allaboutbirds advises to contact licensed wildlife rehab centre or leave them to the place where they were found to increase their chances of survival. The bird appears to be one from Caprimulgiformes.

I agree they look like Caprimulgiformes. We need more info (where you live, where you found them, why you are holding them, etc.) to answer your question. Also, in the future, if you find baby birds, just leave them where you found them. These look fully fledged, and were almost certainly ok and just waiting for mom to come back to feed them...

If you are in Europe they are juvenile common swift (Apus apus).
There is a website dedicated to them, with a page on how to raise them: http://www.commonswift.org/Hand_rearing_Swifts.html
They are very fragile and with the wrong diet they might develop feather deformations. They also require a continuous effort because they eat very often. I raised them a couple of times and when they take off is magnificent but it is easy to do something wrong. If you have some recovery center or expert nearby  I suggest to hand them over.

+1 For the website you linked. I mistook them for nightjars.

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Identifying a spider from coastal Virginia
A spider recently put up a web in my room in coastal Virginia, USA (on the left in the photo).
Rounder/taller body than most species I've seen. Dark brown, not quite solid-color coloration. If laying flat, it looks like its body would be about the size of an American dime. Tends to hang with its underbelly pointed upwards, and the times I've watched it feed it has never attempted to wrap prey in silk –- instead, it immediately eats and discards them.
My best guess from what I was able to find online was Araneus diadematus, but the coloration on all the examples of that species I can find seems much more varied than what I'm seeing, and I'm not particularly well-versed in spider identification, so I'm not sure.
The spider on the right was new this morning, I'm less curious about it and presume it was just a male of the same species.

Please provide some close-up photos if possible. A Photo of the abdomen and the back are preferential. Thanks

@theforestecologist Not sure I can get much closer without disturbing the web, but I'll see what I can do when I get home tonight.

These are very likely one of the common spiders that gets called House Spider, but this variety is one of the comb-footed spiders; the Theridiidae.  They're sometimes also called Tangleweb Spiders or something along those lines.  They make those messy webs, and hang upside down just as you show.  You can tell these guys aren't Araneus or one of the other Araneid orbweavers, because they're not hanging vertically in an orbweb.  This particular spider is probably the very variable and common Parasteatoda tepidariorum, and the smaller one is, as you guessed, a male.  They will share the web for a day or so until he mates and moves on.  You should be aware that the related Black Widow has this same general body shape and habit, and may be stripy and have banded legs like you see in the photo when the females are young.  I suspect that was why TFE was asking for better photos - although you probably would have noted the red hourglass before if that was the case.  I'm inclined to go with P. tepidariorum, for two reasons: Latrodectus generally (but not always) are sensitive to disturbance, where the common House Spiders don't seem to mind, and the abdomen of the female seems to be a little more randomly patterned (as best we can see) than I would expect for a Latrodectus.
Here's a photo of P. tepidariorum with a snack:

https://bugguide.net/node/view/6919/bgimage

Very informative answer, but again please provide some evidence/support/citations/etc to back up your claims. Even if you know all this to be true, a reader may not, and that reader may not be trained to know what is true/not. We're about teaching people on Bio.SE, so by providing links to useful and supportive materials, you're helping out those that read the question a lot more. [Reputable] Support also helps other users feel more confident in your answer, which often leads to more upvotes (e.g., see here). Thanks!


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What is this large beetle from Shirpur, Maharastra (central India)?
I found this beetle in my college in Shirpur, Maharastra (central India). What is it? It is very large, and I have never seen it before. I believe it may be Titanus giganteus but I'm not sure.

Welcome to Stack Exchange! Please take the tour. Could you add more information about the beetle - size (as accurately as possible), anything you noticed about the markings, etc? It doesn't look much like T. giganteus to me - the elytra (wing cases) are the wrong shape and the mandibles are much bigger and shaped differently. Also, as far as I know T. giganteus is found only in south America.

As arboviral said, please add more information.

Clearly not the best picture, but from the poor quality image it does appear you have a longhorn beetle (family Cerambycidae) in the subfamily Prioninae.

They are typically large (25–70 mm) and usually brown or black. The males of a few genera sport large mandibles that are used in fights with other males, similar to stag beetles. These beetles are commonly nocturnal and are attracted to light. The majority of the Prioninae whose biology is known are borers whose larvae feed on rotting wood or roots.

For example, your specimen looks a lot like Toxeutes macleayi from Australia.

 Source: England London - Natural History Museum
I'm not sure whether other closely related species live in India (none of the related Indian species that this site mentions look like your specimen), but I would guess if you look into it you might find a local bug guide that might help you find some other related species.
Based on your location in India, I'd say one place you could start looking is through species in the genus Prionus.

they're also large, generally brown or black, are nocturnal. Additionally,

All members of the genus Prionus have twelve or more strongly toothed or even flabellate antennomeres on their large antennae.

You'll obviously need to provide a better picture for us to examine that detail of your specimen.

I also recommend you examine the list of Indian Prioninae species listed here, including relatives of similarly sized/colored species with large mandibles such as Dorysthenes huegelii and Rhaphipodus fontanieri.
Again, your picture is too low of quality for an accurate ID, but these links should likely help you parse through similar species and hopefully find your answer.

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Reason for specific location of a gnat swarm?
While checking on my yard trees, I noticed a tiny swarm of gnats above one small maple that has a metal cup holder stake used to help train the trunk straighter. Approximate swarm size of 20 - 30 gnats and they hovered about 6 inches above the top of the cup holder.
I know there's studies on the phenomena of swarm behavior, and out of curiosity as to what they would do I put my hand a couple inches above the cup holder. The little swarm repeatedly moved straight upwards 3-4 inches then returned to the original spot as soon as I removed my hand. When I raised my hand up towards the swarm they would move higher and higher and also follow my hand back down as I lowered it. No matter how high I raised my hands if I removed it quickly they returned immediately to the original location. I checked back a half hour later and they are still there and acted the same way.
What might be the reason for that specific preferred location of the swarm? I has been cloudy and humid all morning and I wonder if the metal of the cup holder is changing the air temperature or some other quality that far above itself? I did also notice a stronger sweet smell of the clover in that location but do have clover all over the yard. My other trees, including a very similar sized young maple but without any support next to it, have no swarms so the metal cup holder perhaps is a correlating factor?
I tried adding a picture for reference but can't get it to upload.

'Gnat' is the common name for a number of species of tiny flying insects in the Dipterid suborder Nematocera (https://entomology.ca.uky.edu/ef632), including Ceratopogonidae (biting midges), Chironomid midges (non-biting midges) and Simuliidae (blackflies). Like many other Diptera, a lot of these species mate aerially in swarms: the males gather using visual cues to determine swarm location. I'll try to add more detail to this later on why they go for specific locations, but in the meantime here are some papers on mating swarms in some of the groups normally called 'gnats':
General papers on swarming behaviour in Diptera:

Downes, J. A. 1969. The swarming and mating flight of Diptera. Annu.
Rev. Entomol. 14: 271–298.

Swarming behaviour of the family Ceratopogonidae:

Downes, J. A. 1955. Observations on the swarming flight and mating of
Culicoides (Diptera: Ceratopogonidae). Trans. R. Entomol. Soc. London
106: 213–236.
Campbell, M. M., and Kettle, D. S. 1979. Swarming of Culicoides
brevitarsis Kieffer (Diptera: Ceratopogonidae) with reference to
markers, swarm size, proximity of cattle, and weather. Australian. J.
Zool. 27: 17–30
Zimmerman, R. H., Barker, S. J., and Turner, E. C. 1982. Swarming and
mating behavior of a natural population of Culicoides variipennis
(Diptera: Ceratopogonidae). J. Med. Entomol. 19: 151–156.
Blackwell, A., Mordue, A. J., Young, M. R., and Mordue, W. 1992. The
swarming behavior of the scottish biting midge, Culicoides
impunctatus (Diptera, Ceratopogonidae). Ecol. Entomol. 17: 319–325.

Swarming behaviour of the family Chironomidae:

Gibson, N. H. E. 1945. On the mating swarms of certain Chironomidae
(Diptera). Trans. R. Entomol. Soc. London 95: 263–294.
Oliver, D. R. 1971. Life history of the Chironomidae. Annu. Rev.
Entomol. 16: 211–230.
Fyodorova, M. V., and Azovsky, A. I. 2003. Interactions between
swarming Chironomus annularius (Diptera: Chironomidae) males: role of
acoustic behavior. J. Insect Behav. 16: 295–306.

Swarming behaviour of the family Simuliidae:

Moorhouse, D. E., and Colbo, M. H. 1973. On the swarming of
Austrosimulium pestilens MacKerras and MacKerras (Diptera: Simuliidae). Australian J. Entomol. 12: 127–130
Hunter, D. M. 1979 Swarming, mating and resting behaviour of three species of black fly (Diptera: Simuliidae). Australian J. Entomol. 18: 1–6


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Caterpillar resembling a snake
I found a very interesting caterpillar. It's 5 cm long and  looks like a snake. I discoved it in a greenhouse on a vine in the Czech Republic.

I found two types: a green one and a brown one, both with same length.

What species is it?

Looks like the larvae of an elephant hawk moth (Deilephila elpenor).

