text:
Does every protein starts with Methionine amino acid
During process of protein synthesis we need AUG Codon to start translation .As we know this codon codes for Methionine amino acid so can we say that every protein starts with Methionine amino acid ?

No, not every protein starts with a methionine. When the methionine is removed, it is called N-terminal methionine excision. Abstract excerpt below:

N-terminal methionine excision (NME) is the major proteolytic pathway
  responsible for the diversity of N-terminal  amino  acids  in
  proteins.  Dedicated  NME components have been identified in all
  organisms, in all compartments  in  which  protein  synthesis  occurs:
  cytoplasm, plastids and mitochondria. Recent studies have revealed
  that NME is regulated at various levels and plays an important role in
  controlling protein turnover. NME is essential  in  Eubacteria  and
  lower  eukaryotes  and  is  the target of many natural and synthetic
  inhibitors. Such inhibitors  have  considerable  potential  for  use
  in the  treatment of various human diseases, from cancer to bacterial
  and parasitic infections.

And from a recent review focusing on the methionine aminopeptidase enzyme that cleaves the first methionine:

Protein synthesis is initiated by methionine in eukaryotes and by
  formylmethionine in prokaryotes. N‐terminal methionine can be
  co‐translationally cleaved by the enzyme methionine aminopeptidase
  (MAP). When recombinant proteins are expressed in bacterial and
  mammalian expression systems, there is a simple universal rule that
  predicts whether the initiating methionine will be processed by MAP
  based on the size of the residue adjacent (penultimate) to the
  N‐methionine.

Mitochondria and other organelles also have different start codons. Their alternate start codons are well-characterized (AUA and AUU in humans and mainly - but not exclusively - GUG and UUG in prokaryotes).


text:
A speculative question about sensation
I know this is rather speculative and I am not a biologist, but I have womdered about this for a long time.
I have always been able to pinpoint the central line of any part of my body exactly as if there were some nerve running through it. For example, given a pen, I could trace the line dividing one of my toes precisely. I, in some way, sense that the pencil is exactly at the middle?
 Is there any physiological reason for this? Is this true for everyone or is this an illusion peculiar to me?

given a pen you can trace a line anywhere on your body. This is becasue humans have Proprioception.  we can sense the movement of our muscles, tendons, and joints and track the location of every element of our body. Using this we can control our body precisely without other sensory input. It takes time to completely master this but most people have done so by the time they become adults.

source: Stack Exchange

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sort: votes


text:
Why can't a genetically sound human stay alive for an indefinite amount of time given all the ideal conditions?
I have read that even if we can control our food and lifestyle and keep things as ideal as possible, there are other factors beyond our control like effects from neutrinos passing through our body that would accumulate over time, and may cause harm. More over, Earth's natural radiation, and the Cosmic background radiation may as well play a part.
I wonder what if we somehow removed these as well, will one be able to live forever?!
I have heard people say that this is an impossibility, but I wonder why?!
Thanks.

Your telomeres will kill you long before neutrinos do.

What exactly are telomers @AlexReynolds?...are they the chains at the end of a polymer or something like that?

Related questions: Why does evolution not make our life longer? and Is it possible for a human to live forever if he/she didn't catch any diseases?

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text:
Apply Shannon-Weiner index to evaluate single-cell sample balance?
I would like to identify single-cell clusters where each sample is evenly represented in it. Is it OK to calculate the Shannon-Weiner index from the sample counting data of each cluster? I am worrying that the entire population of each sample is not balanced, therefore I plan to normalize within-cluster counts with total cell number in each cluster.
My naive idea is summarized in these formulas:
$$
E_{i} = \frac{\sum_{j=1}^{N_{sample\,}}P_{i,j}\log_2{P_{i,j}}}{E_{max}}
$$
where,
$$
P_{i,j} = \frac{C_{i,j}}{\sum_{i=1}^{N_{cluster}}} + pseudo\_count
$$
$C_{i,j}$ is the count of sample $j$ in cluster $i$.

What is the purpose of the pseudocount?

Pseudocount aside, you are proposing to estimate a rescaled Shannon entropy onto $[0,1]$ of each cluster. That is fine if that is what you want to know.

@Galen Log2P_ij  undefined if C_ij equals to zero. That is the cluster does not have any instances of the sample. Are there other approaches to avoid this?

That's quite understandable, however by convention we take the right-limiting value $H(0) \triangleq \lim_{p \rightarrow 0^+} p \log_2(p) = 0$.


text:
Genes of the electron transport chain
Where are the genes of proteins that make the electron transport chain of mitochondria?(are they in in the nucleus or they are in the dna of the mitochondria itself?) Thanks for this answering system by the way

Welcome to SE Biology. Please take the Tour and learn about this site. You are expected to do some research before posting, especially for Homework questions. You can easily find the answer to this question by an internet search.  Do this, and then come back if there are particular problems that remain unresolved.

Dear David thanks for your welcoming so much.Honestly I am a student as you guessed but this one was not a school project.It's really nice of you pushing the student's to find the answer themself , instead of just asking them .but I did a search on the web and couldn't find what i wanted since I am not studying in english-there was also nothing on the web in my native language Persian.So if you can help me with the keywords that I have to search to find my answer,I will be really thankful.Have a nice time.

@ArmanJalali Hi, the question can be easily resolved if you try to find articles speaking about each of the four subunits of the transport chain individually. For instance, for the first subunit (NADH oxidoreductase) you can find your answer in the abstract of this paper   Good luck with the rest!

The Wikipedia page on Mitochondrial DNA is an easy first stop. Comes up on the first page of a Google search. You need to search in English, I'm afraid. Your browser should allow you to switch search languages. Firefox does, for sure.

Actually the article is available in Farsi: https://fa.wikipedia.org/wiki/دی%E2%80%8Cان%E2%80%8Cای_میتوکندریایی


text:
What is the meaning of a selection regime in this context?
"Our second approach was based on modeling adaptive regimes
across a phylogeny for each of the groups in our study using an OU
model. We especially focused on the lineage leading to humans, and
tested whether a shift in the selection regime was inferred on this
branch. Under the OU model, species evolve through various selection
regimes that map to branches on the phylogeny. The goal is to characterize the regimes across the tree, and to assess whether a shift in selection regime occurred on the branch connecting Homo to the
other primates."
taken from:
Nunn, Charles L., and David R. Samson. “Sleep in a Comparative Context: Investigating How Human Sleep Differs from Sleep in Other Primates.” Wiley Online Library, John Wiley & Sons, Ltd, 14 Feb. 2018, onlinelibrary.wiley.com/doi/abs/10.1002/ajpa.23427.

I'm an evolutionary biologist. When someone says "selection regime" they simply mean the general conditions (environmental, ecological, etc.) that could have produced a particular evolutionary outcome. For instance, in the example that you mention, they seem to imply that they are interested in knowing if these condtions (i.e. the "selection regime") in the branch that lead to the evolution of humans were somehow different than these of other primates. So, it is a hypothesis, in this case. Unless they state elsewhere in the paper what exactly is this "selection regime", they are simply referring to this idea.

I haven't dug into the paper in too much depth, but I think that it is a little hard to give a precise definition of what they mean by this term in this paper, because it is used in the context of a complex phylogenetic statistical model that they analyze using MCMC simulation sampling or Ornstein-Uhlenbeck (OU) modeling.
For MCMC they appear to be estimating ancestral states (of REM sleep proportion for instance) along the nodes of the phylogeny based on the estimated values of the character for each tip (living organism) of the tree. This is probabilistic and they run the MCMC model until it converges at a reasonable set of parameter values for the overall phylogenetic model, and then they sample reconstructions of these ancestral states. You could view each of these reconstructed states as having its own "selection regime"; however they are not directly describing those regimes. Instead, they are noting only "shifts" in the selection regime, which they are defining as MCMC reconstructions that show a change on the human branch that is larger than that for the rest of the tree of primates. So, it's kind of a black box, because we only know the selection regime in terms of it being "different" between humans and the rest of the tree, as inferred by seeing a large shift in the state of the character (REM or whatever) in humans. That itself is a bit of a stretch of course, because large shifts can also happen without selection. But they're doing their best.
For the OU model, this model itself contains definitions of selection regimes, I recommend looking more into how OU models work to get more information about that. But according to my limited understanding, the OU process is trying to directly model changes in selection regime across the tree. So in looking at the black balls in Figure 2, those are direct OU estimates of the probability of such a shift. Again in this case, what exactly the selective regime is cannot be known from the paper, it is instead inferred to "shift" by the OU model based on changes in values of the character across the tree.


text:
Why the length constant of passive current flow isn't depend on the membrane capacitance?
I read that the equation for the length constant for passive conductance along a neuron depend on the resistance of the plasma membrane, the intracellular axoplasm and the extracellular medium. My question is why it's not dependent also on the membrane capacitance, since it can also affect how far the current can propagate (if for example the capacitance of the membrane is large, more negative charge will be on it's intracellular side, and will cause to the positive current to attract to the sides of the membrane).
Thanks!

Length constants are defined in the 'steady state' regime of constant voltage; capacitance is important for time-dependent electrical functions but disappears in the steady state.
In a real neuron, where you have other time-dependent (dynamic) features like ion channel opening, time constants and length constants interact to determine how current flows in a length of neurite, as you intuit, but these passive properties by themselves are insufficient to describe that behavior: you need to also consider ion channel gating and conductances.
See also https://en.wikipedia.org/wiki/Cable_theory - note how the capacitance is always multiplied by a changing voltage dV/dt in the differential equations.


