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Why humans have the temperature they have?
It is obviously very onerous to generate heat at all, although it has advantages. We don't have to lie on the sun like a crocodile to get warmer. And we avoid the freezing of our body water by out own means. But wouldn't just a little of heat be enough?
Why do humans go as far as 37 C? Couldn't we just have a temperature of 10 C to avoid freezing but stay at it?

Read this article http://www.ncbi.nlm.nih.gov/pubmed/15217694. It says that a lower temperature may have anti-aging effects, but it seems the human body is not 'designed' for other temperature http://en.wikipedia.org/wiki/Human_body_temperature#Human_temperature_variation_effects

If I had to guess, the reason human have the body temperature we do is because the ancestors of placental mammals had that body temperature. You will notice that all placental mammals have nearly the same body temperature http://www.infonet-biovision.org/AnimalHealth/Tools-livestock-care-and-treatment
That being said, birds have a higher body temperature than placental mammals http://www.sciencedirect.com/science/article/pii/030096299190122S
But why the higher body temperature....as you say why not just high enough for muscular activity?
One potential answer is at higher temperature, animals are better able to resist fungal infections for the simple reason that most species of fungus don't grow well at temperature above room temp. Declining by 6% of species for every 1C rise https://www.sciencedaily.com/releases/2010/12/101222121610.htm.  The optimum as calculated in terms of energy cost to maintain that high body temp vs number of fungal species to fight against was estimated to be 36.7 C, about body temp for mammals, and resting body temp for birds.


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Can pandas hunt for meat?
Recently, I learned that pandas have a carnivore's digestive system but that it exists almost exclusively as a herbivore. If pandas hunted would they be able to find meat in their environment? Can't think of any reason why they would 'evolve' to eat only bamboo if this was true. It's like 2 million years ago some bears decided they wouldn't hunt, hibernate or even roar and are slowly committing suicide.

Keep in mind that evolution is not directed. The bears didn't "decide" anything. Natural selection operates when certain genes confer certain traits that end up increasing fitness of the organism. As it happened, for pandas in their environment, eating bamboo and not hibernating were traits that were beneficial, so they persisted in the population.

My question was why becoming bamboo eaters was beneficial. Is there no game in the environment that they can hunt?

Why all the downvotes? I find it quite an intriguing question, given that they are on the verge of extinction.

i was interested because pandas do still eat meat from time to time for example when they find a dead carcass. They are still omnivores. So I wondered if they are too lazy to hunt for live meat, lost the instinctual skill or there is no game in their habitat.

I find the first two options very unlikely since as far as I know humans are the only animals that don't live instinctively.

And while pandas are assumed to be docile and cute, they attack humans just like any other bear.

First: My opinion on why the question has received that many down votes
There were many down votes to this question, not because the question is no of interest. The question actually makes sense and is interesting. The post attracted those down votes because the post and the comments of the OP shows little understanding of evolutionary processes. Here are some issues:

some bears decided. Evolution is not directed. There is no conscious decision from any species (except humans, see eugenics) on how to evolve.

as far as I know humans are the only animals that don't live instinctively. I am not sure there is a common definition of the word "instinctive". But I very much think that the vast majority of people would suggest definitions that forces us to accept that humans behave instinctively. And if the definition would accept that human can sometimes not behave instinctively, then the definition will very likely accept that some animals behave instinctively.
why they would 'evolve' to eat only bamboo. Why did you use quotes?

Eventually the question may show lack of effort as showed in the fact that the OP is stating the 2MYA the panda and the other bears diverged, while it was rather about 36 MYA (according to onezoom and even a bit older according to this reference). This paper however shows that pandas had an omnivorous acenstor 7 MYA only suggesting that pandas modern day diet has evolved less than 7 MYA. More information below.
I don't think that those evident misunderstandings deserves receiving down votes (not sure though).

Can't think of any reason why they would 'evolve' to eat only bamboo

I had a quick look and I didn't find any good answer to your question. It seems that:

In nature pandas has diet consisting almost uniquely of bamboo (ref). They can eat any of the 25 species of bamboo wiki.
Pandas have a digestive track that is very short (like most carnivorans and unlike most herbivorous). Because of their short digestive track they eat a lot (between 9kg and 14kg of bamboo per day!) and they poop a lot (40 times a day) wiki!
As a consequence of its diet, the panda spend little energy and avoid any effort wiki.
Pandas seem to have evolved so that it is able to digest cellulose with the help of bacteria (ref, ref). According to wiki and BBC this microbiome is not herited from the mother but is acquired later in life (it is quite common to see that). This paper suggests that having such a fast transit prevent the ability to absorb other nutrients and therefore limits the benefit of having a more diverse source of food.
pandas size and mouth are adapted to their diet. They have a large size and a round face with powerful jaw wiki.
We actually know what genes are responsible for food preference in pandas (ref). The mutation for the "I prefer bamboo" allele is estimated to be 4.7 MY old (consistent with skull observation ref).
According to many comments online and according to wikipedia (but I couldn't find a trustful reference), as observed in zoo, pandas can eat other stuff when available. Citing from wikipedia While primarily herbivorous, the giant panda still retains decidedly ursine teeth, and will eat meat, fish, and eggs when available.

Given the amount of information we're having there may be tons of possible scenarios. It is possible for example that there is inter-species competition in the wild for access to prey. It is possible that there was for some point a very low density of preys and pandas has shifted their diets. Once, pandas had evolved some features of herbivorous species, they would get stuck there and not be able to get back to a meant based diet (stuck onto a local optima on the fitness landscape). There might be many different explanations involving patterns of competition, parasites, sexual selection, etc... And it seems that we haven't been able to disentangle between all of these.
Hope that helps!

I admit the term that of "decided" was wrong. I know evolution is not conscious. My main point was that a species with so many traits negative to survival shows that survival of the fittest is not a hard rule. Census evidence is now showing minor hope that pandas may not be facing extinction since poaching has been reduced since the population has even INCREASED 17% over last 10 years.

You post positive evolution mostly related to diet. I can post negative aspects related to reproduction also. Did you know that females select only one mate during the tiny heat period and will let all cubs but one die usually?

here is my blog re it although u will see me assuming spiritual awareness behind evolution though i dont really believe. Just that survival of the fittest is not a hard rule. There is survival of the unfittest too. https://epilepsydubai.wordpress.com/2015/05/22/panda-evolution/

Yes. The question was not about panda's biology in general (and hopefully because it would have been too broad) so I did not address pandas reproduction. Btw, many species have similar pattern of letting all the cubs but one dying. Cub cannibalism is not rare either. The expression "Survival of the fittest" was coined by herbert Spencer who has little knowledge about evolutionary biology. Intuitively, "survival of the fittest" relate to the process of natural/articial (eventually sexual as well) selection.

In those terms, then the adage "survival of the fittest" is indeed not a hard rule as not being the only rule, or if stated more correctly, natural selection is not the only process governing evolutionary processes. However, your simple observation of pandas lifestyle is not a demonstration of those other processes. Evolutionary biology is a big field of science. For example, I am personally working in the subfield of population genetics working on the evolution of the species range, the process of range expansion and the evolution of the mutational effects.

I strongly recommend that you make some readings in basic evolutionary biology before writing stuff online that will just allow misunderstanding to spread. Here is a good introductory source of information to learn about evolutionary processes.

My simple question was if pandas have prey they could hunt as omnivores in their environment as they were actually omnivores. Somehow, that was responded to by a post about positive adaptions of the panda. I understand evolution well enough. I just think pandas prove that a species with an accumulation of negative traits can survive too. So mutation doesnt always have to be benficial even in large amounts.