 Green Variant. ©2005 Henk Wallays  (CC BY-NC 3.0)

In the Sphingidae family (like the snake-mimic caterpillar in this post).

Description: typically brown-gray color with black dots along length of body. Young larvae are yellowish-white or green, but some mature larvae also can be green colored. Fully-grown caterpillars reach 7.62 cm in length.

Have a backward curving spine or "horn" on the final abdominal segment.

 D. elpenor color variation. Source: A.R. Pittaway & I.J. Kitching
Range: Most common in central Europe and is distributed throughout the palearctic region.
Habitat: variety: including rough grassland, heathland, sand dunes, hedgerows, woodland, open countryside, and even urban gardens.
Source: Wikipedia

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


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Help me identify these two ants
I recently found these two winged ants near a colony. There were 5, but 3 flew away.
Location: Nassau/The Bahamas. November 19, 2017.
Are they queens? And What species?

The square head and the distance between the abdomen and the thorax lead to Myrmecinae, probably Pheidole, Pheidologeton/Carrebara or some granivorous species.


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What are this designs which I found on curry leaves?
Curry leaves is the plant name where I found designs, but what are the designs present on the leaf?
Location: Argentina

some leaf-mining insect larvae would be the cause. Sometimes such species are specialists (i.e., only attack one narrow range of taxa), while other times the species might be more of a generalist.


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What kind of lichen is it (no. 2)?
I think i found very interesting lichen. I discoved it at 1.15 PM CET in Prague nature conservation area called Divoka Sarka.

I took this picture on the place of my discovery.
One piece of this specious had cca. 6 cm. And it look like a shrub.

And this is micro photograf with magnification about 200X.

This is a fruiticose lichen, meaning one with a bushy growth habit. They are common in my native state of Texas (USA), where they hang off of oak trees. Your photos look much like them. I have seen other examples in the rainforests of the Pacific Northwest, in both Oregon and Washington. I can't name the species.
In the upper left of your first photo, I see a thick, stem-like structure. This looks to me like the holdfast, the place the lichen attaches to the tree or other support.

i know it is hard to try find with this information something more then your answer mister. Of course i know that my discoveri can be put into fruiticose lichen, but i hope for much more accurate answer here. But u know the fruiticose lichen is more often on trees. This one was on the ground and thats fascinated me ! Even more fruiticose lichen is usually pollutation intolerant and i found it in the capital city of Czechia. And u know maybe it not even lichen, but dead moss, shrub. But still thank you :)


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What is this insect in a cocoon climbing a web?
I found this thing hanging from the framework of my garage yesterday:

The size of the object in the picture was about .75 inches tall by maybe a quarter inch wide. This was taken yesterday in a suburb of Jacksonville, Florida, US in late evening (8:30 pm?).
He was (apparently) using his mouth-parts to draw in what appeared to be a strand of spiderweb, and in about 10 minutes had drawn himself upward, towards the top of the garage framework, a total distance of about two feet.
An additional question would be what is that he's in, a cocoon? a piece of bark or something being used like a hermit crab uses a scavenged shell?
Any help would be appreciated!

You're much more likely to get reasonable answers if you remove the silliness from your question and use an informative title. Also make sure you adhere to the species identification guidelines.

I edited the post to remove the alien nonsense the OP included. I opted to edit the post so to avoid attracting further downvotes given that it's an interesting specimen and the post follows the [tag:species-identification] guidelines otherwise. @Chowzen, in the future please keep your posts professional and to the point. Ideally, when asked to edit your post, you should [edit] on your own to avoid closure. Thanks.

That is, probable, a Psychidae (Lepidoptera), commonly known as bagworms. They build those "bags" with pieces of wood, twigs and leaves, and they protect them from predators and parasitoids. One possible species for Florida is this one: https://en.wikipedia.org/wiki/Evergreen_bagworm


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What characteristics of the protein folding process ensure that the energy landscape is a funnel?
The folding funnel hypothesis states that the energy landscape that proteins observe when they fold is funnel shaped with a single global optima. This ensures that no matter what sequence of folds the protein follows, it should eventually end up in the same folded configuration thanks to the laws of thermodynamics.
For example, see this illustration of the energy landscape from Dill & MacCallum (2012) "The Protein-Folding Problem, 50 Years On" Science 338 (6110) pp 1042-1046:

Clearly, the folding works because the energy landscape is funnel shaped. Any other configuration, e.g. a landscape with multiple significant local optima or a flat landscape, would result in a protein folding in all kinds of different ways.
What are the characteristics of the overall system that ensure that the energy landscape is funnel shaped, and that nearly any protein in an unfolded state will reach the global optima? (e.g.: is it because the proteins themselves have certain statistical properties? or it is something to do with how the types of "moves" the protein makes on the energy landscape?)

I'm not sure I follow your question entirely. Protein folding is dictated by both entropy and enthalpy. You may be interested in this: https://en.m.wikipedia.org/wiki/Anfinsen%27s_dogma

Thanks for the link. I guess the question can be rephrased as why is the energy minimum unique and so "easy" to find due to the funnel shape of the energy landscape? Did this property evolve somehow via selection (so there might be folding molecules with multiple energy minimums) or is it inherent in nature?

For any combination of amino acids there is going to be a conformation which is at the lowest energy and, when plotted, this would have to look like a funnel. It is plausible, though perhaps unlikely, that there could be more than one low energy conformation that is stable (the prion protein may be an example). However, since protein function depends on structure, it is likely that evolution would prevent multiple protein conformations that are accessible and stable.

Huh. Isn’t this a seriously outdated hypothesis? The energy landscape of protein folding does have significant local minima, and correct folding often requires specific codon sequences and cofactors. So I think the premise of this question is fundamentally not true.

good point, maybe it is an outdated hypothesis.

I can't help but think of prions, & the potential catastrophic & fatal consequences of 1 alternative folding of just 1 protein - having alternative funnel outputs to the desired one can be seriously problematic, & even 'infectious'..

Naturally occurring proteins are evolved such that this is the case
Natural proteins only occupy a very small amount of sequence space. For a 200 aa protein, there are $20^{200} \approx 10^{260}$ possible sequences. There are nowhere near that many naturally occurring protein sequences, even if you take into account all the different alleles in the different organisms in the world.
What happens when you synthesize and express a random (non-natural) protein sequence? You get junk. It doesn't fold or it aggregates or something else happens. You don't get a stably folded protein. Heck, you don't even need to have a fully unnatural protein. You can take a naturally occurring protein and make a few mutations in it, and end up with non-folded junk.
Evolution has a very strong selective pressure to make sure proteins can fold properly and beat Levinthal's paradox. If a protein can't fold, it can't perform any function in the cell, and thus there's no selective pressure to maintain expression. (The promoters get trashed, and the DNA gets mutated away to "junk" DNA.) Only if the protein is stably folded is selective pressure maintained. So you get the one-in-a-million sequences which does have a decent folding funnel.
So it's not that there isn't protein sequences out there with a flat energy landscape, or an energy landscape with lots of local minima. It's just that whenever such a protein forms, it can't fold. And if it can't fold, it's freed from evolutionary pressure and disappears from the gene pool - either because the organism that holds it can't survive without it, or because random mutations wipe it out with random noise. It's survivorship bias -- you see proteins with a reasonably well-formed folding funnel because they're the only ones you would see.
(There are proteins out there with less-than-robust folding funnels, or with alternative energy states. A brief search of the literature will turn up a number of examples where protein folding requires cofactors or chaperones. Or where a protein has two different folded states, depending on environmental condition. Or where the most commonly folded state is only a meta-stable state, and there's a more stable conformation which the protein will convert to, if given a chanvce - amyloid fibrils being the most common example. These are refinements on the general principle. You don't need a rock solid folding funnel, you just need one "good enough" for the organisms' purpose.)

You can see some of this in the "de novo" protein designs that come out of labs like David Baker's. They're able to take a protein topology and use a computer to design a sequence "from scratch" which folds to that topology. But far from all of the sequences which their computer program spits out actually will fold. Only a small fraction of such designs will actually fold into a compact protein.
But one of the things that they've found which improves their success rate is to check the designs by "forward folding". That is, the computer spits out a design which it predicts will be a low-energy sequence for that structure. But just having a sequence which is predicted to be "low energy" isn't enough. As an additional step they run the sequence through a folding simulation to see if the sequence they designed also has a clear preference for the designed state. Roughly speaking, checking if there is a clear "folding funnel" which will drive the protein toward the desired folded state. By doing this subsequent computational check, they're able to greatly increase their success rate when the proteins are actually expressed.


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What kind of bug is this? I found it on my Cleome plant in Atlanta Georgia

This bug was on my cleome plant in Atlanta Georgia

It is an immature from the order Hemiptera. I am sure of that, but cannot help further.

@KarlKjer If you want to take the time, I think it might be worth posting a canonical immature hemiptera post with some identifying characteristics and any particularly interesting individual examples (you seem to be the most active arthropod ID answerer lately), then we can close and direct people there; although this is the only one I recall recently, I feel like since I've been here there have been a lot of questions on them, especially with the spread of certain shield bugs.