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Interpreting the reciprocal of $R_0$
$R_0$ is the average number of secondary cases arising from a single infectious individual in a fully susceptible population.
In many of the compartmental models for epidemiology, the parameter $\frac{1}{R_0}$ appears frequently.
In particular, in an SIS model, the non-trivial steady state is $(S^*, I^*) = \left(\frac{1}{R_0}, 1 - \frac{1}{R_0} \right)$.

Is there any intuitive interpretation one can give to the reproductive ratio's reciprocal?

I'm thinking some sort of average rate of secondary cases, but this doesn't feel right since $S^*$ is a number.

It's funny: $R_0$ doesn't actually follow as nicely as $1/R_0$ when focusing on the infected class.
In a SIS model:
$$\frac{\mathrm{d}S}{\mathrm{d}t} = -\beta SI + \alpha I \\ \frac{\mathrm{d}I}{\mathrm{d}t} = \beta SI - \alpha I$$
take finding the steady state of $I$. Whether a disease is able to invade is dependent on whether or not the steady state is greater than 0, which means that $I(S\beta - \alpha)$ must be positive. That is, $S\beta$ must be greater than $\alpha$, and $I$ isn't important as to whether or not the infected class changes (unless infecteds are extinct at 0). This means that $S$ must be greater than $\alpha / \beta$ for the disease to invade. Since disease prevalence is $I/(S+I)$ and there is usually a negligible-sized initial prevalence (i.e., $S(0) \approx 1$), we often care about $\alpha / \beta$, which is known as the relative removal rate. This is intuitive because $\alpha / \beta$ is the ratio of the rate of loss to the rate of gain of the infected class. If the rate of loss is greater than the the rate of gain, $\alpha / \beta$ will be greater than 1 and the disease will go extinct.
The reciprocal of the relative removal rate, $\alpha / \beta$, is $\beta / \alpha$, which is known as $R_0$.

1/R0 is the threshold fraction. If fraction of population vulnerable to particular infection is  more than 1/R0, only then infection can spread further. And if it is less than 1/R0 then infection can not progress and eventually goes away
And, 1-1/R0 is the fraction of population which requires vaccination so that we can have herd immunity.
(Reference
http://home.iitk.ac.in/~peeyush/mth426/Epidemiology.pdf
https://www.slideshare.net/singh_br1762/r0-value-herd-immunity)

Thanks for the response - however everything you have said is an immediate corollary of the fact that it is the steady state, so I was aware of this already. I was hoping for a more intuitive explanation for how one could "see" that $\frac{1}{R_0}$ is an obvious threshold from its definition? For example, the reciprocal of the rate of recovery is the average period of infection obviously, but I'm not so sure what abut the definition of $R_0$ means that $\frac{1}{R_0}$ is so important or lending to be a threshold?


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

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

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

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

I would like to understand this process as far as what bacteria or "micro organism(s)" are being leveraged here.  It seems that they are supplementing the soil with some kind of bacteria that acts in this specific way of releasing additional electrons that can then be harvested.
Any idea as to what kind of micro organisms or bacteria have this kind of reaction wherein they release or excrete harvestable energy (and apparently CO2 + H+) upon consumption of plant "excretions" (C6H12O6)?
After doing a bit more digging, I have found some, perhaps, interesting information from Wikipedia:

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

Geobacter is one bacteria that seems to get a lot of attention in the field of developing biological fuel-cells.

I am interested in this. I will lay down the realities of this plan that are probably implied; (the issues with conservation) Persuading large conservative bodies to switch (politics). Large scale farming and conversion of electric current. Nitrogenous waste conversion, It could replace industries that make ammonia therefore Haber process gets replaced. Grass plants are more reliable but Colonization of invasive virus species destroying crops is the reason mono culture went towards DDT and pesticides, besides the fact DDT is a war invention. It is interesting also if mushrooms could supply the

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

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

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text:
What type of Interspecific relationship does this graph depict?
The other day in class, our AP Biology teacher presented us with the following graph and asked us to determine which of the following interspecific relationships it represents:

(A) commensalism
(B) predation
(C) mutualism
(D) competition
(E) parasitism.

She explained to us that since there is not enough information in the graph to explain why species A suddenly drops off after time "x" and species B suddenly rises after time "x", the best answer out of the choices is (A) commensalism.
But to me, that seems to be a faulty line of thinking. After all, my teacher arrived at that answer only under the assumption that the graph/question itself is good to begin with. I tried finding graphs of commensalism using Google Images, and I actually found the original source of the graph that our teacher presented us.
Now, the question on Regentsprep actually gives us a point of reference and states that we are considering two herbivores in a grassland environment, so in my opinion it's reasonable to conclude that the relationship between species A and B is competition.
The problem is that my teacher never gave us a frame of reference: she just told us to identify the relationship in this graph without any "backstory". So what are your thoughts: is it possible to conclude that "A" is the best answer choice if we are not given any information aside from the graph?

I agree that the question as your teacher presented it is very unclear, and even the question as it is presented in the original source is still not a great  question. I would say that commensalism is tied for the worst answer with mutualism, as with commensalism you would expect one population to go up while the other remains the same.

Competition makes the most sense, IMO.
For every other type of relationship, A and B should be dependent and roughly proportional: If parasites kill their host, they die in proportion. If predators eat all their prey, they drop in numbers due to food scarcity until food repopulates, the graph would almost look like a double helix. Mutual/commensals also share a dependent and proportional graph. The inverse proportionality of the sample chart, to me, gives away competition: one organism is flat out winning against another through some method.

Yeah, I agree with why it's competition. That explanation makes so much more sense to me than my teacher's reasoning. EDIT: also, I looked online for competition graphs just now and found a reputable source with competition graphs (bottom of the page) that are very similar in behavior to the graph my teacher showed us: both are steady up until time "x", after which one takes over the other.

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text:
Absence of cytoplasmic Intermediate Filaments in Arthropods
Cytoplasmic intermediate filaments such as vimentins support the architecture of the cell and have been known to aid signaling processes. However, as in this article, it is stated that out of all eumetazoans in Kingdom Animalia, only arthropods do not contain such structures. How is this possible? Are there any replacements to the conventional intermediate filaments present in cells? Do arthropods have special cellular behaviors or signaling networks to correspond with this absence?

It is stated that out of all eumetazoans in Kingdom Animalia, only arthropods do not contain such structures.

I found this paper(1), eliciting an exception (within an exception)- Isotomurus maculatus:

Here, we report the first evidence for the expression of a cytoplasmic IF protein in an arthropod - the basal hexapod Isotomurus maculatus. This new protein, we named it isomin, is a component of the intestinal terminal web and shares with IFs typical biochemical properties, molecular features and reassembly capability.

I would suggest you to read the paper, for more information.

How is this possible? Are there any replacements to the conventional intermediate filaments present in cells?

Both electron microscopy and molecular cloning studies have been unable to detect any cytoplasmic IF protein in these organisms, although they do express a nuclear IF system made of authentic lamins. Other cytoskeletal components have been proposed to have assumed, in arthropods, the mechanical functions that are usually played by cytoplasmic IFs in other organisms. For example, wing epithelial cells are stabilized in insects by a cytoskeletal array consisting of parallel bundles of 15-protofilament microtubules and actin filaments.

Do arthropods have special cellular behaviors or signaling networks to correspond with this absence?

I am not sure if this is what you might be looking for, but the Delta/Notch signalling, which may be involved in posterior elongation in arthropods, does not require IF's.(2)

The Notch cascade consists of Notch and Notch ligands, as well as
intracellular proteins transmitting the notch signal to the cell's
nucleus. The Notch/Lin-12/Glp-1 receptor family was found to be
involved in the specification of cell fates during development in
Drosophila and C. elegans.

1- https://bmcbiol.biomedcentral.com/articles/10.1186/1741-7007-9-17
2-https://en.wikipedia.org/wiki/Notch_signaling_pathway#Mechanism_of_action


text:
Could some identify this bird call? (from the hu - wolf totem)
What species is making this sound?
You can hear the sound it makes at the end of the music video: The HU - Wolf Totem

Before the wolves howling yes?

yes. it starts at 06:16 at the video

You could try the forum at xeno-canto.org, if you don't know about that site yet.

Same bird from Spirited away. There's a part when they get off the train when you can hear it. If you figure that out, you'll find the bird

I believe the bird sound belongs to a member of Gaviidae, specifically Gavia arctica, which has a common name of the Arctic Loon or Black-throated Loon in North America and Black-throated Diver in Eurasia.
The first impression when I heard this was a loon/ diver. Since The HU are Mongolian throat singers, I assumed that they likely used a loon/ diver from Mongolia of which there is one breeding species of the five members of Gaviidae. You can listen to calls and sounds of Arctic Loons here: Macaulay Library
The Arctic Loon sounds much higher pitched than other species of Gaviidae, which is similar the call in the song at 6:16.

Yep, Loon was my thought too. Amazingly eerie calls.


text:
Sickle-cell trait : Why is only one type of beta chain found in any one hemoglobin molecule?
I was reading a textbook (iGenetics, 3rd edition page 71), and came across the following passage:

Homozygous bS bS people make Hb-S, the defective hemoglobin, with two
  normal a chains specified by wild-type a-globin genes and two
  abnormal b chains specified by the mutant b-globin bS allele: these
  people have sickle-cell anemia. Heterozygous bA bS people make both
  Hb-A and Hb-S and have sickle-cell trait. Because only one type of b
  chain is found in any one hemoglobin molecule, only two types of
  hemoglobin molecules are possible—one with two normal b chains, the
  other with two mutant b chains.