Do not feel offended but: No, you do not understand evolution well enough. positive adaptation is not a thing. mutation doesn't always have to be beneficial sounds really weird. Most mutations are indeed neutral or deleterious. People make a Bachelor in Biology, then a Master and PhD in Evolutionary biology and spend 25 years studying evolutionary processes. Evolution is more than what you think it is. You don't need to have that level of knowledge to ask a question on this website but don't rush to conclusion without understanding contradictory arguments.

To cite few examples of basic concepts you may not know about: Fst, Muller's ratchet, probability of fixation of neutral allele present at frequency $x$, heritability in the narrow sense, post-zygotic reproductive isolation, character displacement, Hamilton's rule, Wright-Fisher model of genetic drift, Zaahavi handicap principle, horizontal gene transfer, phenotypic constraints, etc...

I notice that noone has really attempted to answer my actual question. Only try to change my concepts on evolution. That's fine. I believe people are entitled to their beliefs. I shared mine too but was not trying to project it onto others. I was certainly not trying to disprove evolution. If anything, when the this thread devolved into evolution, instead of my question, I only suggested that growth of species that seem unfit to grow seemed possible. If anyone can answer my OP, please do so.

Let us continue this discussion in chat.

At approximately the same time that they switched to a primarily herbivorous diet, pandas lost the ability to taste "umami," or "savoriness." We don't know whether this happened before or after the dietary change, but the umami flavor is a strong attractant for other meat-eating omnivores, like humans. It signals instinctively that a food is exceptionally valuable and should sought out and prioritized over other available food. This is why your mouth waters more at the smell of a steak than the smell of a carrot. Unable to distinguish this quality by smell/taste, pandas would be less inclined to go to the effort to hunt down or scavenge meat, compared to just stuffing readily available but almost inedible bamboo into their craws for sixteen hours a day, even though it often gives them serious indigestion and limits their ability to travel or reproduce.

Hi Edie. Welcome to Biology S.E. :)..any chance you could back up your answer with a (couple of) source(s)? I would recommend to have a quick read through the BioSE Tour (https://biology.stackexchange.com/tour).. in doing so you'll also earn your first badge.

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can animals override instinct?
I would say that one of features that separates human consciousness from animal is the ability override instinctive behavior. A human infant will jerk its hand away from a hot surface. An older child you can communicate with at the basic level may not although experimenting with this is no doubt unethical. An adult can consciously overcome this instinct.
Are there experiments testing this idea with animals? In animals that science claims are self-aware, it would be interesting to know if they can overcome the automatic reaction to negative instincts.
The first step would possibly be to see if one negative instinct can be overcome in the presence of another. Like will a really hungry chimp walk across a painfully hot surface to reach food? This seems likely but I am unaware of any such testing.
A more interesting example will would be cases of real animal altruism. Science is quick to tout what some call animal altruism as hardcoded and evolving genetically e.g. lions defending prides, mothers defending young. And I agree this can be hardcoded and genetic since I am not aware of lions NOT defending prides or mothers leaving young to predators.
However, these links show cases of what some may call true animal altruism. Dogs braving the danger of the highway to help other animals.
https://www.quora.com/Are-animals-capable-of-selflessness-Do-they-have-the-desire-to-help-others
Leopardess adopts baby baboon
https://www.youtube.com/watch?v=j9DOxH5RyWQ

The trouble is our motives don't have labels on them, "instinct", "altruism" etc. Different parts of the brain produce different responses to the same stimuli and it is then the job of the cerebral cortex to calculate which of the competing options to follow, some of these responses are "hard-wired" others not, but there is no single "instinct" which our conciousness, or that of other animals can, "overcome", just a range of competing options almost all of which are processed by the cerebral cortex in every creature that has one.

How do I move a question? Just repost?

@Isaacson You can hold your hand to a hot surface if you wanted. And the videos are indications of animals overcoming instincts. So its very likely consciousness can overcome hardwiring.

@AnoopAlex This is a common misconception that causes few problems in animal studies, but massive problems in human ethics. There is no evidence whatsoever that they are "overcoming instincts", there are just a range of potential responses to the various stimuli in the scenario and the animals are choosing one of them using either learned or novel patterns in the cortex. There is no way of distinguishing "hard-wiring" from "conciousness" in these types of actions, all of them go through the cerebral cortex to be decided on.

Ever housetrain a puppy?  Or consider that a horse's instincts are to flee from perceived dangers, including four-legged wolflike predators, yet with training you can ride your horse around all sorts of scary things, and take your dogs along :-)

@jamesqf: I realize animals can learn percieved dangers are not actual dangers but I was thinking more along the lines of when the threat is real. When a puppy or horse learns the people he sees wont harm him, he no longer fears. But the example I gave of burning hot surface to reach food presents a real threat. I realize there are ethical issues here so am also curious if there have been examples observed in nature.

you may want to look at the vast number of studies done on rats with electric shocks, you would be amazed what behavioral alterations are possible. https://link.springer.com/content/pdf/10.3758/BF03209595.pdf the branch or science you are looking for is called ethology.

What makes you think that altruism isn't instinctual? Certainly certain forms of it are, parents caring for their offspring for example. The examples you mention may be examples of an instinctual behavior applied to a non-typical subject.

Instinct and learning drive almost all behavior in the animal kindgom. We are only considering animals with nervous systems in this discussion, but non-neural learning has been documented.
All animals have instinct. Instincts manifest themselves as desires that elicit "automatic" behaviors. A good demonstration of instinct is to skip a meal and then put yourself in the presence of your favorite snack. You don't have to think "I would like to eat now" before reaching for the bag, it happens "automatically". That is one of many instincts found in Homo Sapiens.
Instincts are encoded genetically and in terms of speciation, population size and generation times insects are more evolved than vertebrates. We would expect them to have instincts just as complex (if not more so) than mammals despite their far simpler brains.
Learning is found in many species, including in jellyfish, earthworms, snails, and many insects. The desire to learn in my opinion is largely instinctual as can be seen by the enthusiasm of a young child. If learning is instinctual, is learning to override instinct actually overriding instinct?
The very smartest animal species can occasionally exhibit "creativity" which goes beyond instinct and learning and can in fact fight against instinct. For example, Orcas beach hunt sea lions which requires overcoming their powerful instinct not to beach. The calves learn this from the mothers (often by doing "dry runs" with no prey within reach), but someone had to come up with this idea in the first place. Whoever that Orca was had to fight their own instinct without resorting to learned behavior.
Humans only have half the cortical neuron count of Orcas but are still above most Cetaceans and are the top non-Cetacean at over twice Chimpanzees and Elephants. Even at such a "lofty" spot in the animal kingdom, truly creative behavior is rare. But imitation is so good that these rare innovations spread around the world and became fixed in collective memory. Eventually, the accumulation of all these inventions led to modern technology (opposable thumbs also helped). There was only one Bitcoin but there are now >12,000 copycats.
Even though no animal species (human or otherwise) commonly breaks out of both instinctual and learnt behaviors, it happens in the smartest species occasionally and can have a big effect given enough time.