This is an instar (nymph) of a shield or stink  bug (order Hemiptera, family Pentatomidae).
Specifically, it appears quite similar to a later juvenile stage (~4th instar) of Chinavia hilaris, the Green Stink Bug.

 4th instar; Source: Oregon Dept of Agriculture

 4th instar; Source: UF IFAS; Credit: Herb Pilcher, USDA-ARS, Bugwood.org.
Alain Hogue also captured a wonderful picture of this species at bugguide.net
From UF IFAS:

Distribution
The green stink bug occurs in most of eastern North America, from Quebec and New England west through southern Canada and the northern U.S. to the Pacific Coast, and southwest from Florida though California. This is the most commonly encountered stink bug species in North America.


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Can anyone identify this insect larvae please?

I found thus tiny creature in my shower its about 19mm in length with a see through body and moves much like a caterpillar.

It would be great if you could add some information where this image was taken.

It looks like a Diptera larva, and it is most certainly not a parasite. I've seen many similar larvae in the Limoniidae subfamily.


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Can multiple cetacean species communicate?
It seems that individuals within the same species have their own communication, but is there evidence to suggest that individuals from different species are able to communicate?

We are starting a Bioacoustics Stack Exchange for people interested in the studies of non-human animal sounds and the impacts of sounds on animals. Please join us! https://area51.stackexchange.com/proposals/126698/bioacoustics?referrer=YjZmYjUxYzJkNDI1YmY5NDk3NzdhMzViMmZlNzI4ZDdiYTAyMWQxNTM5ZWFiNzRhODNkMmFiMzIxZjI3MmY1N_gFvrICTvBsmYNJ2ptRM6lIZEAV-VGkXtIwNyVDja680

Do dogs and humans communicate? What about cats and dogs? I think defining "communicate" is the real question here.
This 2012 study claims to show "the first experimental evidence that the interception of heterospecific vocalizations can mediate interactions between different cetacean species in previously unrecognized ways". In other word, one species is recognizing and responding to the vocalizations of another.
This article points out that "...false killer whales and bottlenose dolphins choose to spend time with specific members of the other species rather than randomly mixing or engaging in brief opportunistic encounters" How could this occur without some form of "communication"? I'd argue it couldn't,

to be fair the second one does not require communication just the ability to recognize individuals in the other species.

It's a reciprocal relationship that involves interpreting signs and signals from the other. What is the threshold at which "recognition" becomes "communication"?

I can avoid riding ornery horses a second time that does not mean I was communicating with the horse, I can prefer my cat to my neighbors cat that pisses on my car, but again it does not mean I am communicating with it.  Favoritism is not necessarily communication.

"I can avoid riding ornery horses a second time that does not mean I was communicating with the horse" Is not the horse's "orneriness" a non-verbal form of communication that it does not want to be ridden? It's not Shakespeare but the threshold in biology for "communication" is quite basic--if a cell emits a signaling molecule and another cell receives it, we call that communication even thought it's nothing more than "recognition".

If you define communication that broadly then the question more or less breaks down, any behavior that impacts another organisms can be communication. Communication does not have only a single biological definition.

And if you proscribe communication so broadly then the question likewise breaks down.FWIW, saying that interspecific congregation behaviors mediated through vocal cues is definitively NOT a form of communication is refuted by the opening sentence from Wikipedia's definition of Animal communication.

making a big leap from what I said to that, interspecific congregation behaviors mediated through vocal cues is definitively not what I was referring to, it is neither of my examples. Also wikipedia is not a scientific source.

I have been trying to have a discussion here but you appear refractory to much beyond defending your ego. I cited WIkipedia because the claim you are making is so fundamentally wrong that I thought a more general source might help you. Guess not. Okay, here's a recent peer reviewed paper discussing a terrestrial analog to the whale example that you took issue with. Unsurprisingly, they consider this to be a form of "communication" as well.


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Identify This Plant (Flower)
I just bought this plant from flower shop, after it flowered it was very beautiful red flower, can anyone tell me what is this flower?

This is a Gerbera, which belongs to the daisy family (Asteraceae). Compare:

There are various species.

The domesticated cultivars are mostly a result of a cross between Gerbera jamesonii and another South African species Gerbera viridifolia.[5] The cross is known as Gerbera hybrida. Thousands of cultivars exist.

(from Wikipedia)


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Identify This Glowing Insect
When I was walking in my garden at night I saw this small glowing insect, can you identify what is this insect?
Location: Middle-East Palestine
Size: Length about 1 CM
This image in the dark (see the light of the insect)

These images taken by flash.

Please [edit] your post to provide your location and the approximate size of the insect. See here for guidelines for writing well-received [tag:species-identification] questions. Thanks

I voted down because we have clear species ID guidelines, and without them your question can, at best, attract guesses. ID questions lacking details lead to answers without details and we end up with a bunch of internet noise. We're trying to be more accurate than sites like Yahoo Answers or Quora where Q and A quality is minimal. Downvoting is my way of enticing users to put in the little bit of extra effort (which will lead you to getting a more accurate ID). Thanks! :)

@theforestecologist np I edited my question bro

Appears to be a larviform female firefly (order Coleoptera; family Lampiridae).
I cannot find a good source for listing/IDing Palestinian fireflies, so I unfortunately cannot give you a definitive answer. I do want to provide some of an answer and an example specimen to get you going on the path of accurately IDing your specimen.
To get you started, your specimen appears similar to Photinus bromleyi (seen here) and below:

Photinus are a group of North American fireflies, so not likely your species.
According to firefly.org, the subfamily Luciolinae is found throughout Eurasia, while the genus Lampyris is a "wastebin taxon" used as a "catch all" for misfit fireflies that is found throughout the world. So I'd start looking in those groups.
I'll dig around for a more Palestinian-oriented bug guide. Again, this is not meant to be an exact answer but just a starting point for you or another user who might have access to Palestinian resources. I'll update if I find something definitive.


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What is this strange flower which I found on an upheaval in Rhodes (Greece) in July?
It looks like it carries berries instead of blossoms. Is it actually a flower or rather a baby tree? I found it in a Google image search (see here: https://goo.gl/images/vfBDSP), but there was no description with the picture.

Looks like the berries of an arum.  Search for "arum berry image" and you'll see what I mean.

I agree, it looks like Arum creticum from the picture.  It is a kind of lily, and these fruits form after the plant has finished flowering.


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What attacked my peach tree?

Help me please! I have to get rid of these!

I Guess Its this http://entnemdept.ufl.edu/creatures/veg/aphid/green_peach_aphid.htm. please feel free to add more information.

Please provide your location, time of year you took the photo, species/cultivar of peach tree (if known) and an approximate size for the pests. Thanks.

I am happy that i was right ať least with that fact that it is aphid.

@L.Diago yeah, nice call! Glad you added the guess as a comment. It helped me form the 2nd half of my answer :).

These are definitely some sort of aphid (small sap-sucking true bugs in the superfamily Aphidoidea).
Based on the coloration and shape of the pest and the host plant, my best guess is that you're looking at Hyalopterus pruni (or the Mealy Plum Aphid).

Note: the scientific name of this species has changed at least 21 times!

 Photo by Jack Kelly Clark

Looks like this person also found this species of aphids on a black cherry tree if you want to see more picture.

Description:

Wingless adult aphids are pale green with three dark green longitudinal stripes on their backs. Their bodies are covered with a white, mealy wax. [source].

Host Plants:
Typically trees in the Prunus genus: cherries, plums, almonds, apricots, nectarines, and -- you guessed it --  peaches. [source].
Damage:
Plant can become stunted from high numbers of aphids, but the primary concern is the development of mold that grows on the aphid's honeydew. [source].
Management:
See this University of California Agriculture and Natural Resources site for management suggestions.
Suggestions:

Biological: lady beetles, lacewings, or soldier flies
Organic: biological control + sprays of neem oil
Pesticides (typically not needed): Phosmet, Diazinon, and others in the fall; neem oil, flonicamid and others in the spring.

Final Notes:
Just because an aphid shares a name with an individual plant (e.g., the green peach aphid mentioned in the comments) doesn't mean that the species is limited to just that plant or that any aphid found on said host is that species. Many aphids feed on a wide range of host plants, so limiting your host to an individual species doesn't necessarily rule out a wide range of pests. However, it is not uncommon for an aphid species to stick to a single genus, narrow set of genera, or narrow set of families of host plants.


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Insect identification - pantry moth vs clothes moth
Are the following insects a pantry moth or a clothes moth? I live in Europe, if geographical location is of importance in this case.

The insects are about 7 - 10 mm in length.
For several months I have been fighting with recurring invasion of pantry moths and those were caught in pantry moth pheromone trap. However, the specimens seem  to be smaller than the pantry moths that I have been fighting a couple of months before (I have read that clothes moths are smaller) and I have seen some flying near the wardrobes. I couldn't find traces of infestation in the food as well. Is it possible for clothes moth to be attracted by pantry moth pheromones?

Although the images are very grainy and oddly lit, the second two images look a lot like a pantry moth. Specifically, it reminds me of a very common pantry pest:
Plodia interpunctella (Indian-meal moth).