(Emphasis mine)
My question is: Why is only one type of beta chain found in any one hemoglobin molecule? Or is this statement simply false?
I did search biology SE for similar questions, and found this one, but it is phrased poorly and the only answer does not address my question.

For one specific hemoglobin molecule, yes it's just one type of beta chain.  In the case of a heterozygote, this hemoglobin molecule could be expressing from the bS gene OR the normal beta gene.  Let's call it a 50/50 chance for each hemoglobin to be expressing bS.  Because RBCs have a ton of hemoglobin in them, this 50/50 or so expression of bS wouldn't be enough to cause RBC sickling and disease, and it also helps explain the heterozygote advantage vs malaria.

"Let's call it a 50/50 chance for each hemoglobin to be expressing bS." What? Hemoglobin is a protein, not a cell , it doesn't "express" anything.
Each hemoglobin molecule has two beta chains: the question is: why do we never find one normal and one bS chain in the same hemoglobin tetramer.


text:
Which is more evolved Rays or Sharks
I know the Theory of evolution explains that life transforms to become more complicated, sophisticated so that it's more equiped for survival, Just like the survival of the fittest, the fittest are the evolved and always survive
I learnt that rays evolved from sharks, but I see sharks eating rays in documentarys, Infact rays are afraid of sharks, they are nothing compared to killer sharks
I also learnt that by skeleton comparison chicken evolved from dinosaur, but dinosaur are like gods to chicken
If man evolved from animals, we've become wiser and they've become pets
What really is evolution speaking, evolved animals do they become stronger than their competitor or weaker?
From unicellular organism to complex organisms, is the pattern of evolution going forward or backward or no pattern
Thanks for your answer

"more evolved" is not a biologically justified statement. See answers here https://biology.stackexchange.com/questions/832/what-is-meant-in-biology-by-the-term-evolved.

Hi Aderinsola, welcome to Biology.SE. There is no such thing as "more evolved". It is just the diversity among organisms being shaped by their environment, their way of living, and so on over thousands of years. We might be "more evolved" than those tiny microorganisms, but come to think about it, we cannot survive inside glaciers or in volcanoes—two behaviours noted in several bacteria. There is no connection between progress and evolution.

Evolution isn't a contest between two species, it's the interaction between a species and its overall environment. The only real measure of evolutionary "success" is the ability to leave behind offspring that survive to have still more offspring.
Tyrannosaurus Rex may have been bigger, stronger, and fiercer than any chicken, but apparently something changed in the environment that interfered with its ability to leave behind offspring. Maybe it was a meteor striking the earth and changing the climate. Giant reptiles wouldn't do so well if the climate suddenly got colder. Smaller dinosaurs that had feathers might have done better. Clearly, in today's environment, chickens are able to produce billions and billions of offspring!
Sharks may eat rays, but they aren't eating all the rays! The rays are leaving lots of offspring behind, and so are the sharks. This means that both species are well adapted to the current environment.

From unicellular organism to complex organisms, is the pattern of
  evolution going forward or backward or no pattern

No pattern. Whatever adaptations allow more offspring to survive will tend to last, and traits that interfere with offspring surviving will tend to disappear.
A good web site for learning more about evolution is Evolution 101


text:
Understanding Research Paper Differences
I'm doing a high-level research which led me to the following paper - https://www.researchgate.net/publication/280389511_Quality_of_life_of_patients_with_chronic_lymphocytic_leukaemia_in_the_Netherlands_results_of_a_longitudinal_multicentre_study
As it's mentioned there are many groups of testing and comparison in the research, which are: the general population, total patient group and three groups of CLL patients.
I'm a bit confused about the definitions' differences between "the total general population" and "the total patient group".
I appreciate every advice / help.

This study enrolled 144 CLL (chronic lymphocytic leukemia) patients ("total patient group"). They further grouped these patients into 3 groups according to the treatment they were receiving.
When they refer to "general population" they are referring to norm scores:

For each patient, an individual norm score was
  derived from age- and gender-matched scores of the general population on the EQ-5D [28] and EORTC QLQ-C30
  [29]. These two studies, as reported in Refs. [28] and [29],
  used a panel consisting of more than 2000 Dutch households, representative of the Dutch-speaking non-institutionalised population in the Netherlands.

So these scores are not part of the current study, but they are estimates from a survey of the wider population rather than patients who have CLL (you can assume they do not have CLL). "Total population" doesn't mean "all CLL", it means "all Dutch-speaking non-institutionalized people".


text:
What are the short/long term effects of chloroquine on fundamental cell processes?
Does chloroquine, which affects the endosomal membrane traffic pathway (by affecting the acid environment used for fundamental endosomal reactions), have short/long-term effects on cell growth/proliferation/signaling?

This paper provides many experiments about changes to the endosomal system and autophagy and should be a good starting point.
Most of the treatments are done in the 5h to 24h range typical for cell culture studies. In theis relatively short time frame Chloroquine is well tolerated by cells. However, long term treatment will very likely be different.

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Is there anything wrong with this objection to evolution?
My friend's argument against evolution goes like this:
It is extremely unlikely that life as we know it evolved from a random mutation process because every organism is like a machine, in that one "mistake" could render the whole machine unworkable. What makes this even more unlikely is that harmful mutations are more likely to occur than beneficial ones. If evolution were true, it would not last very long, most likely.
My rebuttal goes like this:
While it is true that evolution is influenced by a random mutation process, this process is not random in the sense that all mutations are equally likely. When evolutionary biologists say mutations are random, they mean that the environment has no influence on the type or frequency of mutations. They do not mean that all mutations are equally likely to occur. In fact, if you look at certain mutations in humans, you'll see that mutation rates for certain phenotypes are not equal, which means we have unequal probabilities. Also, while it is true that harmful mutations are more likely to occur than beneficial ones, neutral mutations are the most likely of all. Another issue I have is that it only appears unlikely if we are just working with one organism, but if we have a whole population of organisms, mutating and reproducing, then your argument seems to be undermined by this fact.
Was my rebuttal good? Is there anything wrong with my friend's argument against evolution?

The best rebuttal is to point your friend to a resource where they can actually learn about evolution.

There is also the argument from Occam's Razor.  If life on Earth did not evolve, but was created, then whatever created it must have come into existence by some process, either evolution or being created.  Which implies either an infinite recursion of creators, or evolution at some point in the recursion.

@jamesqf Sounds like a futile argument. Surely some creator will have special clause of eternal existence and now the discussion has shifted from the empirical evidence of evolution to speculation about unobservable creators.

@Cell: But we have ample evidence that the universe is not eternal, but has only existed for 14 billion years or so.

I’m voting to close this question because it is not a question about biology in terms of SE Biology but a request for comments on an argument. This is a question and answer site, not a discussion site.

@jamesqf We also have evidence of evolution. This is why the argument is futile becauase you just got sucked into disproving an unobservable creator and you will never win that argument.

@jamesqf So if I rephrased my question without mentioning the fact that the objection came from an debate I was having with my friend, then you would not vote to close my question?

Environment can have an effect on the mutations (type and frequency). Random means that acquisition of mutations is a stochastic process. Doesn't mean that the probabilities are uniformly distributed. Despite all such biases, evolution itself is a non-ergodic process which doesn't have a definite aim or optimum towards which it proceeds.

It is extremely unlikely that life as we know it evolved from a random
mutation process because every organism is like a machine, in that one
"mistake" could render the whole machine unworkable.

Garbage.  Pure garbage.  People in the lab know that you can induce all kinds of mutations and get no effect.  Because as you pointed out, most mutations are neutral.
Your rebuttal was largely correct; most mutations are neutral, and in a population, it doesn't matter if a small number of individuals is killed by their bad mutations, (and obviously a slightly deleterious mutation won't be lethal, or even necessarily noticeable) because there's still a whole population left to host neutral and beneficial mutations.

not only are most mutation neutral, most functional mutations have only small effects, we only notice big effects more easily.

I will henceforth use the word "unfortunately" to describe the predicament of a person who denies evolution.

Is there anything wrong with my friend's argument against evolution?

Unfortunately, all arguments against evolution are invalid, simply due to the fact that evolution has been (simultaneously) observed, deduced and inferred to happen so very multiplicitously. It has been demonstrated beyond any reasonable - and less than reasonable - doubt. It's difficult to know where to begin; throw a dart at any of the innumerable disciplines in biology and you will find overwhelming evidence for the occurrence, contingency and consequences of evolution. Narrow the question down and you will find tomes upon tomes of evidence for evolution within the narrowed scope. Ask an entomologist about a lineage of beetles among cousin species. Ask a structural biologist about a molecular machine in the cell such as a receptor. You will inevitably find unrelated biological subjects converging on the evolutionary hypothesis, even without meaning to. After all, almost any biologist working today is 'accidentally' adding to the overwhelming mountain of evidence for evolution on a daily basis. Such evidence in 2020 is virtually unpublishable in scientific literature because demonstrating that evolution is real is very 'low impact', just as novel demonstrations of heliocentrism would be unpublishable in astronomy journals. The logic and predictions of the theory work, so much so that some theories of evolution have transcended biology into the other sciences.

But one "mistake" could render the whole machine unworkable!