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Parametric Bootstrap Capture Recapture
I am using the (one sample) capture recapture for estimating hidden human population. One sample method uses purely frequencies of capture to estimate population. One of my colleague suggested parametric bootstrapping method to assess the variability of the population size estimate. I tried to research online a little about this parametric bootstrap method but I just still don't understand how it is performed. I know bootstrapping is basically resampling data with replacement and then calculating the variance of it. However how do I perform parametric bootstrapping (I assume the frequencies of capture follows Poisson Distribution) on capture recapture data? Do we treat the frequencies as datas, i.e. so if f(1)=100 and f(2)=9, our data has 100x 1 and 9x 2 and then resampling this? Is probability of daily capture the parameter $\lambda$ in Poisson distribution?
I guess what I am trying to ask is, how do you perform the sampling bit of a parametric bootstrap [in capture recapture]?

I'm a little confused when you say "[your method] uses purely frequencies of capture". Is there any 'recapturing' going on?

@CactusWoman So unlike the normal capture recapture where they have discrete timings and capture history, my capture recapture is a continuous model (since only 1 individual can be captured at a time) and only frequencies of encountering individuals are noted. So the only data I have f(1), frequency of capturing individual once, f(2), ... Does this make sense?

I did a little research and I think it works like that:

Collect a dataset of $n$ observations.
Fit a parametric model to your data. If you want to model the recaptures, I would suggest a Poisson-GLM. You can also estimate the parameter directly from your data and simply parametrize a Poisson distribution. However, this approach would not model the random variation in your data.
Use the fitted model to draw a sample of size $n$
Calculate your desired metric based on the sample. I guess in your case this would be human population size (calculated as ${N} = \frac{nM}{m}$?)
Repeat steps 3 and 4 many times (1000+)
There you go! Now you can easily assess the variability in population size based on the estimates from your bootstrap samples.

Im confused with step 2, I thought for estimating parameter from the bootstrap sample we use the same method we use for the original data?

I was referring to the parameter $\lambda$ of a Poisson distribution. You can estimate lambda based on your data using maximum likelihood. Some function to do this should be included in every serious statistical package. So what 2 says: Build a model from your data (a glm or a parametrized Poisson distribution) and use this model in steps 3 and 4 to for bootstrapping.


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Why do some women have menstruation-like spotting throughout their pregnancy?
An interesting question that was asked during a lecture about human reproduction: what is the biological mechanism behind some pregnant women getting monthly spotting that they mistake for a regular period? I've found articles and research papers about bleeding during zygote implantation, ectopic pregnancies and problems with the placement of the placenta, but nothing regarding menses-like bleeding during otherwise unproblematic pregnancies.

Related: How common is it to be pregnant with periods?

Here are some causes of bleeding during pregnancy:

early pregnancy (first trimester):

implantation bleeding [1]
infection [1]
after intercourse [1]
miscarriage [2]
ectopic pregnancy [2]
cervical changes [3]

second part of pregnancy:

abruptio placentae [1, 2]
placenta previa [1, 2]
miscarriage [2]
vasa previa [2]
preterm labour [1]

References:

American Pregnancy Association. Bleeding During Pregnancy. Available from http://americanpregnancy.org/pregnancycomplications/bleedingduringpreg.html (accessed 29.07.2014)
U.S. National Library of Medicine. A.D.A.M. Medical Encyclopedia. Vaginal bleeding in pregnancy. Available from http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0003748/ (accessed 29.07.2014)
WebMD, LLC. Bleeding During Pregnancy. Available from http://www.webmd.com/baby/guide/bleeding-during-pregnancy (accessed 29.07.2014)


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Why do beta-1 and beta-2 adrenergic receptors result in two completely different effects (though both use Gs pathway)?
$\beta_2$ adrenergic Receptors are $G_s$-coupled 7-TM proteins. Considering that $G_s$ , by activation increases $[\text{cAMP}]_\text{cytosol}$ which inhibits MLCK of smooth muscles (and causes relaxation as in bronchial smooth muscles).
But at the same time, in cardiac myocytes ($\beta_1$), $G_s$ activation activates PK-A (through cAMP) which in-turn activates L-type $\ce{Ca^{2+}}$ channels. Thus there is prolonged plateau phase and positive inotropic and chronotropic effect.
I think these two results are contradictory. Why and how are these two seemingly completely opposite effects mediated through similar signal transduction pathways?

Madamanchi A. Beta-adrenergic receptor signaling in cardiac function
and heart failure. Mcgill J Med. 2007;10(2):99-104.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2323471/

The autonomic nervous system is composed of the parasympathetic and sympathetic nervous systems. The sympathetic nervous system is stimulated via adrenergic receptors.
Adrenergic receptors are G protein-coupled receptors stimulated by norepinephrine (noradrenaline) and epinephrine (adrenaline).
There are 4 sub-types of adrenergic receptors:

Beta1-adrenergic receptors
Beta2-adrenergic receptors
Beta3-adrenergic receptors
Beta4-adrenergic receptors

Yes, Beta2-adrenergic agonists reduce bronchial Smooth muscle contraction.
Yes, Beta1-adrenergic agonists increase heart rate.
Here we can see activation of different tissues from different receptors, that activate the same pathway. Thus, despite the example explained - the activation of the same path-way - different responses ensue.

In the human airway - Smooth muscle cells express Beta2-adrenergic receptors the most (100%).

In human heart tissue (Cardiomyocytes/Cardiac muscle cells), of Beta-adrenergic receptors - Beta1-adrenergic receptors are expressed the most (75–80%).

"...the cAMP pathway generally promotes contraction in cardiac muscle; however, in Smooth muscle, activation of cAMP causes relaxation."

Source
cAMP inhibits myosin light chain kinase, the enzyme that is responsible for phosphorylating Smooth muscle myosin and causing contraction. Thus no contraction takes place in smooth muscles cells.
Inhibition of myosin light chain kinase increases intracellular cAMP, which further inhibits myosin light chain kinase thereby producing a lower contractile force (E.g. promoting relaxation).
Source

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Can we develop a virus which is amicable for us but deadly for SARS-CoV-2 and HIV?
I am not biologist and do not have special education in it etc.
It is know that in the wild, some species have their deadly enemies.
What I am suggesting is can we humans find/create virus that is amicable for us, but super deadly for SARS-CoV-2, HIV etc?
If I am not mistaken, there are plenty of native bacteria/viruses in human body.
As an option can we genetically modify one of them to turn them worst enemy for some kind of viruses like SARS-CoV-2  for restricted amount of time?
P.S
I am not a specialist, therefore I apologize if my questions are too naive.
With regards,
Almas

Viruses are obligate intracellular parasites. They act like a living organism only when they infect a cell. Apart from some protein structures which help them to attach and enter specific kinds of cells, viruses don't have enzyme systems that can be used for activities like "destroying other viruses".
A virus can not infect another virus as this would be a one time action. Viruses infect cells in order to replicate, a virus can't replicate by using another virus. So if you engineer a virus which will attach and destroy another kind of virus, it will be no longer a virus, it will be an unnecessarily complicated antiviral drug.
In addition to this point, you should consider that our bodies have leukocytes (white blood cells) which can identify and destroy viruses. Some kinds of leukocytes also produce antibodies to fight with the infection agents. If you aim to engineer a bacterium in order to fight with a virus inside our bodies, first you have to provide that the bacterium will stay in the tissues of our bodies for a sufficient amount of time and/or its secretions which attacks to the virus will enter and stay at least in the blood stream. It is obvious that this approach is way more complicated and hard to achieve.

This is an interesting question I have not considered, however it does have some caveats.
The ultimate question is how is COVID-19 going to be assaulted? What is the interaction to eradicate the pathogen? If we understand this, we don't need to create a bio-weapon to destroy a virus.
Also if we understand this interaction, we should arrive at a suitable vaccine as a solution. There are many methods to develop a vaccine, as outlined here.
Bacteria and viruses are very different and are in-fact different organisms.
Within our gastrointestinal tract (The hole from our mouth to anus), live approximately 100,000 billion bacteria. Typically viruses - speaking generally - stay with someone for a short time-frame. So you never have more than one at a time really and most people live their life without any viruses.