 Source: Urban & Structural Entomology, Texas A&M University, USA
Range: [source]
The Indian-meal moth can be found on all inhabited continents. Although it is primarily tropical, it can live in a range of habitats and is a very common nuisance pest in food storage facilities and people's pantries worldwide.
Description: [source]

7-10 mm long (wing span ~ 1-1.5 cm)
Wing color:
-Posterior 1/2 of wing red/brown/bronze
-Anterior 1/3 of wing is white/light gray / ochre-yellow

Separated by dark band

Body color: reddish-brown

Pest Info: [source]

Adults live 5-7 days
Females lay 60-300 eggs
Eggs hatch in 2 - 14 days
Larvae do all of the destruction

Can even eat through plastic to get to food! [source]
Common Foods: Cornmeal, flour, dried fruits, nuts, seeds, health foods, pet foods.

The first picture is of a Clothes Moth (Tineola bisselliella). The uniform gold colour of the wings (with shiny dust that easily comes off) is diagnostic.
The second and third pictures appear to be Pantry moths.
I could not find a scientific reference, so I describe my own observations below. Happy to delete this if it is not appropriate.
Both species mostly are caught in the trap with the matching pheromone. A few are caught in the "wrong" trap, and both are caught on a trap with no pheromone at all (a control).
In this case it looks like the moths pretty much are attracted to their own pheromone trap, and only caught in the wrong trap by accident.

Clothes moth trap (with pheromone bait above it)

Pantry moth trap above

Control trap above - no pheromone


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Is this a bedbug? Found in my bathtub
I found this bug crawling in my bathtub

Yes it seems like bedbug. If you want to make it certain put it on your skin and let it suck some blood. After sometime kill that bug by pressing it against your nails. If your nail is smelling awkward then it is definitely a bed bug.
Try comparing your bug against this post.


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Why and how does uniprot list around 150,000 proteins in the human genome?
Using organism:"Homo sapiens (Human) [9606]" as a query in uniprot returns about 146,000 proteins. I was under the impression that there were only 20-25,000 protein coding genes in the human genome. Is this something to do with splice isoforms, like those from SpliceProt, or another splice isoform database or tool?

Well you are assuming one sequenced genome/proteome per NCBI tax id. That is no longer true. So if you click on the proteome filter it decreases by half.
Which gets you into the 60,000 range. Now not all of these are "different" conceptual proteins, many are artifacts from the way GenBank/EMBL/DDBJ interact with the TrEMBL section of UniProtKB i.e. they are not normalized in db speak.
So for the human case you also want to add the Swiss-Prot filter to get a decent proteome that gives you about 20,000 proteins. Corresponding to the predicted/confirmed human gene count.
In all bioinformatics databases you need to pay attention to difference between database records and biological concepts. They rarely map cleanly one to one. In this case an UniProt record is not a protein, but information about a protein and a different record could have information about the same "protein". Or at least the same under some definitions of "same".
See the announcement of the draft human proteome in UniProtKB
The known isoforms are most often stored in the alternative products section of an UniProt entry. In some rare cases when the splice variant has a completly different biological function they are described in separate UniProt entries. For UniProtKB/Swiss-Prot Human there is a near 1 to 1 relation between genes and proteins. Cases as above and fusion proteins are the exceptions to this rule.
TrEMBL tries to automatically reduce redundancy in INSDC by auto merging entries in the same taxid and now proteome that have an identical reported sequence. However, variations of single gene products due to mutations and or limit what auto merging can do. For example there are 8 records for the P53 gene in TrEMBL today. Many of them from mutants, i.e. cancer genomes etc...

Since most proteins exist in more than one isoform, the number should be higher than 20.000.

@chris in UniProtKB isoforms do not get an independent record. See neXtProt for an isoform centric database of human proteins.

Very insightful answer, thanks. To be clear, these some 100,000 isoforms and artefacts are coming from GenBank, EMBL and DDBJ and are presented as TrEMBL entries?

The key point is that there are more proteins than genes because so many genes exist in multiple splice forms. You should not expect number of genes and number of proteins to match up.

There are 20+ thousand genes in the genome, but each of these can produce multiple proteins. In addition to this, you have protein fragments and cleavage products further increasing the number of entries.

I was also hoping to find out specifically where or how uniprot finds the information on those additional products.

@GoodGravy Proteomics data I presume

@GoodGravy A lot of them come directly from papers and other databases like NCBI. For example, B7U540 is an entry originating from me (via NCBI, since I never submitted it directly to UniProt).


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Can plant roots absorb dissolved oxygen from water, or do they require actual bubbles in the water?
Plant roots generally require some exposure to air.  Deep water culture is a form of hydroponics where plants' roots are left to soak in water.  To keep the roots from "suffocating", most online sources recommend some kind of aeration mechanism, such as an air stone.
These systems normally wind up filling the water with bubbles, right under the plants.  So my question is: are the bubbles responsible for keeping the plants alive, or is the dissolved oxygen keeping the plants alive?  So for example, could plants live immediately downstream of a waterfall (a natural aerator), even out of range of its bubbles?


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What is possibly wrong with my gel electrophoresis when i don't see bands of DNA ladder?
![enter image description here][1]
What was possibly wrong in my gel electrophoresis when I didn't see bands of DNA ladder?
I'm running a 2% electrophoresis gel (65v for 2h) to confirm the presence of qPCR amplification products, I can see the gDNA bands, is only the ladder that don't appear.

Try a new batch of ladder, rerun the gel. Without more info this question cannot be answered.

Can you add a pic?

Already added, the ladder should appear in the first lane.

did you try rerunning with new ladder?

no, this was the last ladder available in the lab with the base pairs i needed.

As one attempts their daily Sisyphean challenge of uncovering a new fact there is one truism, or platitude, that informs all of our efforts at troubleshooting an unanticipated experimental outcome.  This can be paraphrased as:
The number one cause is pilot error.
Accumulated experience of bench scientists everywhere shows that their own human errors are the simplest explanation whenever they try to deduce what could have gone wrong.  In the real world this translates into an operating axiom:
Don't waste time and energy coming up with new physical laws, or multi-step explanations that require you to remake and test all of your reagents, just repeat the experiment and see if this phenomenon is reproducible.
With that new information, that it is, or is not reproducible, you can decide if there is any hypothesis to test. But please, don't just take my word for it. Survey experimentalists, and the more experience they have the better.


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How do signal transduction pathways utilize transcription factors to express a specific gene?
I have an inquiry regarding the regulation of genes via extracellular signaling.
To my knowledge, in autocrine, paracrine, and endocrine cellular communication, large protein ligands that cannot directly diffuse through the plasma membrane of the target cell(s) use surface receptors to perform their desired action on the target cell(s).
I have learned that some of these ligands activate signal transduction pathways such as the MAPK/ERK and JAK/STAT pathway and drive the expression of specific genes by utilizing transcription factors (of course, in eukaryots). A simple example of this would be the action of epinephrine (adrenaline) on hepatocytes (liver cells), where the amino acid-based hormone uses the transcription factor CREB to express the gene coding for Glycogen Phosphorylase to engage in glycogenolysis.
Here I have two questions:

How does the transcription factor chemically indicate which gene to express? (Is there a gene indexing system like a computer filesystem?)
How does the transcription factor locate and bind to the promoter of the gene it is trying to express?

Thank you.

1: by recognizing the promotor sequence. 2: trial and error. TFs don't have eyes nor a brain or ways to propel themselves. Somehow the answers are in the question it seems, as 2 answers 1, while 2 is basically chemistry in a way.

@AliceD But don't most genes have similar promoter sequence patterns? How could we specify a set of transcription factors to express a specific gene? If trial and error was used, signal transduction pathways that involve gene expression would pitifully fail most of the time.

Subquestion 2 does not have "specificity" included. As of now, it looks like you wish to know how it gets to its target. maybe refine your question a bit and perhaps the whole story on signal transduction is not really relevant?

Most genes have a similar core promoter but varying proximal and distal promoters which contain specific TF binding sites. Signalling pathways are integrated with other signals and the status of the cell in order to correctly express genes.

This is a combination of multiple regulatory systems. Most genes are not regulated by a single factor, but by many. Moreover in eukaryotic organisms there is also epigenetic, which "inactivates" permanently certain areas of the genome by compacting these zones forming heterochromatin.
Moreover, even when we are interested in a single function a TF might have, that does not mean that it only has this function in the cell. We view it as humans, and maybe for us it is logical that a response to a high metabolite in the environment simply leads to expressing the protein that metabolizes it. However, probably it is interesting for the cell to also activate other pathways and gene networks (i.e. anabolic pathways that feed off this metabolite, compensatory pathways to mantain homeostasis...). Because that normally TFs affect more than one gene naturally.
The mechanisms of action of the TFs are multiple, but they tend to simply allow or deny the access to the adequate RNA polymerase. For more information about this check the wikipedia article on TF structure
In this image we see a typical mechanism of action, DNA bending
Different domains interact in activating a gene, enhancers which are usually long distance, promoters which tend to be in the upstream region, though they can be downstream or in the gene sequence, and epigenetic factors that change the compaction of DNA, making it inaccessible to proteins.
Just as a last thing to point out, you should acknowledge that the biological systems are far from exact and yes, a single TF might activate 200 genes, even when its main objective in that moment is to activate one, but it won't really matter as long as the those 199 activated genes express at a very low rate (for example by not having the right RNA polymerase subunit accessible, being marked as inactive by epigenetic systems or having their own inhibitors).