Plenty of mutations kill and maim organisms. We can't even count how many organisms 'could have lived' if it were not for deleterious mutations, because they didn't make it. We see mutations. Yet we see life. Hence this is a non-argument, unfortunately. And you cannot debate non-arguments.

[Where do we stand on arguments for/against evolution?]

These questions are valid and important to discuss, they are very formative and central to the progress (scientific and otherwise) of humanity.
However, the context for this discussion is abundantly clear. The occurrence of evolution is no longer debated in science, and hasn't been in many decades (centuries perhaps?), just like the theory of heliocentrism (Earth orbits Sun) or the shape of the planet (it's most certainly not flat). The debate is long closed and relegated to history.

Wikipedia says that roughly 30-50% of human conceptions do not result in a live birth, and prior to modern medicine, a large fraction of those died before adulthood. Among plants and many animals, hundreds to millions of fertilizations occur, but on average only a pair survive to reproduce.  Evolution DEPENDS on eliminating the excess whose genetic differences (AKA mutations) make them less likely to survive.

It is extremely unlikely that life as we know it evolved from a random
mutation process because every organism is like a machine, in that one
"mistake" could render the whole machine unworkable.

Consider this. We have two processes called gene duplication and exon duplication . These 2 processes "Copy" a gene or part of a gene and "Paste" it somewhere in the genome. Therefore even if a bad mutation happens in one gene , there is a probability that its function/concentration would be balanced by the other (wild) gene. (It's also worth mentioning that this situation would create a recessive (and harmful) allele for the original gene.)
So you can improve your "machine" by simply duplicating it , editing one of "machines" would not do any harm since there is a backup "machine" . That will eventually result in a more complex "machine" over time by evolution.


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What is the rate of bacterial cell death due to viruses on land?

"The rate of viral infection in the oceans stands at 1 × 10^23 infections per second, and these infections remove 20–40% of all bacterial cells each day." - https://www.nature.com/articles/nrmicro2644

What are the equivalent figures on land?

"On land" is pretty vague in this context. Are you just interested soil? Would you include surface waters? Wetlands? Animal-associated microbiomes? I think it's a simpler calculation for oceans, as marine biomass is largely dominated by microorganisms, whereas terrestrial biomass is dominated by plant life.

True, it is vague. I'd be interested in figures for any non-ocean ecosystems. Animal and soil microbiomes in particular.


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Does Japan have an ageing population?
I often hear Japan has a declining/ageing population.
It seems to be the prime example for this kind of thought.
Yet after moving to Japan and after having been there for travel several times already. And in comparison with my native country Germany as well as Europe in general, I think this concept seems questionable.
While I hardly see any children outside in Germany and it's mainly parents with one child.
Everywhere I go in Japan I meet a lot of children. Especially in the greater Tokyo area, if I go to restaurants there's always a bunch of kids. And usually you see at least two children per parents, if not three.
I can understand that in general this concept might be true but might not be applicable for bigger cities.
Where does the concept come from? Is there any proof it's actually true?

This seems better asked on Skeptics.SE, and would require a notable claim. I don't see any biology in the question. Your comment on the one answer makes me even more skeptical that you are actually looking for a biology answer here.

Thank you, actually I want sure either if it's good here but it seemed the best fit. Skeptics sounds better though. I didn't find that one.

I hate to sound rude, but you could easily answer this yourself with even the most minimal look into well-tabulated demographic information, rather than highly non-representative observations. About 13% of Japan's population is 0-14 years old, the third lowest fraction in the world. (https://data.worldbank.org/indicator/SP.POP.0014.TO.ZS ; easy to find with Google)  The fraction of the population over age 65 is 28%, the highest in the world. (https://data.worldbank.org/indicator/SP.POP.65UP.TO.ZS?most_recent_value_desc=true) The population density is high, so you'll certainly see more kids than in many other countries, though not proportionally more. I will leave it as an exercise to look up the numbers for Tokyo itself.

Of course I looked up those numbers. But I'm not sure how they come into place. Are they really representative?

How about the corollary: how representative are your observations?


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What is the scientific name of this green insect/bug?

(Picture from Internet)
I want to know the scientific name of this insect. They are very small in size and they do not like to stay at one place so taking pictures is hard. Following are some information which will help in identification.

Location: India
Size: Miniscule. About some millimeters
Color: Green. Sometimes a black dot appears on its wings
Survive during the post-Monsoon duration i.e. Late July to October. Hence sometimes referred to as Post-Monsoon bugs.
Attracted to lights. Large number of those swarm around any source of light
Causes a great deal of damage to crops
Does not bite but causes local itching on contact with skin
The name in our native language roughly translates to "green insect" (because of green color)

From the google search I did,guess they are green leafhoppers.
To find more on the leafhopper of the second half, this link should help .Reach the site and give a search on green leafhoppers in the searchbar.
Well,there are a large no of leafhoppers under the family Cicadellidae and I believe the ones in the picture differ.
If my findings are correct,Cicadella viridis is the scientific name of the leafhopper of the 1st half,the second one comes under Nephotettix sp.
Hope it has helped!

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Please don't post text as images. You can rewrite key points from the source in your own words while citing the original source of the information.

I did some research based on your info and found that indeed they are diffierent typrs of planthoppers/grasshoppers. 1st image is Cicadella viridis which is primarily present in Europe, so let's exclude that. The second one is one of the species under Nephotettix genus. The image I included might be Nephotettix nigropictus or Nephotettix virescens, the latter one most likely.

To complete this post, I want to include my answer based on my research which will server as a complementary answer to @BactiPrabha's answer.

As @BactiPrabha pointed out, they are "green leaphoppers". There are different types of leaphoppers which implies that the 1st image and 2nd image are not same.
The 1st image is Cicadella viridis. This species is present in most of Europe and in the Indomalayan realm which does not match with my location. So let's exclude that.
The 2nd image is one of the species from Nephotettix genus and from the characteristics, it could be either Nephotettix nigropictus or Nephotettix virescens, the latter one most likely. Along with N. cincticeps, they are the most common Asian pest species in this genus and causes diseases like tungro disease in rice. Hence they are also called "Pest of Paddy".
For more information, go through these links:

https://www.cabi.org/isc/datasheet/36200
https://agritech.tnau.ac.in/crop_protection/rice/crop_prot_crop_insectpest%20_cereals_paddy_2.html


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What species of thermophilic prokaryote is present in hot compost that creates white mould like threads?
A method known as the "hot composting" method aims to create the right ratio of carbon rich and nitrogen rich materials in the pile in order to encourage thermophilic organisms to thrive in order to accelerate the process of making compost.
The following source 1 explains:

Need optimum temperature of 55-65 degrees Celsius. At temperatures over 65 degrees Celsius a white “mould” spreads through the compost, which is actually some kind of anaerobic thermophilic composting bacteria, often incorrectly referred to as”fire blight”. (It appears when the compost gets too hot – over 65 degrees Celsius and short of oxygen. It disappears when the temperature drops and aerobic composting bacteria take over).

What specific species is this organism?
I say prokaryote in the question title as I'm aware it may be a bacteria or archaea. Many sources incorrectly refer to archaea as bacteria.
Hot Compost – Composting in 18 Days

sorry i don't have enough time to answer this completely but here's a reference incluing a list of common bacteria they found. It really sounds like you are talking about a fungus, but cross referencing this list could make a complete post.


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What is the typical concentration of Calcineurin (PP2B) in CA1 dendritic spines?
I am trying to find the concentration of CaN (PP2B) in dendritic spines, there is a computational model (doi:10.1073/pnas.0804672105) that uses the quantity of 1uM in the dendritic spine. I think this value is not correct since it was measured long time ago (Goto Brain Res. 1986 Nov 5;397(1):161-72) and was given as Hippocampus 1.45 -+ 0.39 (ug/mg of protein).

Why do you think the data is incorrect simply because it is old? The concentration can be high because the volume of the dendritic spine is very less.

This article says that CamKII concentration (different subunits) is ~60-140µM. Calcineurin should be in similar range, I guess.

I think that this measurement is incorrect for the spine because CaN localization is found in the spine neighborhood, not the whole neuron (that diluted the concentration). Being old is not a problem, sometimes it is gold, like Magee and Johnston (1995) VGCC measurements. A Lisman paper guesses that CaN concentration is maybe 20uM in the spine (CA1), but they don't provide the reference ...

Do you know how CaN and CamKII are correlated? I could not find any article on CaN concentrations but see my previous comment for CamKII concentration. You can at least make an informed guess for your computational model. I do believe, you would do some kind of sensitivity analysis with your model parameters; so a perfect value may not be essential.

How they are correlated? one is a phosphatase that presumably dephosphorylates (CaMKII), an experiment in 2015 is saying that is not the case but they didn't look into the dynamics with enough temporal resolution, as Chang/Yasuda 2017 did. For CaMKII there are several estimations of the spine concentration, which is really good. For CaN, the spine concentration is hard to trust. And there are values in literature from 1uM to 20uM.

Kuno et al., J Neurochem, 1992, PMID 1313851 give 0.96 % total hippocampal protein = calcineurin (both isoforms).
Goto et al., 1986 give ~ 0.15 % total protein = calcineurin
In rat brain, there is ~ 10 % protein / total wet weight (Clouet & Gaitonde, PMID 13398827).
Stefan, PNAS, 2008. 1uM
Lisman and Pi, 2008. 20uM

I don't know how they are correlated; not my area of expertise. I just suggested if you know there is a correlation then you can guess an approximate value.