This does not provide an answer to the question

In fact, there are many gastrointestinal viruses that are present indefinitely, they are bacteriophages that use intestinal bacteria as hosts: https://pubmed.ncbi.nlm.nih.gov/31295677/
However, there are no "virophages" for animal viruses--the closest thing I know of is hepatitis delta virus, which exclusively infects cells that are already infected with the hepatitis B virus. However, while HDV is a "parasite" of HBV in this sense, it doesn't eradicate HBV (doing so would be evolutionarily "stupid" as it eliminates its own host).


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Carotene in Dracaena draco
I'll keep this question straight and simple:
Some succulent plants produce carotene, a red pigment, in response to great heat, turning their leaves red. The dragon blood tree (Dracaena draco) is among the succulent plants. Does it exhibit this behaviour too?

Looks like they do.
What We Know and What We Do Not Know about Dragon Trees?

Numerous phytochemical studies of resins from the Dracaena species
  resulted in the isolation and subsequent identification of sterols
  [135–138], steroidal saponins [110,138–141], lignans [138], and
  terpenoids [131,135,142–144], flavonoids (recently reviewed by Sun et
  al. [129], bioflavonoids [145,146], carotenoids [109,138], and
  aromatic compounds [107,147–151].

Citations are behind a paywall but apparently carotenoids are in the sap.


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Design primers for PCR from given DNA sequence

Given the sequence: 5’-ACTGACTATGTAGAA………GGCCCTAAGGGCCAA-3’ (1)
You wish to do PCR of this dsDNA to add “overhangs” on the ends of it. On the 5’ end of you will put
  the restriction site for NdeI enzyme (5’-CATATG). On the 3’ end you will put the restriction site for
  MspI (5’-CCGG).
Write the sequences for the “forward” and “reverse” primers to do this. Each primer should be
  16-18 nt, with 12 nt for hybridization and 4-6 nt for “overhang.”

I am a little confused as to how to write the forward and reverse primers for the sequence. From videos I have seen that I should write the complementary strand of my giving strand. Which would be:
3' -TGACTGATACATCTT........CCGGGATTCCCGGTT-5' (2)
Then from sequence (1) I should get the reverse primer and from sequence (2) the forward primer. However, this doesn't allow me to add both restriction enzymes because both primers would be from 5' to 3'.
Or should I simply take the given sequence and write the primers only from that? So that the primers would  be:
Forward primer:
3’-GGCCTGACTGATACAT
Reverse primer:
GGATTCCCGGTTGTATAC - 5’
where the bold nts are the restriction sites.
Thank you!

This question is a bit confusing, in part because the convention is to always write DNA/RNA sequences left to right as 5' --> 3'. Is this a homework question?

Also, where you write "Should I simply take the given sequence..." You appear to in fact be using your complementary strand for both F and R primers, rather than the given strand, I'm not sure if this is intentional.

As alluded to in the comments above, remember that you are amplifying double-stranded DNA, so two new reverse-complementary strands should be generated from each cycle (so that they can hybridize with eachother). As written in your answer, both of your primers would hybridize with your given strand, and the amplicons would not overlap (one binds at each end, but both would amplify in the same direction).
To fix this, you need one primer that binds to the target sequence, and one that binds to the reverse complement strand, which you have already generated. The new amplicons extend 5' -> 3' (from the 3' end of the primer not the template), so your primers need to bind at the 3' end of their respective strand. This link has a good visualization of that.
The 3' end of the primer needs to hybridize tightly with the template, since this is where extension happens (discussed in this guide). So your flanking restriction site sequences will always be on the 5' end of either primer (notice that the question actually hints at this by indicating the 5' end of each flank).
The primer given as your "reverse" primer will actually bind to the 3' end of your given sequence in the appropriate orientation, but you may want to put your 3' flank onto the 5' end of that primer sequence, as this will be theoretically be the 3' end of your amplicon. Your other primer will need to bind the 3' end of your reverse complement (which is the 5' end of your target), so it will have the 5' restriction site flank.
By convention, primer sequences are always given in 5'---3' format. So make sure your answer follows that convention. (i.e. 5'-Flank-primer-3').
If all of this sounds really confusing, that's because it is. I do this for a living, and I still always double check my primers in a program like Primer3


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Would I still exist if
I've been wondering for some time, but say that my mother's egg chose another sperm cell, and a baby was eventually produced. Would I still be born, but end up with different characteristics/features?

Sorry but this is not a real question. What makes you you? If you have different characteristics how can you be you? Also, the egg does not choose sperm, where did you get that idea?

I, as in being an entity that can perceive the world. Let's Ignore the extra features like hair, eye color, etc.

Well, yes, just about any sperm with any egg would produce a human being that could perceive the world. How would we decide if that's 'you' or not?

I was hoping someone would have an answer to that.

consciousness and awareness and in fact a brain develops long after fertilization.. i hope that clears your doubt

@terdon This is a legitimate philosophy question. Not biology, though.

For every sperm that fertilises an egg there are millions/billions/"a sh**load" that don't make it. Within that pool of unused sperm there is considerable genetic variation. If we assume that DNA is the only factor which makes "you you" then the chance of picking one of those  sperm and it having the exact same DNA is small. Of course environment also has a large effect so even two identical sperm and egg combinations would produce two people with different physical and mental attributes.
If this does not answer your question then this is not really a biological question though and should really be on the philosophy SE.


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Are there any enzymes in cytoplasm to help the newly-synthesized polypeptide to form tertiary structure?
Polypeptides made by ribosomes which attach to rER will go into the rER to form the tertiary structure. Those polypeptides made by free ribosomes usually stay in cytoplasm. So are there any enzymes in cytoplasm to help them to form tertiary structure?

What about the chaperone?

There are several types of proteins that do this, all of which fall under the category of molecular chaperones. In particular, chaperonins such as GroEL/GroES complex in E. coli, sequester newly-formed polypeptides to allow them to fold their tertiary structure and avoid aggregation. Another widely studied class of these proteins are heat shock proteins (Hsps): these are involved generally in acclimating cells to stresses (such as heat), and some of these Hsps have been specifically implicated as chaperones. I'm a new user, so I can't post a 3rd link, but just google Heat shock proteins and you'll find plenty of information.


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Which monkey species features two distinct male phenotypes?
I remember coming across a popular science article years ago about a monkey species which featured two male genotypes: the first were good looking males who acquired social status (as alphas or betas) within the group and could thus achieve reproductive succes. The alternative (less frequent) phenotype achieved similar fitness by adopting an outgroup (omega) lurking rapist kind of reproductive strategy.
Does anybody know which species and whose observervations I could be referring to? I'm curious to find out if this was a valid observation and if any further research has been done on this phenomenon.

Related behaviour in lizards: http://en.wikipedia.org/wiki/Common_side-blotched_lizard

Search term 'alternative reproductive strategy' for lots of related behaviors in various organisms.

Patas monkeys exhibit "sneak mating" where a male other than the resident male sires offspring. Resident males do sire more offspring than sneaker males, but both strategies do co-occur. I'm pretty sure there are other species that have a similar mating strategy as well.

Although I'm pretty sure that this is not the species I was looking for, this behaviour resembles the description in my question closely enough, so I'm accepting your answer.