Thank you so much!! You just clarified my understanding of gene regulation!

I'd also like to add with respect to many text figures, that while the coactivating complex Mediator isn't necessarily required in all instances of gene regulation, it does give the transcription a level of robustness you wouldn't otherwise get without it. More on mediator here.


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How can E. coli affect C. elegans expression?
Plasmids can be transferred to E. coli. These transformed E. coli can be fed to C. elegans to silence its gene expression by RNAi.
How can E.coli release RNAi to C. elegans? Even if we assume E. coli could enter cells of C. elegans for being intracellular Bacteria, it is hard to imagine that RNAi will exit E.coli directly and enter C.elegan's cells? Normally, no cells or bacteria will release RNA or genomic material outside of their cells?

@Chris Is there a way of merging this question with this one http://biology.stackexchange.com/questions/38586/how-c-elegans-is-used-for-siliencing-genes/38597#38597 ? While they are duplicate questions, this one asks the question in a clearer, more precise manner?

"Normally, no cells or bacteria will release RNA or genomic material outside of their cells?" Horizontal Gene transfer in Bacteria. Human immune system Neutrophils and Neutrophil Extracellular Traps...

This post provides some additional information on how dsRNA is taken up by C. elegans

Yes, as bizarre as it may seem, that is what happens. The E. coli express a double-stranded RNA hairpin (under the regulation of an inducible promoter), and the RNA contains a sequence derived from a C. elegans gene.  When the worms eat the bacteria they grind them up in their pharynx, and release the cell contents (including the induced RNA) into the worms' gut. The gut cells are able to absorb the dsRNA  and transport it to other cells as well. The RNAi pathway processes the inhibitory RNAs to down regulate the target gene.

Now that is surprising! +1. I tried to edit the question. Could you check if it's OK? It's not really my expertise.

You can also add a note on RNA transporters in C.elegans (Sid1/2). Though I am not sure, I guess that C.elegans (or perhaps related organisms) expresses these transporters more than other organisms that we know.

@WYSIWYG Ilan amd you had given similar answer to a question of mine about c.elegans. I think my question cud be merged with this one. ( amnt able to provide the link.... using app)

First of all, gut cells can absorb the dsRNA, but we are talking about the whole body's cells in C.elegans! If we transform RNAi of EGFP, it will silence the whole body's EGFP... or not?
Second, RNAi is made by E.coli or C.elegans? I am not talking about dsRNA. If RNAi is made by C.elegans, it means C.elegans must absorb the dsRNA releasing from E.coli. As far as I know, dsRNA might be bigger than proteins... is it possible to absorb the dsRNA directly? And also, back to the first question, how can dsRNA expend to the whole body of C.elegans to silence most of cells' gene in the whole body?

@RogerL. You are confusing the term RNAi, which is a biological regulatory mechanism that degrades mRNA, with small dsRNA, which can trigger the RNAi pathway. The bacteria synthesize the dsRNA, and this is released when the bacteria die. The C. elegans cells absorb, or incorporate those bacterially synthesized dsRNAs AND contain transporters that spread the dsRNA between adjacent cells. So yes, EGFP expressed in bodywall muscle will be silenced by dsRNA ingested in the gut. The RNAi complex exists in all worm cells.

Two worm genes that regulate other worm genes using this pathway are let-2 and lin-4. They do not encode proteins; they encode small interfering RNAs that bind to mature mRNAs from other genes--protein coding genes. Once the lin-4 transcript binds to its complementary target that dsRNA triggers the RNAi degradation pathway.  You can also inject dsRNA into worms (but is is labour-intensive), or you can synthesize dsRNA in vitro and just soak the animals in it for the same effect as feeding them engineered bacteria.


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Why alcohol can't help with OCD?
I was thinking about influence of ethanol on our brain.
We know, that ethanol can affect GABA receptors and increase flow of chlorine in our brain cells. So it makes signal weaker and slow our CNS activity down.
People with OCD usually take minor/major tranquilizers (and many other ofc.) that have similar effect.
I understand, that alcohol (ethanol) can't stay in our CNS as long as tranquilizers do and it also causes many bad influences, but if we put these bad effects away, could alchohol potentionaly help people with OCD for a short time?
I guess no, but i don't know much in neuropharmacology, so explain me please.
Thanks.

Interesting idea. How do you know it doesn't work?

The close-vote on the question being self-help is off. It is a legitimate question, especially in the light of the tendency for psychiatric patients to self-medicate. +1

https://www.quora.com/Why-alcohol-cant-help-with-OCD Got some answer on quora, if smb is interested.


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CRISPR/Cas for editing the human genome
I know, that the CRISP/Cas approach for "cutting" the human genome is not completely suitable if we can't say not suitable at all. Because we have many repeats and this approach can bring to our genome additional breaks in DNA and after DNA-repair it causes unwanted mutations. If so, why scientist still continue to play with it (See the link, only 16% success chinese scientist got) ? And what other DNA-editing mechanisms we have? I might be wrong, so correct me please.
Thanks for explanation.
Chinese Scientists Defy Ethics, Double Down on Editing Human Embryos

It's not clear to me what you're asking. Editing the human genome is not at all the same as editing the genome of human embryos. The vast majority of all work with CRISPR is for editing genes in isolated human cells grown in laboratories, not in people. In the laboratory setting, 16% is an excellent success rate; before CRISPR, that number was much, much lower --- small fractions of a percent. Very few scientists "play with it" in human embryos, because of the major ethical problems involved. So are you asking about molecular biology or ethics?

Ofc about molecular biology.

In terms of molecular biology, how do you come up with the idea that CRISPR is "not suitable" ? The success rates and level of specificity achievable with CRISPR is pretty darn revolutionary. That's why scientists continue to play with it -- in the lab, and in model organisms. Using CRISPR in humans is a whole different question though, and most scientists would say it's too early for this yet; but this depends a lot on what specific application you're thinking of. For curing a recessive genetic disorder for example, 10% success rate might be fine. You need to be more specific I think.

I'm interesting in how we can avoid unwanted mutations that CRISPR/Cas causes.

Well that's an entire research field ... If you're asking about the current rate of off-target effects, that can be answered (Keith Joung's paper mention by Tom is a good example). But in the study you cite, I don't see any data on off-target effects. They only looked at the CCR5 locus, and 84% of embryos that were not "successful" were either not edited at that locus, or contained indels (unsuccessful homology repair). So that is more about efficiency of homology repair, which is unrelated to Cas9 specificity.

This question has been flagged for closing. I think if dshulgin and @roland bundle the comments into the question and an answer then this is a productive question.

Repeats aren't the problem with CRISPR. They stop you from editing repeats and repeat-like sequences, but in principle they can be worked around through careful design of guide RNA. CRISPR techniques right now do have problems with off target effects, but these problems may yet be solved. The CRISP/Cas approach to gene editing already has a lot of different variants and is under continual improvement, so there's no reason to think it won't get better. There's also no reason to think that the 16% figure there is only influenced by the use of CRISPR/Cas - it's an experiment with lots of other variables.

Could you be more clear? Under repeats i meant that our genome has thousands similar to our target sites and we have big probability of incorrect interaction with Cas protein. Can you explain your point in more details? Sorry that's still unclear for me.

"thousands similar to our target sites" is not true of all sites. It's true only of sites resembling repeats. Most sites in the genome can, for instance, have specific PCR primers designed against them. This would not be true if they all resembled repeats.

"can" but is that true in general? I mean, we should have big confidence of that to process CRISPR/Cas on human's genome.

It is true in general yes. But not in every case.

The accuracy of CRISPR to its target is not necessarily a problem at this time, because scientists have developed a more accurate version of it, CRISPR hf, which has almost no off target effects.  Here's a report on a study with a very accurate version of CRISPR


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Cell biology books
I'd like to know, what is the best list of books for non-biologist to understand, how signalling between organels is organized inside of eukaryotic cells. I really want to get how cell as separate system works until apoptosis happen.
Of course, any useful online courses (like MIT ocw) are appreciated.

BOOKS

If you want to learn about cells in detail from scratch to advanced level I recommend you two books:

Molecular Biology of the Cell, 6th Edition. 2014. Bruce Alberts, Alexander Johnson, Julian Lewis, David Morgan, Martin Raff, Keith
Roberts, Peter Walter
http://www.garlandscience.com/product/isbn/9780815344322
Essential Cell Biology, 4th Edition. 2013. Bruce Alberts, Dennis Bray, Karen Hopkin, Alexander D Johnson, Julian Lewis, Martin Raff,
Keith Roberts, Peter Walter (This can probably be considered the
"light" version of the first book above)
http://www.garlandscience.com/product/isbn/9780815344544

Then if you really want to put everything you learn into practice and learn them in-depth, you can try the Problems Book of the first book mentioned above:

Molecular Biology of the Cell 6E - The Problems Book. John Wilson, Tim Hunt garlandscience.com/product/isbn/9780815344537

ONLINE COURSES

Crash Course in Biology -- on YouTube
Introduction to Biology - The Secret of Life -- available on exd.org
-- provided by MIT
Simply just search for "Biology" on coursera.org and you will find dozens of good courses

Finally, I highly encourage you to look into the first book I mentioned (Molecular Biology of the Cell, 6th Edition). It's a fantastic book and it will teach you much about biology and cells.