Thanks! I will let this rest on my head.


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Can monoclonal antibodies be used to transport insulin
Quick question
Monoclonal treatments in cancer require the drug attached to the antibody which then attaches itself to the neoantigen on a cancerous cell, would it be possible to
transport insulin in the same way?

There are no quick questions on SE Biology, only good questions and bad questions. Good questions are on topic, explain the problem clearly, and demonstrate an attempt to research it yourself. Your question does not explain the problem, and is really focused on your own answer. Where do you wish to deliver insulin to? Why do you think it cannot reach there already? What problem is doing so going to solve? Unless you edit your question accordingly it is likely to be ruled “off-topic” as “unclear what you are asking”.

Thanks I'll keep that in mind

Technically you can link two proteins together, but why would you want to do this?
Antibody drug-conjugates are used to specifically target cells which can be differentiated from the healthy cells by their cancer neoantigens. This provides a high specificity of the drug delivery and also limits side effects on healthy cells.
For insulin on the other hand this is not necessary, since insulin receptors are ubiquitous thoughout cell surfaces in the body, hence supplementing insulin is enough.

I think “most likely yes” is a comment rather than an answer. As the question is unclear I would suggest it comes under the category of “not all questions should be answered”.


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Where to find data on different crops
Hello I'm not sure if this is the proper place for this question. If not, I am happy to move it.
I'm trying to find a source of data on different crops, is there some governmental database that houses this kind of data? After looking for a couple hours on google and reading a few different articles, I have not really found what I was looking for.
For example, consider the crops maize, wheat, sorghum and sugarcane. I could be looking at the different kinds of carbohydrates an their proportions in these crops, or I could be wanting to know the amount of water needed to produce some yield, what kind of soil each crop likes as well as how different hybrids and mutants have different needs or qualities.

Did you try a google search? I got these results, hope they are useful:
http://www.fao.org/land-water/databases-and-software/crop-information/en/
https://world-crops.com/home/
http://www.ecpgr.cgiar.org/resources/germplasm-databases/eccdb-list/


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Do blood vessels expand during angiogenesis?
I know that there are two usual ways of creating new blood vessels:

A new vessel sprouts from the wall of an old one,
A wall of cells grows down the middle of a vessel, splitting it into two.

I also know that capillaries are all the same size (about wide enough for a single red blood cell to get through). I also know that in between the major blood vessels and the capillaries, you have a hierarchical branching of differently sized tubes.
So my question is to do with, like. So if a new blood vessel starts to sprout, does it start off as wide at the base, as it's always going to be? (E.g. does it already know how many times it'll have to branch before getting to the capillaries, and choose its width accordingly?) Or does it start off smaller, but widen at the base as its ends keep branching?


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What species is this golden fly?
Last summer I was visited by this unusual golden fly, whose kind I have never seen before. It was impossible to scare away so I could take relatively good pictures.
The pictures on this hobbyist page suggest, it is a  "Golden blowfly". Those pictures were taken in Australia. The only paper I could find on golden blowflies locates the species in Australia as well. However, I took my pictures in southern Germany.
What is this fly? Is it an invasive species or native to Germany as well as Australia?

is it tachina fera?


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When telomere length is measured, is the method performed on a collection of cells yielding an average?
What are the methods used in measuring telomeres in human or animal subjects?
Can it be done on an individual cell?
Has the following concern been raised and addressed before:
What if there exists a natural variance in telomere length on a cell by cell basis and various methods exist (strenuous exercise etc) that exert selection pressure on telomere length, then if the measurement method in some way involves multiple cells you have the effect of the average length increasing while something else actually occurred. Resulting in all these studies concluding that telomere length increased.

Welcome to Biology StackExchange! I suggest you to read policies related to homework questions (https://biology.stackexchange.com/help/homework). This will greatly increase the chances that you receive appropriate answers.

A telomere can be measured using a flow-fish test. Basically fluorescent markers that bind DNA are introduced to the nucleus of a cell, and then those markers can be counted using a method call flow cytometry.
It can be done on one cell
I'm not sure I understand the last part of the question, but I can say that if the average telemore size increases in a particular sample size, then scientists will not conclude anything based on that data.
If there is a scientific conclusion on telomere size with relation to external selective pressures, there would be statistically significant data that properly accounts for the variations observed in different cells.


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Lower optimum temperature of plant Catalase
Most resources give an optimum temperature of 35° C for Catalase. after performing the AP Catalase enzyme lab in school, using blended potatoes, our results gave a greater reaction rate at a room temperature of 25° C. we hypothesized that this is due to the fact that potatoes cannot regulate body temperature, so catalase works better at room temperature. The only source we could find that backed up its claim was an excerpt from a Pearson textbook: Here

Do plants have a lower optimum temperature like the textbook suggests, or was something wrong in our experiment?

(75 students, half did potatoes, half did liver)

There are two points you need to do here. 1. Tell us clearly what the results were for catalase from the two sources. You do not do this and therefore I cannot see what you are trying to explain. Please rewrite it. 2. Find whether your results contradict published results. Although the generalization in Pearson is reasonable, it need not apply to all enzymes. There is no reason why an enzyme in an organism that metabolizes at ambient temperature might have greater activity at a higher temperature that it never encounters. I can’t see this being selected against.


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regenerative capacity of human body
Is liver the only internal organ in human body with regenerative capacity? How about endometrium?and what is the difference between regeneration and renewing?

No, many tissues regenerate, otherwise we'd never grow or heal from wounds. Skin, muscle, lining of the intestines, bone, to name just a few.

I'd say renewing refers to a constant process wheras regeneration applies to wholesale rebuilding due to trauma.
For example, your skin is constantly "renewed" by the undermost cells, adjacent to the basement membrane, dividing to produce new cells that migrate outward. These cells are modified to protect and eventually slough off to feed the mites in your bed. Ditto to cells lining the stomach which are replaced/renewed about ever three days due to abuse of stomach acid and salsa.
Humans can regenerate much of the last joint of a finger, bone and all. I'm not sure if this is age dependent nor how much of the knuckle needs to remain. Search "regeneration of fingers in humans" to find many references to this.

Some of the information contained in this post requires additional references. Please [edit] to add citations to reliable sources that support the assertions made here. Unsourced material may be disputed or deleted. Specifically, please provide a reliable scientific reference for the claim made in your last paragraph. "I just saw a show" is not a reliable reference.

Yep, a search turns up a third of a million references to 'regeneration of fingers in humans'. Maybe it was my colloquial parlance that triggered your comment. As an educator, I try to taylor the response to the student, but maybe it was too homely for this forum. I've removed it. Uncommon theories and arkane assertations should be referenced. Referencing each and every fact detracts from the clarity of the discussion. Imagine your comment to the OP, replete with references.

No, referencing facts does not detract from the clarity of the discussion, it enhances it. References provide suggested additional reading, allowing those who are interested to learn more about the topic. And since we're on that new-tangled "internet" thing, you can make inline links and continue with the flow of your prose without those annoying superscripts. We've discussed this on Meta, and the consensus is to link all but the most basic facts. Wikipedia is frequently used. Your thumb claim should be linked, as it is not common knowledge. I'd also link "basement membrane".

However, your refusal to put even a basic link into your text is just petty. It tells people "oh, you should know this, but if you're too dumb to, I'll tell you to google it because you probably wouldn't think to do that on your own." I've found that some of the best answers on here have tons of supporting links, but they're there for reference, and usually not quoted from directly. Instead, the authors synthesize what's contained in them, but leave the link if you want to know more, or want to check their claims. Your answer does none of that.

It wasn't a refusal, nothing petty on this end. I honestly thought my edits would satisfy your complaint, my mistake. I also though it was good pedigogy to provide general direction as opposed to choosing one of 300,000 plus hits. I feel your damning comments ill deserved.


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How are the very first telomeres added?
Here is an image of telomerase adding telomerase.

As we can see, the telomerase sort of binds to a bit of the existing "3' flanking end of [the] telomere" - it's almost half and half.
My question is, where did that existing telomere come from? And the telomere before that?
Essentially, the telomeres must have begun from some point on the chromosome/DNA, but how were those telomeres added if the telomerase has a preset RNA sequence that it uses to bind to specific nucleotide bases? Does our human DNA coincidentally end with TTAGGG as well or something?

See telomerase and TERT.

So I understand that it has to use reverse transcription to do it, but I cannot find anything specific to telomerase adding the first telomeres. Any help?

I won't be able to help you, as I know little about molecular genetics. But given the number of upvotes, you will probably get the attention of someone who will be able to answer such as Chris or WYSIWYG.

Telomere might have evolved from a retrotransposos. http://www.nature.com/scitable/content/t-loops-and-the-origin-of-telomeres-26791

Telomeres are maintained by telomerase (in certain cell types, not all of them) at every replication. So, the answer to your questions "where did that existing telomere come from? And the telomere before that?" is: "because there was already a telomere to extend at the end of this chromosome".
Your questions boil down to "how did telomeres appear in the first place?" (because once telomeres and a maintenance mechanism have been established, they will simply remain unless some major genomic catastrophe happens), and this is a difficult question. As Whitney pointed out in the comments of your question, some hypotheses about the origin of telomeres are discussed in this article.
Interestingly, Drosophila doesn't have telomerase, and maintains telomeres by a transposition mechanism. Somehow this is a clue about how telomeres appeared: Drosophila telomeres could be an intermediate between circular chromosomes and telomerase-based maintenance of linear chromosomes.
This is a complicated topic, but the scientific literature about the appearance of telomeres is fascinating. Some bacteria (Borrelia and Streptomyces taxa) have linear chromosomes, but maintenance mechanisms that have nothing to do with transposition nor telomerase.
Here are some references:

Drosophila: https://doi.org/10.3389/fonc.2013.00112
Borrelia: https://doi.org/10.1146/annurev.micro.112408.134037
Streptomyces: http://link.springer.com/chapter/10.1007/7171_2007_090

If you can read French, you will find more info in the introduction of my PhD thesis.