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What are the implications of tigers being susceptible to SARS-CoV-2?
It was recently reported that a handful of tigers and lions tested positive at the Bronx Zoo for SARS-CoV-2 (see here and here). Does this imply that the SARS-CoV-2 strain in humans mutated into a form that can infect these other species? I thought these sorts of mutations required a long time and prolonged contact between the species (which I wouldn't have thought would be present with such large cats).
Alternatively, is it possible that a single strain of the virus is capable of infecting multiple species?

A partial answer, to the question of how the virus might spread to animals I found several references

The HongKong dogs, the New York tiger, the Netherlands mink farm and the French cat have been sequenced and can be seen on nextstrain. Note the low amount of mutations in each case, which is intriguing because we expect for example that different ACE2 genes will induce some adaptation at in the viral spike. Those animals had an infection and detectable RNA in the nose for several days. For the dogs the viral load was low and in one case the sequence was identical to the owner. The minks and tiger had noticeable symptoms. A Wuhan cat partial sequence has been uploaded too, as well as a full-length French cat sequence.

A lab paper said "SARS-CoV-2 replicates poorly in dogs, pigs, chickens, and ducks, but efficiently in ferrets and cats", in particular dogs can't transmit the disease efficiently. According to them subadult cats are susceptible while adult cats are not, and the disease is upper respiratory tract.
There is a new preprint on a 4 month cat who developed severe disease, dyspnea, and had to be euthanized.

A paper found antibodies in several Hubei cats from animal shettlers and vet clinics, some of the positive cats are "stray cats", others are sick cats, and a few were cats owned by covid positive people, in those the antibodies were found to be neutralizing the virus much better than in others.

Another one found that ferrets are efficiently infected in lab and transmit the disease to each other, even if it is mainly upper respiratory tract (no severe pneumonia).

Rabbits are susceptible though less than ferrets, and asymptomatic.

Mice are not succeptible but human-ACE2 transgenic mice are and develop a mild pneumonia. Note that SARS-CoV and OC43 produced instead a deadly encephalitis.
However, through 6 ($10^{5.8}$PFU) passages into mice lungs the researchers could adapt SARS-CoV-2 through acquisition of a single mutation in the RBD allowing the virus to produce a moderate pneumonia into both young and aged mice.
The same researchers after 30 more passages obtained a super-deadly mouse adapted strain effective even at $10^2$PFU with 3 mutations in the RBD and 9 others mainly in nsp3-4-6 and N. Of note, two of the RBD mutations are in the South African variant N501Y.V2.
Something similar had been done with SARS-CoV.

The Baric lab has compared the RBD from SARS-CoV-2 and previous sarbecoviruses,
the human and mouse ACE2 protein, and through computer simulations they could find two amino acids to change in order to switch the virus from humans to mice. With 10 more passages they obtained a deadly strain in aged mice.

There are several mink farms in Netherlands where the animals got infected, this is possibly the most promising species for inter-species transmission. Edit : as predicted (first reported case) of animal to human transmission is believed to have occurred in such a mink farm. A detailed story including severe pneumonia is described in a paper.

In lab, SARS-CoV-2 is provoking a severe disease in minks as well as in Roborovski dwarf hamsters.

The Pangolin outbreak(s) : not SARS-CoV-2 but the newly discovered Pangolin-CoV in the same lineage, it killed 16 of 21 Malayan pangolins in March 2019. The virus was identified only in February 2020. The Pangolin-CoV whose RBD is very similar to SARS-CoV-2 was in this outbreak.

Cats can transmit the virus to each other. In the nose the peak was $10^{4.5}$ PFU / ml which is a medium viral load.

Similar for hamsters and macaques, the latter are used for vaccine development.
Racoon dogs show high shedding and can transmit the virus through present only minor clinical signs.
This kind of result is not surprising, most human viruses can transmit to some species and not to others, often producing a different and milder disease, which is a problem for vaccines and antibodies development.

This paper https://onlinelibrary.wiley.com/doi/pdf/10.1002/jmv.26621 has a lot of references on zoonotic potential of SARS-CoV-2

Your question may be based on a misconception. Mutations occur all the time. In almost all cases, it leads to decrease in reproductive viability. For a virus with one or more established host species, it has already evolved to be quite efficient at reproducing within those species. For it to jump to a new host species and spread in that other species, it must not only be able to infect the new host species, but must also have the opportunity to cross over. If it cannot normally infect the new host species, then it has to acquire some mutations. But mutations occur all the time, whereas the opportunities are not always there. So this is a matter of relative likelihoods. The more contact between wild animals and humans, the greater the likelihood of such inter-species infection happening, because of low prior contact between humans and wild animals.
Since we now have probably 10 million or more humans infected, we have provided a great number of opportunities for the virus to jump to other species, many orders of magnitude more than the original opportunities for the virus to jump to humans. This is why such large-scale events can have knock-on effects of much bigger scale than the events themselves.
While zoo visitors may not go close to large cats, they may sneeze or cough and thereby transmit the coronavirus in mucus droplets that can last very long even if alcohol-based disinfectants are applied. The zoo keepers themselves may be infected and have close contact with the animals. It is difficult to trace the source of infection when we have so many cases. Although the Bronx Zoo was supposed to be closed from 16 Mar onwards, it is not impossible that some animals were already infected prior to that, so any hypothesis is going to be guesswork.
Furthermore, viruses that already regularly infect more species tend to be able to infect more new species than other viruses. So once the coronavirus managed to jump to humans, it is reasonable to expect it to be able to infect other new species more easily than the strain in the original host species. So the fact that tigers are susceptible to the strain that infects humans does not imply anything about whether that strain has acquired some new mutations or not.

A single strain of virus (such as rabies) can infect multiple species of hosts.
The big question is whether domestic cats also get infected?
If they do, two main problems.
There would be a reservoir of virus circulating in cats allowing reinfection of humans. And worse, the virus may acquire mutations in the cat population that make it more virulent in humans.
Personally, I recommend keeping a good distance from all big cats to be safe.

Lol agreed.  Only one thing is worse than being bitten by a tiger, and that is being bitten by a tiger with coronavirus.

Interestingly I got quite a lot of downvotes and negative criticism for this (inc. request for citations). Never make a joke on an intercultural site unless it’s OK for people to miss it.


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kcat in uncompetitive enzyme inhibition
Why doesn't $k_\text{cat}$ change in uncompetitive inhibition, given the fact that uncompetitive inhibition lowers the enzyme–substrate complex efficiency (which is the reason for lowering of $V_\text{max}$ as well)?
Source of information: https://youtu.be/0ZiCqwtFMTs

Welcome to the Biology community! Aside from grammar and punctuation fixes, your question needs attention to the following issues: 1. Please mention the source of the information (kcat remaining unchanged in uncompetitive inhibition) and the context in which it was given. 2. 'enzyme–substrate work efficiency' is not a well defined term in biology. Can you word it better? Please edit your question to incorporate these changes. Thanks.

The source: https://youtu.be/0ZiCqwtFMTs

Enzyme- substrate complex.

Please add these changes to the question itself (comments might not be read by everyone).