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Can immortality of the Turritopsis dohrnii be learned or adapted by other species?
I have heard that Turritopsis dohrnii is a species of jelly fish which is immortal, as it can grow old and then back to growing young.
So, how is it possible?   Can other species (marine and/or land) species adapt or  evolve into such a system?

Possible duplicate of Why is the Hydra Biologically Immortal?

@AliceD I had a look at that question, and I don't think this is a duplicate of it.  This asks whether some other species can adapt or evolve itself to have such features which helped Turritopsis dohrnii with the immortality characteristics

The answers of linked question answers the 'how' part and the theory whether other species could evolve such a system is opinion based and open-ended. Knowing how it works (stem cells, telomerase activity) can be extrapolated to other species, in theory and in theory only.


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How do two parents, recessive and dominant genes and two complimentary nucleotides end up in one DNA?
In the basic school, I was taught that half of genome is received from father and another half comes from mother in the form of double-helix DNA, whose first helix consists of dominant nucleotide bases and second helix is a kinda inverted copy of the first helix. I feel like 3 different concepts are mixed here into one DNA spiral and I cannot sort them out. Can you explain exactly how is every concept (parent material, recessive genes and complemenrary nucleotides) are represented in the DNA? The professional and wikipedia explanations are too full and I cannot extract this basic information from too much detail.
For instance, mother and father could donate non-overlapping sections of the double helix, e.g. you inherit a head of DNA from father and tail from mother. I can also guess that first helix consists of primary nucleotides whereas second helix is complimentary. I also understand that despite it is natural think that primary = dominant whereas complimentary nucleotide stands for recessive, it is unlikely coz dominant is a full gene rather than a single nucleotide and dominant is independent and can differ from recessive whereas complemntary implies deterministic relationship between two. Furthermore, receiving dominant from parent1 and recessive from parent2 contradicts the fact that only one of the parent alleles enters the offspring DNA. Probably both are inherited and only one is expressed in phenotype but I am not sure and ask to clarify this. In other words, I would like to know how both parent1 and parent2 chromosomes live in the child DNA if not in the form for helix1 + helix2. Particularly, what are these two chromosomes, next to every person, if not two helix of one DNA

and where are they located? Are these just two DNAs which exist only during meiosis, during first moments of fertilization? How do you end up with only one DNA in the end?
I would also like to know if individual's eggs DNA is coming from his own DNA or is formed in parallel, from his parents' DNA? That is, when individual's eggs' DNA is produced: during fetation of the parent, during his lifetime from his DNA or during fetation of the child?

Welcome to Biology.SE. Your question is very broad and therefore the answers cannot be complete. Try to limit your post to one unique and accurately defined question. Note also that your last sentence is not finished (I would also like to know which parts of the offspring DNA are produced during ....)

I agree with @Remi.b,  it is quite a wordy question with a lot of buried subquestions.

I will talk about humans only and I will not talk about the special case of sexual chromosomes (and anomalies such as trisomy 21) from the answer just to keep things easy. There is a lot to say, so I am just making a very short overview of different subjects. Get some coffee first, read slowly and don't hesitate to click on the wikipedia links to further your knowledge.
Pairs of chromosomes
We all have 46 chromosomes. The chromosomes can be arranged in 23 pairs. By definition the 3rd pair of chromosomes is the 3rd longest pair of chromosomes as you can see on this karyotype

You'll note that the 23rd pair is the pair of sexual chromosomes but I won't talk about them. Note by the way that species that have chromosomes present in pairs are called diploid. Some species are haploids (not pairs), some are tetraploids (4 chromosomes of the same type together), etc... While the terms "diploids species" is often used to refer to mammals for example, it is actually more correct to talk diplontic species. Diplontic species, are those species who are diploid most of the time and haploid only for a short period. Our ovules and spermatozoids are indeed haploids.
Pairs of chromatids
Chromosome are more-or-less X-shaped. Each "vertical line" of the X is a double stranded (double helix) chromatids. Two chromatids of the same chromosome are called sister chromatids. Two chromosomes of the same pair are called homologous chromosomes. Note that chromosomes don't always look as they are represented here, it depends on the phase during the life cycle of the cell but this is a story for another time. As you said, one chromatid is made of two strands that are "anti-parallel". The point of the junction in the center (although it is note always in the center as you can see) of the X-shape is called the centromere.
Inheritence
In a pair of chromosomes, one chromosome is inherited by the father, the other one by the mother. Therefore we receive exactly the same amount of genetic information from each parent (but see this post). The egg actually receive 2 single chromatids (one from the ovule and one from the spermatozoid). At some stage of the life cycle each chromatid duplicate to make those X-shaped chromosomes. Therefore, two sister chromatids are exactly (except exceptions!) identical. However, because one chromosome come from the father and the other one from the mother, two homologous chromosomes are not exactly identical. Note that mutations occur during replication of DNA (especially during meiosis). Note also that at the moment of producing our gametes (=spermatozoids and ovules), chromatids from different chromosomes (within the same pair) can exchange DNA. This process is called crossing-over. Here is a schema of this process

Crossover is the process by which two chromatids from different homologous chromosomes exchange their DNA. Chromatids do not merge into one (as suggested in your below comment). Look at the above picture. Top left are the two homologous chromosomes. Top right are the two homologous chromosomes after crossover (a little pink piece is now attached to a blue chromatid and vice-versa). In the bottom are the four resulting gametes (the 4 independent chromatids) after meiosis.
While crossover refers to the mechanism, recombination refers to the statistical association between two loci. On the above picture there are two loci represented and both are heterozygotes (see below for definition) as at one locus are the alleles aA and at the other locus are the alleles bB. Of course, on the sister chromatids both alleles are the same given that the two chromatids are just copy of one another where one comes from one parent. Therefore, a is always with b and A is always with B on the same chromatids. In the absence of crossover, we say that they segregate non-independently. If the offspring get A, (s)he will necessarily get B as well. However, if crossover can occur in between the two loci, then some gametes can carry a and B and some others can carry A and b. The statistical association between two locus is referred to as recombination. the recombination rate between two loci indicates the rate with which a crossover will occur between these two loci.
DNA
When talking about DNA, we usually refer to one double helix (one chromatid). DNA, is made of different chemical compounds including the nucleotides. There are 4 types of nucleotides that we are reffering to by the first letter of their names, A, T, C and G. Every time there's a T on one strand there is a A, in the other strand (and vice-versa). Every time there's a G on one strand there is a C, in the other strand (and vice-versa). In consequence one strand is some kind of a negative (photography) of the other strand.

From gene to protein
You can refer to a position on a chromosome as a locus. At different loci are different types of sequences. Without going into the details, a gene is a type of sequence that is used to make a protein. In order to make a protein from a gene, the double helix has to open up over a short region, some proteins come, read the DNA and make up an RNA out of it. The RNA is some kind of negative of the DNA strand that has been read (except that the Ts are replaced by Us). From the RNA some other mechanism (ribosomes; ribosomes are actually made of other RNAs but this is also a story for another time) make a protein our of the RNA. Here is an extremely simplified schema of this process.

Effects of the genotype on the phenotype
As I said above, there are some differences between homologous chromosomes. Consider for example that in a population, at a given locus (let's assume this locus correspond to a gene for simplicity) different chromosomes carry different variants. These variants are called alleles. The words recessivity, additivity or dominance refer to the relationship between two different alleles at the same locus in terms of how the two alleles affect the phenotype. Referring from wikipedia A phenotype [..] is the composite of an organism's observable characteristics or traits, such as its morphology, development, biochemical or physiological properties, phenology, behavior [..].
Recessivity, additivity and dominance
Let's call one allele Aand the other allele a. Given that one individual has two chromosomes, this individual at the locus under consideration can be either aa, aA, Aa or AA. The difference between aA and Aa is that in one case the A allele comes from the mother while in the other case it comes from the father. It essentially makes no difference, so let's just call these two types aA. a and A are said additive if the phenotype aA is the average phenotypes between the phenotype of aa and AA. If the phenotype aA is closer to the phenotype AA than tow the phenotype aa, then A is said to be partially dominant and a is partially recessive (or vice-verse for the opposite scenario). In the extreme case where the phenotype of aA is exactly like the phenotype of AA, then A is said to be dominant and a is recessive (or vice-verse for the opposite scenario). Overdominance is a third type of relationship where the phenotype of aA lies outside the range of phenotypes of aa and AA. Such as for example individuals having both aa and AA genotypes are small while individuals being aA are big. Btw, AA and aa individuals are said to be homozygous while aA are said to be heterozygous regardless of the functional relationship between the two alleles.
Consider for example a disease that is expressed only in the aa genotypes. In such case a is recessive. If two AA individuals mate together there is no risque for the child to carry the disease. If one aA individuals mate with a AA individual the child is either aA (with probability 0.5) or AA (with probability 0.5). If two aA individuals aA mate together, than a child is aA (with probability 0.5), AA (with probability 0.25) or aa (with probability 0.25). In other words, if two heterozygotes individuals mate together, they have a probability 0.25 that a given child will carry the disease if the disease is recessive. This probability reaches 0.75 if the disease is dominant (but the two heterozygote parents would both express the disease as well).