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Difference between viral and native RNA
I am a data scientist with really next to no training in microbiology.  I hope you'll all forgive my ignorance to entertain these questions.  The attention COVID-19 has gotten recently got me thinking:  What is the fundamental difference between viral RNA and the RNA native to a particular cell?
What I mean is, we are often told in school that viruses hijack the cell's protein manufacturing facilities to express their own genetic material.  The cell produces so much of the viral protein that it eventually lyses (for example).  But what is it that makes the cell produce so much of the viral proteins?  How does the cell not produce too many proteins from the cell's own DNA?
I suspect the answer comes down to the lack of gene regulation for the viral RNA.  But is every gene that is native to the cell really subject to some sort of regulation?  If so, is the real danger of viruses that they lack any kind of regulation?  Then that seems to be a fairly easy thing to detect- at least theoretically.  In other words, a cell, or a scientist could label a sequence of RNA as dangerous simply because it is unregulated, regardless of whether it came from a virus.
A second question is, we are told that the viral proteins self-assemble and encapsulate copies of the viral RNA just by chance.  Doesn't this seem unlikely?  Are the virus's components really so ubiquitous in the cell that the virus will self-assemble including all its necessary components a significant portion of the time?  I suspect for this to happen, the virus's RNA would need to be copied many times so that it would be plentifully available.  Then it comes back to the same question as above.  Is viral RNA unique in that it gets copied indefinitely?

There is no fundamental difference between viral RNA and and native cellular RNA other than the sequence of RNA bases in them.  The sequence differences are not biochemically apparent in the RNA, only in the protein products produced from the RNAs.
Regulation of native RNA is done in a huge variety of ways (nothing in the cell is designed; everything is ad hoc, so any random happenstance can become established).  Native regulation is essential, otherwise runaway production will happen leading to cell death or to cancer.
Much, if not most, of the native regulation is done by regulating transcription of DNA into RNA. Once the RNA is in the cytosol, little further regulation is done, so viral RNA in the cytosol has the run of the cellular protein factory.  But at least some viruses have acquired further advantages which help their RNA out-compete the native mRNAs for use of the protein machinery (see, e.g., Hijacking the translation apparatus by RNA viruses)
So it is not really an easy thing to "label a sequence of RNA as dangerous simply because it is unregulated" as the wide range of normal RNAs in the cytosol does not provide a basis for determining if any are "unregulated" and the cell cannot be protected in that manner.
Self-assembly is widespread in normal cellular functions as well as in viral production.  The molecules involved have long-honed attractive points for their mate molecules, and in the jiggling molecular soup of the cell the molecules can soon bump into each other and join up.  Thanks to the virus's uncontrolled production, new viral particles have plenty of component molecules available for this assembly.

(If you wonder I'm posting two answers, it's because this q-post asked two questions in one.)
Regarding the issue of virus self-assembly... studying it has indeed been a challenging issue. There's a recent (2019) PNAS paper on that:

Despite decades of study, how capsids self-assemble has remained a mystery, because there were no methods to measure the assembly kinetics of individual capsids. We surmount this obstacle using a sensitive microscopy technique based on laser interferometry. The measurements show that a small nucleus of proteins must form on the viral RNA before the capsid assembles.

Overview of the measurement. (A) A structural model of the MS2 capsid (PDB ID: 2ms2) shows its small size and T=3 structure. The 2 coat-protein dimer configurations are shown in gray and purple. (B) We inject a solution of unassembled dimers over a coverslip on which MS2 RNA strands are tethered by DNA linkages. As dimers bind to the RNA, the resulting particles scatter light. The particles appear as dark, diffraction-limited spots because of destructive interference between the scattered light and a reference beam. (C) We monitor many such spots in parallel. Shown is a typical image of the field of view, taken 126 s after adding 2-μM dimers and representing an average of 1,000 frames taken at 1,000 frames per second. (D) The intensity of each spot is proportional to the number of bound proteins within each particle and changes in the intensity as a function of time reveal the assembly kinetics of each particle. The darker the spot is, the larger its intensity. (D, Top) Time series of images for the boxed spot in C. (D, Bottom) Intensity trace for the same spot using a 1,000-frame average. We discuss the relationship between intensity and number of bound proteins, as well as how we calculate the spot intensity, in Materials and Methods and SI Appendix.

Some videos posted as well in the Supplemental.
And a bit more on the observed dynamics:

We find that the “growth time,” the time required for a particle to reach the size of a complete capsid after it nucleates, varies from particle to particle, ranging from 30 to over 200 s (Fig. 2A and SI Appendix, Fig. S1). Of the particles that grow into a complete capsid, some grow at a constant rate, others slow as they approach completion, and still others contain intermediate pauses lasting up to 25 s (Fig. 2A and SI Appendix, Fig. S1). Despite these differences, essentially all of the traces are monotonic, with little or no observable disassembly steps.

So yeah, quite interestingly, the virus capsid just build and builds itself; even if it takes "lunch break" it's not a problem reversing the build progress in a significant manner.
The failure mode(s) of this self-assembly process are actually related to building/attracting "too much stuff", or two (or more) viral RNAs getting entangled by common protein shards they both (all) attract. Basically too much density of building materials can lead to problems...

The growth times also decrease with increasing protein concentration, but less rapidly than do the nucleation times (Fig. 4A) [below]. Thus, we conclude that the RNA, which promotes nucleation at low protein concentration, creates a competition between nucleation and growth that can lead to overgrown structures at higher concentration, as sketched in Fig. 4B. This pathway provides a possible explanation for the “monster” (5) and “multiplet” (19) structures observed with other RNA viruses.

I mostly agree with mgkrebbs (+1), but note that while viruses generally have some kind of RNA replicase subunit (RdRP) to help them out, viroids completely lack those, yet manage to reproduce:

While RNA viruses encode subunits of the enzymatic complex (RNA replicase) that catalyzes initiation and elongation of viral RNA strands, viroids must rely for this replication step on pre-existing host RNA polymerases.  In principle, the best candidates would be RNA-dependent RNA polymerases, whose existence in plants has been known for a long time. However, viroids do not use these enzymes for their replication, but DNA-dependent RNA polymerases redirected to accept RNA templates.

The closest thing to a viroid in humans is Hepatitis D. Until last year, it was thought that it was mostly a human disease, but a 2019 survey found that HepD analogs are quite widespread in invertebrates, fish, snakes etc.
Viruses are "much more nasty" than viroids in that replication regard because

Positive-strand RNA viruses replicate by using virally encoded RNA-dependent RNA polymerases (RdRPs) that provide a direct RNA-to-RNA replication function not found in host cells.

Some recent research suggests that RdRPs have been independently lost in many animal clades. Ironically, the roles of these (former) host RdRPs was [most likely] to provide an anti-viral mechanism via RNA silencing (see [section] below for details), but evolution has provided with alternative host mechanisms for producing the same.
While it's possible to recognize the [core of the] viral RdRPs in software, it's not clear/known how to translate this into a general anti-viral strategy, as far as I know, due to their fairly substantial variation. (In general it's not enough to know the genetic sequence encoding the RdRP of some virus to even screen inhibitor drugs for it; additionally one must know the crystal structure of the RdRP complex for that virus.)

If you're curious about "intra-cell" (i.e. RNA-based) anti-viral defense... there exist mechanisms like that, but are substantially more complicated (that what you suggest), being based instead on RNA silencing:

In eukaryotic RNA-based antiviral immunity, viral double-stranded RNA is recognized as a pathogen-associated molecular pattern and processed into small interfering RNAs (siRNAs) by the host ribonuclease Dicer. After amplification by host RNA-dependent RNA polymerases in some cases, these virus-derived siRNAs guide specific antiviral immunity through RNA interference and related RNA silencing effector mechanisms.

Key steps in RNA-based antiviral immunity induced in Drosophila
melanogaster by infection of positive-strand RNA viruses such as flock house virus.
Following entry and uncoating of flock house virus (FHV) virions, the genomic
positive-strand RNA ((+)RNA) serves as both mRNA for the translation of viral
RNA-dependent RNA polymerase (RdRP) and as a template for the synthesis of
antigenomic negative-strand RNA ((–)RNA). Preferential production of (+)RNA by viral RdRP
is achieved by multiple rounds of initiation of RNA synthesis from the 3ʹ end of the low
abundant (–)RNA. The resulting double-stranded RNA (dsRNA) formed between the
5ʹ-terminal nascent progeny (+)RNA and the (–)RNA template is recognized by Dicer 2
(DCR2) and cleaved into small interfering RNAs (siRNAs), thereby triggering RNA-based
antiviral immunity. The viral siRNAs are assembled with Argonaute 2 (AGO2) into the
RNA-induced silencing complex (RISC), methylated at the 3ʹ end (depicted by a black
circle) by HEN1 and used to guide specific clearance of FHV RNAs. As a counter-defence,
FHV encodes a viral suppressor of RNA silencing, the B2 protein, which targets two
steps in this immune pathway: inhibition of viral siRNA production by binding to viral RdRP
and the viral dsRNA precursor, and sequestration of viral siRNAs by binding duplex siRNAs.
Loqs-PD, loquacious-isoform PD.