Sorry, and thankyou

Short answer
It all depends on how you look at $k_\text{cat}$ and enzyme concentrations

Long answer
The effect of an uncompetitive inhibitor on $k_\text{cat}$ can be interpreted in two ways.
Interpretation 1:
This is followed in the lecture series mentioned in the question.
See the video https://youtu.be/rNBEUGYu034 from 7:37 to 11:01 minutes. The instructor says:
... the turnover number basically describes the ability of that active site to actually transform the substrate molecules into the product molecules per unit time. Now because when the inhibitor is not bound to that particular enzyme-substrate complex, the active site's ability or efficiency to change that substrate to the product doesn't actually change, we see that the $k_\text{cat}$ value in uncompetitive inhibition also doesn't actually change...
Mathematically, $k_\text{cat}=\frac{V_\text{max}}{[\ce{E}]}$ (where $[\ce{E}]$ is the concentration of enzyme, excluding that which has been inactivated by inhibitor). Now, uncompetitive inhibition reduces both $V_\text{max}$ and $[\ce{E}]$ by the same factor. Thus $k_\text{cat}$ remains unchanged.
Interpretation 2:
Some people do things differently. They regard $k_\text{cat}$ as $\frac{V_\text{max}}{[\ce{E}]}$, where $[\ce{E}]$ is the total concentration of enzyme in the mixture (including inactivated forms). In this treatment, the uncompetitive inhibitor reduces $V_\text{max}$ but $[\ce{E}]$ stays the same. Thus $k_\text{cat}$ is reduced.
Qualitatively, the enzyme in the mixture is now a combination of active and inactivated forms, and thus has lower "efficiency" overall, i.e. lower $k_\text{cat}$.

Thanks for the answer.


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Why do cells not spread on soft substrates?
I recently read a paper discussing how cells (primary mouse embryo fibroblasts) fail to spread and proliferate properly when plated on a soft substrate (i.e. soft PDMS pillars with stiffness k = 2.3 nN$\mu$m$^{-1}$), but spreading and proliferation can be restored with cyclic stretching of cells.
http://www.nature.com/ncomms/2015/150223/ncomms7333/full/ncomms7333.html
My question is if we understand why cells need to be on a hard surface to do normal operations (proliferate and spread)? It doesn't seem to me that a soft surface would be any more difficult for a cell to attach to. I would think that a "slippery" (I'm not sure of a correct biological term for this) surface may have this effect, but I wouldn't expect this from a soft surface.

Some cells need a matrix to adhere. Adherence relays proliferative signals in these cells. If you coat the PDMS pillars with polt-D-lysine or collagen then the cells may grow well.

Please keep in mind that this is about a single cell type (MEFs), and not extensible to all cell types and environments.

@WYSIWYG so are you saying that it's harder for cells to adhere to a softer substrate (or matrix)? for some reason, it's just not intuitive to me that that is true.

@MattDMo is this not a general trend observed for most cell types? Am I way generalizing a result from one paper by thinking it would extend to most cells? I suppose fibroblasts don't typically need to move that much, but would you expect this result to hold for macrophages or any other cell that needs to move a lot?
My apologies if these questions are too general -- my background is not in biology!!

@NaiveHalmos it is not about being soft. Cells need some kind of interaction with the substrate. Some proteins allow this interaction because of their functional groups. This article says that hydroxyl groups in the substrate facilitates cell adhesion.

@WYSIWYG Oh, so the paper I presented above didn't need to include that they used a soft substrate? They could have just mentioned that before cyclic stretching, the cells weren't adhering to the PDMS pillars? Thanks!

@NaiveHalmos Please note that texture and other surface properties of the material can play a role in adherence but not the bulk properties such as tensile strength etc. I am not really sure if by soft they mean smooth or not-rigid. I haven't read the paper yet. Will read it and let you know. As far as I can understand from the title and abstract they say that when the cells are attached to PDMS then mechanical stimuli like stretching promote growth.

@NaiveHalmos no, this is not a general trend. Some cell types, including the many kinds of white blood cells like T and B cells, grow and proliferate just fine while growing in suspension, with no substrate needed at all. Others form colonies in soft agar. Just like any research paper, you need to look carefully at what the investigators analyzed, and how they drew their conclusions. If they did all their work with a single cell line or cell type, and didn't look at any others, then the results are not necessarily generalizable at all.

As both @MattDMo and @WYSIWYG have already so succinctly answered this question in their comments I'm just going to attempt to expand a bit on their answers.
@MattDMo and @WYSIWYG have explained that the aforementioned paper from the question has results that are "not extensible to all cell types and environments" and "Some cells need a matrix to adhere. Adherence relays proliferative signals in these cells."
I'm just going to expand a little bit on these points... I know this addressing an erroneous assumption in the question rather than the question itself but bear with me.
Ok, so as has already been mentioned, different cell types in a multicellular eukaryote (like a mouse, or a human) only grow in certain environments and this is really important . Think about it like this, a mouse's body is made up of many different cell types all working together to create functional organs and systems and to ultimately make up the mouse. The individual cells don't know they are all coming together to make an entire animal and a cell is designed to grow and proliferate in order to make more copies of itself and spread. So why don't all cells just grow all over the place, on top of each other and spread to all parts of the body.
The reason you and the mouse aren't a formless mass of undifferentiated cells - like a big soft tumour - is because different cell types develop in such a manner that they can only grow in a restricted, structured way in a certain environment in your body. There are mechanical and chemical signals along with unique sets of growth factors that are found in different environments in the body that make it possible for certain cell types to grow in one area while not in another. It's why only blood cells can survive suspended in the blood not adhered to anything and your fibroblast cells (they make up your structured connective tissue can't, they need to adhere to a surface to grow. The different cell types only get their signal to keep growing when they are in their proper environment.
This is why when scientists are growing various mammalian cell cultures they have to be aware of what environment and growth factors the specific cell type they are working with requires in order to grow. Some mammalian (e.g. mouse) cells need a structured scaffold to grow them in culture and some can grow in soft or liquid culture.
Source: Hallmarks of Cancer: The Next Generation http://www.cell.com/cell/abstract/S0092-8674(11)00127-9?_returnURL=http%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS0092867411001279%3Fshowall%3Dtrue [This is a classic paper that explains this far better than I can hope to - look for the section 'Sustaining Proliferative Signaling'.]


text:
Is EGF-mediated proliferation symmetric?
It's known that the MAPK signaling cascade (say, ERK) is downstream of EGFR in epithelial cells, and that EGFR activation can cause proliferation in some cell types in some situations. My question is the following: if an epithelial cell with active EGFR (and hence active ERK activity) divides, will the two daughter cells have the same amount of ERK activity as the parent, both have half as much ERK activity as the parent, or divide asymmetrically? I suppose ERK activity should be defined here as ERK phosphorylation... though I would certainly welcome better definitions!
If you need better context, I would be considering wound healing of mammalian epidermal skin. There are plenty of sources suggesting that in response to  a wound puncture, EGF is released and stimulates proliferation.
Thank you!


text:
Introductory book in genetics?
I am working in the field of neuroscience with a background in computer science. I try to find new ways of analyzing brain imaging data (mostly MRI, EEG, MEG, fMRI) with modern machine learning methods.
I would like to take a step up by adding genetics to the data arsenal. My work this far has found connections between some X and Y but not really shed insight to why things should be like that. I hope I could get a partial answer from biology.
To get started, I would need some good material to read. It does not matter if the content would be difficult in mathematical/statistical/technical aspects, but it should be approachable with limited knowledge in biology and/or chemistry and physics.
Suggestions?

What type of genetics?

You should clarify what you really require in detail. Else this would count as duplicate of the abovementioned post.

GENETICS: Analysis and Principles, 4th edition, Robert J. Booker
This book is used in my school's ( NYU Poly) undergraduate genetics class.