You exaggerate the number of questions I have asked. Particularly, I did not ask anything about RNA-proteines. I also understand what does dominant and recessive means. I just asked where are they located. The fact that mom chromotide is paired with father chromotide and I carry both separately throughout my life is everything I wanted to know. This explains how dominant allele is homologously coupled with recessive one. I still wonder which crossover are you talking about if the chromotides exist independently? Crossover/recombination is a process of merging two chromatide into one, right?

Maybe I oversee the number of questions but that would just mean that the post is a little unclear instead of being too broad. But anyway, we might get to the answer you're looking for before the question get closed. Please see edit in the "inheritence" paragraph below the picture.

@ValentinTihomirov Recombination/crossover is when elements of sister chromatids are exchanged between the two chromatids, see this wikipedia page. They do not merge into one.

I think you really need to go back to the very basics and try to understand the DNA molecule, what a chromosome is, DNA replication and mitosis, what homologous chromosomes are, what non homologous chromosomes are, what sister chromatids are, what non sister chromatids are before you attempt to understand meioses. And I would definitely recommend you learn all of these things well before you attempt to understand molecular inheritance, but let me see if I can at least begin to clarify some of your misconceptions.
If you are having a hard time understanding the concepts as written, try looking up the articles on Simple English Wikipedia first. The try to make their articles easier for novices to understand.
There is no such concept as Dominant Nucleotide Bases. The two strands of the DNA double helix are complementary and antiparallel. Genes can reside on either strand.
You are also getting really mixed about recombination via crossing over in meiosis. The chromosomes that are being recombined in the mother are from her parents, so technically the chromosomes that are being recombined are the grandparents chromosomes.
The same is happening when the father produces gametes. The chromosomes from his parents are swapping pieces of DNA.
At the end of meiosis, each gamete has a random assortment of 23 chromosomes, either from the father or the mother of the adult male or the father or the mother of the adult female.
The 23 can be recombined meaning that the chromosome is part grandma and part grandpa, or it is a grandmother's chromosome that has not recombined or a grandfather's chromosome that has not recombined. Just looking at the possible ways that 23 chromosomes can randomly assort without taking into account recombination to produce a gamete, there are about 8 million combinations. Add recombination and it gives you a huge amount of genetic diversity.
So those are the haploid gametes. When fertilization occurs the sperm from the father donates its random assortment of 23 chromosomes and the ovum from the mother has 23 randomly assorted chromosomes of its own. This gives you at total of 46; 23 from the father, made up of a random assortment of chromosomes from his father and mother (or chromosomes recombined by crossing over to be part his mom and part his dad), and 23 from the mother with the same pattern of random assortment and recombination.
Also, the double helix doesn't dissociate (come apart) during crossing over [NOTE: for those who know, please do not jump on me for not explaining strand invasion here and the need for homologous sequences for crossing over]. One part of a grandparent's chromosome is exchanged for the exact same part of a chromosome from the other grandparent's chromosome, assuming normal cross over events. The alleles (versions) of the genes in that segment may vary, which is why you have a chromosome is part grandmother and part grandfather.
As for dominant autosomal genetic traits versus recessive genetic traits. A dominant trait means that a heterozygous child will express the phenotype even though they only have one copy of the dominant allele. If it is a disease, then we say the person is affected. If it is a recessive trait, then the heterozygous child will not express the phenotype, so they are not affected by the disease, but they carry the allele and can pass it on to their children. This person is said to be a carrier. If a person is homozygous for a recessive trait, then they will be affected by the disease and show the phenotype.
As for inheritance, you have to draw the punnet squares. This will show you the different patterns and probabilities of inheritance.
UPDATE
I think that you are getting confused by the idea that you inherit one set of 23 chromosomes from your mother and one set of 23 chromosomes from you father. While this is true, meiosis happens in their reproductive organs before fertilization (for the most part, but the important part happens there and then).
The example of the father is easier. He has two sets of chromosomes, one set that he inherited from his mother and one set he inherited from his father. At the beginning of meiosis all 46 chromosomes replicate. They make an exact copy of themselves and are joined at the centromeres. You have 2 sister chromatids on each of those chromosomes. Now the the homologous chromosomes will pair up, so one of the chromatids on the paternal chromosome (say chromosome 4 from Grandfather's set) will join with a non sister chromatid from the maternal chromosome (Grandmother's chromosome 4). So you have four chromatids from chromosome 4 lined up at the metaphase plate. The two non sister chromatids that are joined will recombine when the kinetochores move along the microtubules towards the poles of the spindle. At the end of all of this you have two cells that contain 23 chromosomes, each with a sister chromatid, however the sister chromatids are no longer identical because one of them recombined with the the non sister chromatid of its homologous chromosome. The thing you must remember is that each chromosome assorted independently of the other. For Chromosome 1 the maternal chromosome may have gone to the left cell while the paternal chromosome went to the right. Then for chromosome 2 you might have the maternal chromosome go right and the paternal chromosome go left. And so on and so forth. The number of possible combinations of how you can arrange two sets of 23 chromosomes is 2^23 or about 8 million different combinations.
During meiosis II the 23 chromosomes again line up at the metaphase plate and they are attached to the spindle by both sides of their centromere / kinetochore complex. When the migrate the two sister chromatids migrate towards opposite poles. Again it is completely random as to whether the recombined chromatid or the chromatid that did not undergo recombination will migrate to the right or the left. Again, there are 2^23 possible combinations for EACH cell.
So you end up with an incredible amount of genetic diversity on how chromosomes are assorted within the gametes. You will still only have four possible outcomes  in the copies of any single gene that you get. You will inherit either your paternal grandfather's copy or your paternal grandmother's copy and you will inherit either your maternal grandmother's copy or your maternal grandfather's copy. That is why if a genetic disease is caused by one gene, it depends on which copies you inherit.

I do confuse crossover with recombination indeed. Here in IT, we have a simplified picture where you need crossover to combine features of two survivors and you achieve recombination through crossover. I use recombination with crossover, interchangably, as long as DNA is linear, for this reason.

You seem to say a very non-obvious, sensational thing that instead of combining the features of fittest individuals, nature combines genes of their parents. This is very sensational because the well-qualified features, that favor the mom-dad fitness and survival, may be due to crossover in their proper DNA rather than their parent qualities. It is therefore that nature discards the parent DNA and starts over. There are good chances that I become good painter if nature tested my parents but my chances are reduced if it will use DNA of my grand parents to recreate mix of genes of my parents.

@ValentinTihomirov Your post is really too broad (and it gets upvotes probably because it got 2 answers) but you should consider no extending your set of questions any further and rather open new post for new questions. If you want to ask what is the difference between crossover and recombination then you can do so in a new post (note however that a google search will probably answer your question).

I asked my question because I seen this statement A dominant trait means that a heterozygous child will express the phenotype even though they only have one copy of the dominant allele many times. I want to know where are those alleles stored in. I always pictured them as a section of DNA sequence, whose first helix represents dominant gene and antihelix represents a recessive gene. It seems attractive, despite wrong for explained reasons, because you always speak about dominant and recessive as they always come in pairs.

Genes are semi randomly dispersed along each chromosome. I say semi randomly because gene duplications can result in genes that are very close to one another. Also most genes are not found at the very end of chromosomes. The estimated is that humans have about 25,000 genes distributed over 23 chromosomes. That averages to about 1,000 per chromosome, though some have more and some have less. There really isn't any order to where they are in a chromosome or which chromosome they are found on. The just are where they are as a result of how each germline evolve.

@ValentinTihomirov  I am not sure what is non obvious or sensational about what I said. Independent assortment was understood by Mendel before we knew about DNA. While meiosis ensures that each gamete gets a single copy of each chromosome, how those 23 get distributed from the 92 possible chromatids is entirely random so long as one if each type of chromatid makes it into a gamete. The traits that get passed on are solely dependent on the chromosomes contained in the egg and the sperm that fuse.

"I want to know where are those alleles stored in. I always pictured them as a section of DNA sequence, whose first helix represents dominant gene and antihelix represents a recessive gene" @ValentinTihomirov. This is wrong. One copy of a gene is on the chromosome that you get from dad and the other gene is from mom's chromosome. Each chromosome is a separate molecule of double stranded DNA. Dominant just means having only one copy, say gene from dad's chromosome is enough to make you sick. Recessive means the gene you get from dad and mom have to be the same, otherwise you won't get sick.

I understand that water is wet. I am asking if I carry both dominant and recessive alleles or only dominant one enters my body?

@ValentinTihomirov Whether you have dominant or recessive alleles is a function of the trait you are looking at. Eye color is an easy example. Brown eyes are Dominant; Blue eyes are Recessive. In order to have Blue, you need to have both alleles be recessive to produce the blue phenotype. To have Brown, you only need one brown allele, as that will produce the brown phenotype. If you have a parent with blue eyes and a parent with brown eyes, then you will be heterozygous if you have brown eyes, One dominant and one recessive. If you have blue, then both are recessive.