And yes, the RdRP of viruses (the most significant part of the self-copier machine they come with) is an important drug target, e.g.

CoVs employ a multi-subunit replication/transcription machinery. A set of non-structural proteins (nsp) produced as cleavage products of the ORF1a and ORF1ab viral polyproteins (5) assemble to facilitate viral replication and transcription. A key component, the RNA-dependent RNA polymerase (RdRp, also known as nsp12), catalyzes the synthesis of viral RNA and thus plays a central role in the replication and transcription cycle of COVID-19 virus, possibly with the assistance of nsp7 and nsp8 as co-factors (6). Nsp12 is therefore considered a primary target for nucleotide analog antiviral inhibitors such as remdesivir, which shows potential for the treatment of COVID-19 viral infections (7, 8). [...]
The efficacy of chain-terminating nucleotide analogs requires viral RdRps to recognize and successfully incorporate the active form of the inhibitors into the growing RNA strand.

So while it's not so simple to detect/fight viruses' as you suggested, some replication-targeting strategies involve either "jamming their own (RdRP) copier with fake parts" (as e.g. remdesivir does) or producing [hopefully] as many "copy cancelers" as possible, for which the RNA silencing machinery actually uses parts from the virus copies themselves.


text:
In north America is their mammals that can survive from falling from hundreds of feet?
Like animals have great attributes but is their any mammals that have unique attributes to survive such fate of death?

There are quite a few, including Corynorhinus townsendii virginianus, Eptesicus fuscus, and many others.

No I’m asking about resilience animals to surrive such fate

Like surviving falls. That can kill people but mammals are munch stronger then human so they have more of chance of survival


text:
Why animals haven’t yet evolve in 2020?
In past when I was born like 1990s I notice most animals haven’t evolved in 30yrs. Example  cats haven’t gain more muscular body as to be strong to defend themselves from predators like well many animals of coyotes, raccoons, possums, red fox, bobcats, birds of prey, wolves and others

Are you looking for the evolution of cats, mammals or animals in general? And what exactly makes you think there is no evolution? Not all changes are visible on spot, especially given that 30 years are not a long time span in context of evolution.

I wonder why so many downvotes for this.

Yeah I'm a bit confused why so many downvotes. I was curious for live chat @Arsak

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. In particular, your question needs: 1) clarity, and 2) evidence for the assertion that "animals" haven't evolved. ——— In general, we encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Thanks!

I have found that when learning about a new area starting with a relatively accessible and reliable source like Khan Academy is very helpful. Wikipedia is also generally a good starting point and you can then check their references. Online platforms called MOOCs offer free (or very low cost) courses on a wide variety of subjects — two I am familiar with are Coursera and edX. Finally, textbooks with a good level of detail are also freely available online e.g. from NCBI.

In particular, I encourage you to check out some of the online resources available for learning more about evolution. For example, this a useful introduction to evolutionary theory from UC Berkeley.

But still feral cats of 2020 are new generations from 1990s feral cats that 20yrs later of generations possible over 100 generations had passed since cats breed very quickly in feral life

Evolution takes either many generations or strong evolutionary pressures (or both).  For your example species, domestic cats, 30 years is only about 30 generations.  Most domestic cats (as opposed to feral ones) are bred by humans, and are selected for attributes - call them collectively "tameness" - that make them good house pets.  These attributes are not those which would help as defenses against predators.
Now if you looked at populations of feral cats, you might find them evolving such traits, since they'd be under strong selection pressure.  (Though stealth & avoidance behaviors would seem to be more likely than size & strength.)
Conversely, wild animals can be "evolved" under human selection in a fairly short time, as for instance in the Russian fox domestication experiment: https://en.wikipedia.org/wiki/Domesticated_red_fox  You could also consider the evolution of the coywolf in eastern North America: https://www.csmonitor.com/Science/2015/1108/How-did-a-canine-hybrid-coywolf-emerge-in-front-of-our-eyes
Likewise, if you go to organisms with shorter generation times, examples of evolution, such as antibiotic resistance in bacteria, are quite frequent.  Indeed, if you have been paying any attention at all to recent events, you might have noticed that a variety of coronavirus has recently evolved the ability to infect humans.

But I seen many cats they look and same behavior. My cat was born from the streets so he ten years old. He quite small but seems tough but not really a dog can kill him with one bite :( I mean dogs are stronger, faster, smater high stamina and more resilience then cat. If cat could gain some those then cat wouldn’t have so many predators. I think dogs are smater then cats but cat people not true even though I’m cat person

@John Pass: I strongly doubt that the many cats you've seen are an appreciable fraction of all the cats there are, or that you've made any statistical study of the differences between feral cat populations and domestic cats.  (FTM, search for 'new cat breeds" to see how cats have evolved in recent decades.)  As for dogs being stronger &c than cats, it really depends on the dog. My bear-chasing Plott Hound, yes (except maybe the smarter part :-)), someone's toy poodle, not so much.  And of course there are enormous differences between dog breeds, too.

But the feral cats I seen are small like average size. They lived with coyotes, raccoons and birds of prey. If pack of coyotes chase a cat then the cat is no match to defend themselves. My cat ran out one night because we accidentally left door open he  gotten attack by raccoon at night we took him to the vet he got scars that was few years ago. I turn the lights on the raccoon ran off

@John Pass: Certainly feral cats defend themselves against coyotes. (Otherwise they would all be eaten, no?) They do so by evasion, not combat: climbing trees, going into small holes, &c.  If they were to evolve towards larger size/strength, they would lose those advantages, and would have to become large enough that they would be competing directly with coyotes for that evolutionary niche.

Oh I understand but I seen YouTube videos that coyotes hunt feral cats like 1-2 coyotes is enough to kill them. Cats can’t run long distance compare coyotes

@John Pass: So what you're seeing is evolution in action.  The ones that get eaten by coyotes are the ones that couldn't evade the coyotes, because they e.g. got too far from a safe refuge.  You don't see videos of the cats that don't get eaten because they were smarter, more cautious or whatever, yet these are the cats that will be passing on their genes to following generations.  That's the way evolution works: if all cats (or any other creature) that were born survived to reproduce, the world would soon be buried in cats. "Thus, from the war of nature, from famine and death..."

Like tigers are big cats they been hunted by poachers why they never evolved or adapted to gain more intelligence or smaller sizes to hide or faster bodies or tougher body for gunshots those who did survive by a bullet to next generation

@John Pass: Once again, the really too obvious reason is TIME.  Humans have only had guns for a couple of hundred years.

but its been like 200-300yrs why isn't that enough for evolution

@John Pass: No, it's not.  Why can't you seem to understand this?

You are witness to the COVID-19 epidemic, an example of evolution.
True, there are not weird bipedal cats walking around.  Actually Youtube shows quite a few, but you get my meaning.
But there is a new virus ravaging the world.  Where did it come from?  It came from predecessors that were not so pathogenic for humans, got a purchase in humans, and a new strain evolved.
COVID-19 coronavirus epidemic has a natural origin

Evidence for natural evolution
The scientists found that the RBD portion of the SARS-CoV-2 spike
  proteins had evolved to effectively target a molecular feature on the
  outside of human cells called ACE2, a receptor involved in regulating
  blood pressure. The SARS-CoV-2 spike protein was so effective at
  binding the human cells, in fact, that the scientists concluded it was
  the result of natural selection and not the product of genetic
  engineering.
This evidence for natural evolution was supported by data on
  SARS-CoV-2's backbone -- its overall molecular structure. If someone
  were seeking to engineer a new coronavirus as a pathogen, they would
  have constructed it from the backbone of a virus known to cause
  illness. But the scientists found that the SARS-CoV-2 backbone
  differed substantially from those of already known coronaviruses and
  mostly resembled related viruses found in bats and pangolins.

A rare thing - the evolution of a new and dangerous life form in your time on earth!

I don't understand what you mean on corna virus for a cat? I'm asking about why cats haven't evolved. My cat is ten years old so he was born almost 10-20yrs after i was born in the 90s. My cat and any other cat that was born after 2010, all the same, no extra attributes

The cat thing was a joke.  I believe you have not seen new cat types.  But you have seen or heard of a new virus type.  A new virus has evolved during your lifetime.  Get it?

I understand but I’m asking about cats in streets or feral cats not evolved from predators

@John Pass: And you've been told the obvious reason why there are no readily apparent evolutionary changes to feral cats: not enough time.