MIT Open Course Ware has a course on genetics, which uses the following text:
"An Introduction to Genetic Analysis", Griffiths, Anthony J. F., Jeffrey H. Miller, David T. Suzuki, Richard C. Lewontin, and William M. Gelbart, 7th ed. New York: W. H. Freeman, 2000.


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Is it possible that the DNA of an individual changes significantly over a period?
Is it possible that the DNA of an individual changes significantly over a period ?

What do you mean by "significantly"?

Not that significant that changes your identity, but that significant that may change your life.


text:
What kind of insect is this found in North America in April?
I noticed this small insect that probably measured 5 mm in length on my coat lapel. Not sure whether or not it had been inside or landed outside on my coat. Photos were taken in Nashville, Tennessee, USA in April. It was alone and I have never seen an insect like this one before. Just trying to figure out whether this bug is harmless or something that could be a problem. . Here is another photo taken of the same insect.

It is a ladybug larva.  They eat aphids.  I have handled many and never been bitten.
https://test.whatsthatbug.com/2010/10/25/ladybird-beetle-larva-ladybug/


text:
How can I render a protein non-functional to avoid problem during expression?
We're expressing a protein in a model organism for crystallization, however it seems the protein has some toxic effect on the cells.
Is there something we can do to make it non-functional during expression so it won't affect production, in such a way that we can restore function later (ex. after purification) in a simple way?
I know there are other approaches available but I'd like some inputs on this one alone.

That would depend on the specific protein being expressed. You could try secreting the protein or targeting it to inclusions and then refolding.

Can you provide more information? Are you expressing the protein in yeast or bacteria?

@user22542 in yeast, however I'd be interested to hear approaches that can work in different vectors too

I assume the toxicity is limited and not lethal.  Is the protein showing the toxic effect being secreted during production or retained in the cells?

@user22542 It is secreted in the medium

With limited knowledge and information, but intrigued with the question, I can only hazard to ask if it might be possible to alter the pH of the media (or another parameter) enough to render the protein temporarily "non-functional" or at least "less toxic" while maintaining a permissive environment for the growth of the production yeast? Beer becomes a questionable environment yet the yeast don't seem to mind to a point.

@user22542 could be an idea, I guess

You need to add more details or else the question would be considered too broad and most likely put on hold.

Inclusion body (IB) is a technique used to express proteins that are toxic to the host cells. IBs are aggregate of highly similar or the same kind of proteins in the cytoplasm formed as stress reaction, resulting biologically inactive precipitated proteins. Such stress reactions can be induced by high temperatures, pH-shifts or occur due to high feeding rates (1,2). Active proteins can be acquired later via purification and mild solubilization of inactive IBs (1).
The second method is to use special host strains. In terms of E. coli, some strains are specifically mutated and selected to withstand the expression of toxic proteins (3). e.g. C41(DE3) and C43(DE3) are developed to enhance membrane protein production (4).
Another method is to express proteins in the periplasmic space. In E.coli, you can achieve that by fusing your recombinant protein with a proper signal peptide, which targets the recombinant proteins to the periplasm via post-translational Sec-dependent pathway (3).
In addition, I also found this product list that provides several solutions for toxic protein expression, including expression in yeasts. But in that case it is similar to your situation so I am not quite sure why it doesn't work out for you.
Resources
(1) Slouka C, Kopp J, Spadiut O, Herwig C. Perspectives of inclusion bodies for bio-based products: curse or blessing?. Appl Microbiol Biotechnol. 2019;103(3):1143-1153. doi:10.1007/s00253-018-9569-1
(2) Slouka, C., Kopp, J., Hutwimmer, S. et al. Custom made inclusion bodies: impact of classical process parameters and physiological parameters on inclusion body quality attributes. Microb Cell Fact 17, 148 (2018). https://doi.org/10.1186/s12934-018-0997-5
(3) Rosano Germán L., Ceccarelli Eduardo A. Recombinant protein expression in Escherichia coli: advances and challenges. Frontiers in Microbiology 5, 172 (2014). https://www.frontiersin.org/article/10.3389/fmicb.2014.00172
(4) Kwon, SK., Kim, S., Lee, DH. et al. Comparative genomics and experimental evolution of Escherichia coli BL21(DE3) strains reveal the landscape of toxicity escape from membrane protein overproduction. Sci Rep 5, 16076 (2015). https://doi.org/10.1038/srep16076
(5) https://www.neb.com/-/media/nebus/files/brochures/proteinexp_trifold_0912.pdf?rev=3ade8cf2c18b47afb7cc57113df43147&hash=7BEDC3D4DBDAE53A09EC37ADE808C450


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confusion in types and kingdom system of classification
I am a high school student and I want to ask: is the 'kingdom system' of classification (two-kingdom, three-kingdom etc.) different from artificial or natural classification? I am asking this because my teacher told me that these two are different things. He says that you cannot categorize the two-kingdom classification as artificial or any other type.
But I am little confused as to why we cannot categorize kingdom system classification into artificial, natural or any other type. For example, Linnaeus selected only a few characters to propose the two-kingdom classification. Then why can we not say that it is an artificial classification?

This question is very unclear. I don't know what "2kingdom", "3kingdom" are or what "artificial type, natural type etc." refers to. It seems at the end you're wondering about whether the classification of living things is arbitrary or not?

@Oosaka The OP is referring to the description of biological classification systems as artificial or natural. They then ask whether the two-kingdom classification is a natural system, an artificial system, or something else entirely. (I have suggested some edits to the question, hopefully they will make the meaning clearer.)

2 kingdom ,3 kingdom are the systems of classification which were used by earlier scientists to classify organisms, and natural ,artifical are also types of classifications which were based on the characters selected by them, i think i have cleared this in my question,,and my confusion is that whether the kingdom system can also be mixed/categorize in artificial,natural etc. types of classification or not?

@Adhish Thanks, I think I better understand what they mean by "2kingdom, 3kingdom" but I think your edit might not be totally accurate, in that OP talks of "classifications" and "types" where "natural" and "artificial" modify "types" and "2kingdom" etc modify "classification" and you've conflated things so that "artificial", "natural", "2kingdom" etc all modify "classification". Either way it doesn't answer the question of what OP means by "natural" or "artificial" types of classification... I can infer a meaning but I don't know if it's what OP is thinking.

@ArunBhardwaj As I said I think I understand now the 2kingdom, 3kingdom thing (you mean Linneaus had plants and animals, right? And others added fungi, prokaryotes, etc?) but I still don't know what "natural" and "artificial" types of classifications are. You say "based on characters", are both based on characters? What is the difference? Is it a difference in the characters, if so which ones? If you are talking about a definition you learned, can you give a source that explains that definition?

I would recommend adding this source to your question, else it will be downvoted: https://onlinelibrary.wiley.com/doi/10.1111/j.0107-055X.2007.00098_12.x This gives a good distinction between natural and artificial systems.

@Oosaka yes that is my question,,,thats,why i have asked this because i am also confused why these two systems of classifications are different i.e why one cannot be categorized into other

In earlier days, biological classification systems were often described as artifical or natural, with natural systems reflecting the 'real' relationships among living beings, and artificial ones allowing classification only for some limited purpose (Gilmour, 1937). Natural systems were supposed to be based on a large number of characters, with a focus on characters 'fundamental' to organisms.  Artifical systems were supposed to be based on fewer, arbitrarily chosen characters.
As an example, consider Linnaeus' works on the classification of plants. Linnaeus' Systema Naturae (1735) classified plants based on floral morphology alone. However, his later work Genera Plantarum (1737) included more characters, such as the morphology of fruits. Linnaeus therefore regarded the latter classification as being more natural. (See the Encyclopedia Britannica entry on Linnaeus for a more detailed discussion of this.)
As for the two-kingdom classification, I couldn't find any sources calling it either artificial or natural.
However, the natural vs artificial dichotomy is not always straightforward. For instance, how do we know which characters are 'fundamental' and will help us develop a natural classification system? To quote Judd et al (2008):
For hundreds of years, botanists tried to develop classifications that were "natural"... Unfortunately, the word natural has no fixed meaning; rather, authors have used it to mean something that agrees with their own ideas about nature or about constructing classifications or systems. Eighteenth-century systematists had ideas about nature that were very different from ours—they were certainly not evolutionary—and their systematic practice and classifications are best interpreted in terms of how they understood nature.