@ValentinTihomirov If you have the case where one parent has Brown eyes and one parent has Blue eyes and you end up with Blue eyes, that means that your brown eyed parent was heterozygous and had a brown allele and a blue allele and you ended up inheriting their blue allele along with your other parent's blue allele. As the blue parent was homozygous for blue, you were always going to get one blue allele, so there was a 50% chance that you would get the blue allele from your heterozygous brown parent and have blue eyes and a 50% chance that you would inherit the brown allele and have brown.


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Identify hematophagous insect
There's a small insect that seems to enjoy residing near trees and takes blood meals. The pain is sharp, comparable to being stung by a wasp.
I'm located in Serbia, Eastern Europe, bordering Hungary and Romania. It's currently August, warm and very moist from the grass being regularly sprinkled.

This is an "aphid lion", a larva of a lacewing (family Chrysopidae). They eat aphids and other small animals, not blood, but are capable of biting humans. Here is a text about that (seems reasonable even with the silly title). It also says that "When a lacewing larva bites a human, it’s likely that any persistent itch or redness is due to the saliva injected at the site of the bite" so that would explain your pain.

Great! Apparently, they seem so beneficial you can't simply swat them off your person.

yes, just keep them off your skin!


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Selective herbicides
There are several herbicides available that claim to kill lawn weeds but not the lawn grass. This seems amazing, to me. How does this work? How can a chemical be lethal to a broad range of plants, but not to grass? What’s the difference between weeds and grass?

I suggest you investigate C3 vs C4

Thanks. I see that wheat and rice are C3 plants. I’d guess that lawn grasses are similar to these?? But I also see that 95% of plants are C3, which suggests that most weeds are C3, too. Are you suggesting that lawn grasses are C4?

Those two articles are good but don't suggest any reason for selective action

From the second paper: “the underlying molecular mechanism of how auxinic herbicides selectively kill dicots and spare monocots is not understood yet”. So if dicots = weeds, and monocots = lawn grass, then I’m asking a question that didn’t have an answer in 2013.

Hmmm. To a lay-person like me, glyphosate seems like a good example of a herbicide that is NOT selective: as far as I can tell, it seems to kill everything. It certainly kills grass.


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Shrimp in rainwater puddles
After rain, we often find shrimp-like creatures in the puddles left on our concrete patio. We have also found them in the cat's water bowl (on the same patio). They are pink in color, and around 3mm long.
The idea of shrimp on land seems absurd, but that's certainly what they look like.
We live in Okinawa, and even long-time local residents don't seem to know what they are. We're on a cliff 10 meters tall, right next to the beach.
My questions: what are they, and how do they magically appear after rain? From eggs that are lying dormant on my patio, waiting for rain??
The alleged duplicate is quite helpful. My question is slightly different because I live beachside in Okinawa, not in central Florida, and my creatures are much smaller. Probably a related species, though one that doesn't seem to be familiar to the locals.

Is there any chance you could take a good picture and add it in your post?

I thought someone would ask for a picture. I'll try next time it rains. But meanwhile, after some research, I suspect that they are some sort of amphipod. Weird that the local folks don't know about them. Maybe a new arrival in Okinawa??

or maybe water fleas...

@BryanKrause: Thanks. I saw the post you cited. My creatures are quite similar, but about half the size. Just another species, I suppose.

does any match https://openi.nlm.nih.gov/imgs/512/352/3253665/PMC3253665_ZooKeys-163-013-g017.png


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Why doesn't telomerase activity cause DNA to get longer each time a cell undergoes DNA replication?
Telomerase extends the ends of the lagging strands in order for all of DNA to be be copied. Doesn't this also mean that DNA gets progressively longer each time it undergoes replication? Why is this not the case?

I will assume that you are referring to humans, though much of the research to elucidate telomerase function was performed in yeast.
The first reason is that only a small subset of somatic cells express telomerase. Most somatic cells are terminally differentiated and mitotically inactive, so they are not called upon to replicate their DNA and divide. And when they do, their telomeres get shorter due to the 3' end replication problem.
The end replication problem arises due to the biochemical limitations of DNA Polymerase. Pol requires a primer, 5' to 3', in order to bind to the template strand and begin to catalyze the elongation reaction. So when DNA Polymerase gets to the 3' end of the template strand, it is unable to catalyze the reaction because it doesn't have a free 3' hydroxyl. When the end RNA primer that was used to catalyze the Okazaki fragment just before the 3' end is removed, there is no place left on the template strand to prime, so there is no 3' hydroxyl to begin the elongation reaction and you are left with a 3' overhang of single-stranded DNA.
On the 5' end of the Template Strand, even though the polymerase is able to catalyze the reaction all the way to the end, the end of the chromosome is processed and nucleotides are removed to make a single-stranded 3' overhang on this end. The overhangs are necessary to do strand invasion to form the T-Loops of the telomeres. So every time a chromosome in a cell that has inactive telomerase replicates, it gets shorter.
For the cell types that have telomerase actively express, such as lymphocytes, partially-differentiated stem cells, and the precursor cells to sperm, there is a negative feedback loop based on the length of the telomeres, which in turn regulates the activity of telomerase. Telomerase maintains the ends of the chromosomes, especially in these mitotically active cells, but it will only elongate them to a certain point.

It has long been known that telomere length is regulated by a negative feedback loop (reviewed in Smogorzewska and de Lange, 2004). Long telomeres contain more negative regulators that limit further telomere elongation by telomerase. Because of this, the enzyme preferentially acts on the shortest telomeres in the cell (Hemann et al., 2001; Zhu et al., 1998).
  - Loayza, et. al.; Cell; Volume 117, Issue 3 30 April 2004


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How does RNA polymerase achieve higher processivity?
DNA polymerase uses a sliding clamp in order to replicate DNA. RNA polymerase does not require one. What allows RNA polymerase to hold on to DNA just like DNA polymerase?

Hi @notorious. Could you add a citation for this sliding clamp usage? I'm rather intruiged!

The structure in the presence of s (holoenzyme) is on the right; note the open channel for DNA binding. The structure in the absence of s (the core enzyme) is on the left.  Note that the channel is now closed, as if the fingers and thumbs of a hand now closed to make a circle. This striking conformational change that occurs when s dissociates is thought to confer high processivity on the RNA polymerase.
SOURCE: http://biowiki.ucdavis.edu/Genetics/Unit_III%3A_The_Pathway_of_Gene_Expression/10%3A_Transcription%3A_RNA_polymerases

DNA Polymerase III Holoenzyme has processivity of 500,000 bases. High isn't a number,

If you have nothing to add to the discussion and if you continue criticizing other people's answers without giving a proper explanation to the question, then you really shouldn't be using StackExchange. Also, you still haven't corrected the error in the question.

And here is another point that you are missing. RNA polymerase need only associate with the template strand of DNA and transcribe from that, where as DNA polymerization is a far more complex process involving leading and lagging strand synthesis, laying down or RNA primers, producing Okazaki fragments and performing exonuclease error correction with DNA polymerase working with both strands of DNA at the same time.

Perhaps you can add some details on processivities of DNA and RNA polymerases. This will clarify the point. Also cite references for those. BioNumbers is a good place to look for figures such as these.

@AMR DNA-polymerase, unaided by sliding clamp has a low processivity. Highest seems that of viral polymerases (7200 for EBV).

@AMR I remember being scorned for almost exactly the same thing in a college (UK) biology class. I said there was a "high amount" of something I can no longer recall. I now fear the words "high" and "amount". Specificity is key for, if nothing else, not angering teachers and biologists.


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How does exercise cause weight loss if the corresponding chemical reactions have the same mass on the LHS and the RHS?
How does weight loss take place in the body during physical activity, given that the corresponding chemical reactions would have the same mass on the left hand side and the right hand side?

What chemical reactions would these be? We cannot answer question if you don’t specify the problem.

Please give example of chemical reactions you're referring to, It will help us answer your question.

Better yet, look yourself at the reactions and think about what might happen to the products...

I don't know what chemical reactions take place. I just remember studying years ago that the metabolic activity in the body is basically chemical reactions. And chemical reactions don't involve a change of mass between LHS and RHS is another thing I remember studying. So how does weight loss take place then (apart from sweat and bodily waste being expelled from the body)?

This is a layman question -- I have no knowledge of biology or chemistry beyond high school level which was years ago

Excretion. You've really answered your question in your own comment, except that you don't seem to have realized that there is no "apart from sweat and bodily waste being expelled from the body".
Simplistically, say the body has some stored fat, which has the general formula CH3(CH2)nCOOH.  When you exercise, the fat is burned for energy, converting it to CO2 and H20.  The CO2 is exhaled, the H20 leaves either as perspiration or urine. https://en.wikipedia.org/wiki/Lipid_metabolism#Lipid_catabolism

Thanks, this is exactly the answer I was looking for.


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Why were the earliest humans hunter gatherers instead of fruit eaters living on trees?
How is it that the earliest humans who evolved from primates (who live on trees and mostly eat fruit) became hunter-gatherers (which seems like a harder, more stressful and more dangerous way to find food)?

Perhaps because living in trees and eating fruit rather limits you to living in places where there are fruit-bearing trees.  Becoming a hunter-gatherer allows a species to greatly expand its range.