Can u explain not enough of time. That’s why I don’t get it. Feral Cats been around 1900-2020 that 120yrs that hundreds of new generations


text:
Can human pathogens present on plants become plant pathogens?
Since human pathogens sometimes live on the surface of plant leaves(read here and and here), and there are plant-pathogen microbes also living on leaf surfaces, is it possible for plant virulence genes to transfer to the human pathogens (perhaps via horizontal gene transfer) and make the human pathogen also pathogenic to plants? Has there ever been evidence of this happening?
This review paper addresses why plant pathogens haven't "crossed the Kingdom border" to being human pathogens, but what about the other way around (human pathogens affecting plants). Since there is such a wide array of plants out there with a wide range of pathogen interactions, it seems to me that it would be statistically more likely that a human pathogen could mutate to be pathogenic to some plant, than some plant pathogen could mutate to be pathogenic to specifically humans. Is that assumption valid? Also, I am talking about human-animals specifically, since it looks like there is a known virus infects both animal and plant cells in the lab (Lepidoptera/ cow pea)
As a currently-relevant example, could some plant virus, say Southern Bean Mosaic Virus, somehow share genes with a coronavirus strain and become a morph plant-human pathogen? (I know this last question is a little "out-there"). I chose that example plant virus since it is a positive-strand RNA virus like SARS-CoV-2. Thank you!


text:
Why do the two sexes have different reproductive costs and capabilities?
Is there an evolutionary explanation that shows why the reproductive costs are mostly on the female sex?
And therefore, why do males can potentially have more offspring?
Does that happen to create more competition in sexual selection?

I may have misunderstood your question, but there is no theory why usually reproductive costs are on the female, as this is a fact. Females have usually larger (and fewer) reproductive cells (gametes), they frequently have to carry the embryo until birth, and sometimes they have to attend to the offspring during the first stages of their lives. To put it very simple, females are stuck with their offspring from the moment of conception until they are born - sometimes even longer - while males generally can mate with many females in a short period of time, potentially having much more offspring.
A consequence of this is that, usually, females are choosy (they want good mates), whereas males just try to mate as much as possible. Female choosiness generates sexual competition, as females prefer to mate with males having certain characteristics that hint to a superior genotypes/phenotype that may be passed to their prole (e.g. beautiful plumage, social status, size of the wallet). Sometimes the costs of attending offspring after birth are higher than the costs associated with reproduction alone. In some of these cases, we may observe unusual behaviors, e.g. male-only parental care and choosy males.
This is a very broad and complex topic and a short answer here cannot cover all of it. John Maynard Smith developed the game theory approach most commonly used to investigate the consequences of different pay-offs for the two sexes and to explore how these can influence the behavior of the parents. Moreover, this topic is also covered in many behavioral biology textbooks. I have had very positive experiences with Krebs & Davis Behavioural Ecology (ISBN-13: 978-0865427310), which I would recommend.
Hope to have clarified some of your doubts.
Cheers,
Emilio

Thank you very much for this answer! Unfortunately I don't have a very strong education in biology so I apologise for being unclear. In the question I was specifically referring to pregnancy and calories investment in giving birth(and maternal care as well). I guess the main evolutionary advantage that enabled sexual reproduction to evolve in this way lies in the competitiveness it generates among males (another reason may be reduced costs and easier reproduction). I will definitely check out those books! Thanks!

I would say that sexual reproduction has the big advantage of DNA recombination. Then, how sexual reproduction is actually carried out, it varies a lot even just inside the animal kingdom. One sex needs to give more resources to the embryo just from a cellular physiological point if view. Largest Investments cause competition in the other sex, which does not necessarily means females choose the best partner. For instance, an optimal choice is conditional to the environment and specific situation. I would thus be cautious interpreting sexual selection as evolutionary advantageous in general.

Within a two-sex species, there are roughly three possible evolutionary strategies for reproductive investment:
Sex A and Sex B invest equally.
Sex A invests more than Sex B.
Sex B invests more than Sex A.
The last two are practically equivalent if you don't project your assumptions about differences between the sexes.
So the only alternative to different reproductive investments is equal reproductive investments. That option is not stable since sex A can invest 10% less at only 5% (assuming a linear relationship between investment and reproductive success, which is not accurate) reduced viability since the partner is not investing more yet. This means sex A can use the saved energy to reproduce with 10% more partners. This is a constant evolutionary pressure, so eventually one sex will invest a lot less than the other.
The other sex will probably not invest 5% less too, since that drops offspring viability by another 5% meaning they gain 10% more partners at the cost of 10% less offspring. There is no advantage here, so there is no evolutionary pressure. Alternatively, they could invest 5% more leading to 5% more reproductive success. This also gives no advantage.
The only reason for any sex to increase investment is if the reproductive success gets so low that it it is worth a larger investment to keep reproducing. There is no reason to assume the investment will primarily come from the smaller investing sex, so that won't change the difference in investments.


text:
Are there poisons that affect only mammals but not reptiles
Are there poisons that affect only mammals but not reptiles or crustaceans?
E.g. hemotoxins which affect hemoglobin but not hemocyanin or specific Na+ channels?
Looking for a "nice" poison/disease as idea for a fictional story to explain survival of reptiles/crustaceans vs. mammals.

"Reptiles" are not very different from mammals (compared to crustaceans).

Good candidates would likely be poisons originating from reptiles/crustaceans themselves...


text:
Do wild birds eat the egg shells of their own offspring?
Background:
I'm a volunteer who is monitoring nest boxes that were established for American Kestrels (Falco sparverius). This spring I've cleaned several boxes that were newly-installed the previous spring, with no intervening monitoring until I showed up a year later. They were obviously used last season (poop, pellets, prey remains), but no egg shells.  So either the inhabitants never laids eggs, or they laid eggs and ate the shells.  Seems to me that the shells would be a good calcium source.
Question:
Do wild birds eat their offspring's egg shell?

Did you try Googling this first? I immediately came up with an answer.

This may unusual for a Q&A site, but we require evidence of an effort on the asker's part that they tried googling (or a book/whatever) to try to answer their own question. Yes/no answers here will be deleted, and this does fall into that kind of answer. The concept is that the more effort you put into your question, the more effort we put into our answers, even to the point of often/usually giving you "proof" that you can trust the answer you receive on this site. You can edit your question by clicking on the edit button. Thanks. (And what a great volunteer "job"! I'd like that.)


text:
Why insects are attracted towards light?
Many insects like bees, dragonflies, wasps and other small insects are attracted towards light. Sometimes they are in groups, sometimes they are in solitude. When the light source source is switched off, they do not fly, rather stay still. What causes them to be so attracted towards light?

They think that the light is the "sun", so thry go towards to the light.( insects are guided from the suns position ).

@Orphee this is likely a myth

No it isnt.Its true.

Not a myth, but is among the current theories. Except it is more likely the moon. To fly in a straight line, an insect might use the moon as a stable landmark. An artificial light however, used as a landmark in this way, would result in flying in a spiral.

Phototaxis is a common behavior to many species, including insects but not only (e.g. most fishes do phototaxis).
The ethological reason is quite simple: with light you can see, and if you see you can find food, avoid predators and increase your survival chances. Phototaxis is thus a very strong innate reflex: at the neural scale in many species it is "hardwired".
I would say that the initial "purpose" of this reflex was to avoid shade areas during daytime, the light during nightime being pretty rare before man invented artificial light. The fact that insects gather around artificial lights during nightime is, to me, a side effect of this reflex.


text:
Nastic movements in Insectivorous plants
Questions:

What type of plant movement is shown by each of Sundew, Venus Flytrap and Pitcher Plant? What is the mechanism of the movement?
Can a movement be both Chemonastic and Thigmonastic? If yes, so any plant in Question 1 show both?
Give example(s) of exclusively chemonastic and exclusively thigmonastic movement.

Description:
Sundew (Drosera sp.), Venus Flytrap (Dionaea sp.), Pitcher Plant (Nepenthes sp.) are 3 examples of Carnivorous Plants.
These plants use rapid movements to capture their prey and then digest them to fulfill their Nitrogen requirement as they grow in Nitrogen deficient soil.
My Attempts:
I have found different answers according to different sources.

According to one source, tentacles of both Sundew and Venus flytrap curve in response to soluble proteins placed in the centre of the leaf. So, both of them are Chemonastic.
According to another, Chemonasty is exhibited by long peripheral tentacles of sundew. Closing/Bending of glandular hairs of sundew in response to nitrogenous compounds.
According to Wikipedia, Sundew and Venus Flytrap shows thigmonasty.
Interestingly, none of the above sources mention Pitcher Plant. According to a friend, Pitcher Plant shows free movement (moves its leaves at its own will). Is that true?
Finally, according to me, all three should be thigmonastic. Because all three trap the insect once the insect touches it. So, it is influenced by touch, thus, thigmonastic. Maybe some of them are chemonastic as well (I don't know which ones).

Hi everyone! Sorry for making the question too big. For a smaller version, just read the Question: part.

Also, in our school, a T/F question was: Chemonastic movement is noticed in Pitcher Plant. This is a reason that I am asking this question.

So, I studied abo them a little more, and came to a conclusion, which I am adding as answer.

Answers:

Sundew and Venus Flytrap show both Chemonastic and Thigmonastic movements. Pitcher plant doesn't move at all. Reasons in Description.
Yes, Sundew and Venus Flytrap show both Chemonastic and Thigmonastic movements.
Mimosa pudica, bunchberry and mulberry plants show exclusively thigmonastic movement. Still didn't find any plant that shows exclusive chemonastic movement.

Description:

In Sundew and Venus Flytrap, trigger hairs contain some proteins that sense touch. Although the in response to nitrogenous compounds part is hoax (since even if you put a stone in the trap and move it a little, then it will shut. After a day, it will spit that stone out.)

In a Pitcher Plant, no movement occurs. Rather, a slippery substance on its opening lid makes the prey slip in. Watch this video.

I still didn't find any exclusively chemonastic movement, and also still don't know for sure if the mechanism in venus flytrap and sundew invokve something chemical (not exclusively thigmonastic) since according to Wikipedia, Venus flytrap shuts its leaves even if a non-living thing falls in.