Thus, in modern biology, 'natural classification' and 'artificial classification' are better regarded as historical ideas than as useful descriptors. The focus is now on classification that integrates an understanding of evolutionary relationships, i.e. phylogenetic classification.

You still don't explain what "artificial" systems are, and neither does the Wikipedia article that you linked to, other than saying that such systems were based on arbitrary criteria, without giving any examples.

Linnaeus' sexual system was artificial. ("In contrast to systems based on arbitrary divisions (including his own sexual system), a system based on natural characters could accommodate the growing number of new species..."- from the source you have linked).

Thanks for the comment @MattDMo, I have edited the answer accordingly.

Thanks @Bipasha too, I hope the edits address your point.

@Adhish thanks, that explains it a lot better.


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what is “a group of living things that can interbreed and produce full interfertile offspring”?
lets call this term "collection" Example: group of humans.
what is not a "collection" horses and donkey: can't produce full interfertile offspring, lions and tigers: can't produce full interfertile offspring, Camels and Lama: can't produce full interfertile offspring.
And no this is not "species". Polar bear is a species grizzly bear is a species they can produce interfertile offspring, they are of the same "collection"
Two species can belong to the same "collection". Two different "collections" can't be of the same species.
And no this is not a homework question.
Why is this not defined in biology?
Why is this down-voted? I know what ring species is. First and last generation do not interbreed naturally. But it does not say they can not interbreed at all or can not produce full interfertile offspring.
The question is about having the ability of intebreeding and producing full interfertile offspring.
I will add more details:
The term species is a fuzzy term and makes a lot of confusion. I'm not asking about it.
There is a clean cut for all living things that intebreed and produce. For a given group of living things they either can intebreed and produce full interfertile offspring or not. There are many example.
Why is this clean cut not have a term in biology?
Again. This is not a "species" and from my point of view the term species should not be used in biology. Anything is a species... Homo sapiens, Neanderthals two different species although they had interbred and produced full interfertile offspring.....
Different dogs "races" are sometimes called different speices although they can intebreed and produce full interfertile offspring.
I already know about the fly experiment where the author claims that he got two different "species" of flies after some year of combination of sexual isolation and interbreeding. But no, all flies during the whole experiment of the same "collection" even if the author says they are different "species". The author did not make sure that they intebreed, he let them naturally decided whether they want to interbreed or not. They did not because they are not attacted to each other, but this does not mean they can not interbreed and produce full interfertile offspring.

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and then edit your original question rather than posting a new version. Also, note that "homework"(https://biology.stackexchange.com/help/homework) can apply to questions even if they are not assigned as homework. ——— We also 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!

This version of your question is clearer, but part of the reason that previous version was closed was because you don't demonstrate that you have done enough background research. ——— I recommend that 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. You should also do reading on "species concepts", which I think may ultimately be what you are trying to understand ...

I am going to upvote this back.  The species question is not trivial - the above link to species concepts illustrates this in quotations, but this is not truly a matter of species.  The questioner's example of U. arctos and U. maritimus is a good one.  Typically we apply the species concept to what does interbreed, not what can interbreed.  There is no a priori limit to how far interbreeding could take place, and some genera such as Aquilegia are known for looser limitations.  Well researched answers here should make interesting reading.

Part of the problem here is you are using an overly narrow definition of species, by many schools of thought neanderthals are not a separate species nor are brown bears and polar bears. It all depends on whether you are a splitter or lumper.

Based on the biological species concept, you're referring to two different species that experience ecological isolation (also called "habitat isolation") as a prezygotic reproductive isolating mechanism.
See here for a simple explanation of various concepts regarding species.
This, of course, is just one of the many reasons (see here for more) why we have multiple species concepts. Some might argue that these organisms are the same species based on their ability to produce interfertile offspring. If said researcher wanted to do so, they would define these organisms using a different concept.
Recognize that “species” is an artificial construct to allow conceptualization and organization of an incredibly complex, dynamic, and otherwise continuously variable genetic world.
We have not found a perfect way to "cut up" the world neatly/consistently into describable and functionally useful units, and --in fact -- we likely never will. Why? Because the lives of these organisms do not care about our cataloging and description systems -- these concepts are strictly for humankind to functionally relate to and react to their presence. The concept chosen almost inherently relies on the underlying motivation of the describer for naming the organism in the first place.

And remember the problem with defining species when you include fossil specimens, where you cannot test for inter-fertility. As I point out to my students if allow a single species to be distributed in time, (Aka a fossilized horse and a living horse are the same species), all of life can be one gigantic complex ring species.


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Is it possible to reduce maturity time of plants with biotechnology?
I've heard of speed breeding which makes use of optimal circumstances in glasshouses and growth chambers. Is it also possible to shorten a plant's maturity time (i.e. the time it needs from being planted until the time its yield can be harvested) using genetic modifications?

Pick up a packet of seeds at a garden shop. Most will have "days to maturity" . And there will be choices of time(growing season) .Such as a 70 day corn or a 100 day corn. Growing conditions such as moisture an nutrient level have a secondary affects.

Your use of "growing season" is confusing, since it almost always means the length of time plants will grow - basically from the last frost in the spring to the first frost in the fall (for those of us in temperate latitudes).  What you're asking is more often "days to maturity" or "time to harvest".

@AlexReynolds thanks for the reply and links. I also suggest you post this comment as an answer to get some reputation.

@jamesqf thanks for the clarification; I've edited the question accordingly. Is there any other word for what I mean other than "days to maturity" or "time to harvest" (or as I said maturity time)?

Perhaps investigate the families of YUC genes that synthesize the growth hormone auxin (ncbi.nlm.nih.gov/pmc/articles/PMC6941117) and ARF genes (ncbi.nlm.nih.gov/pmc/articles/PMC4737911) that respond to auxin. Auxin overproduction or changes to ARFs might speed growth. But some herbicides are synthetic auxins (e.g. 2,4-D) and work by exhausting and killing weeds (en.wikipedia.org/wiki/2,4-Dichlorophenoxyacetic_acid), so modifying these pathways may have unwanted side effects, depending on the crop.

Independent of the hormone manipulation suggested by Alex Reynolds, perturbation of transcription factor UPB1 has been found to have an effect on plant growth by Tsukagoshi and colleagues -- Transcriptional regulation of ROS controls transition from proliferation to differentiation in the root.
In short, disrupting UPB1 activity in model Arabidopsis roots alters the balance of free radicals, leading to delayed differentiation and continued cell growth. UPB1-deficient roots were faster growing and composed of larger cells. Artificially increasing UPB1 activity resulted in slower root growth.
Taking OP's definition of maturity time --

the time it needs from being planted until the time its yield can be harvested

-- the agricultural utility of this mutation depends on the crop.  If the goal is to increase the amount of biomass as fast as possible, this is likely a beneficial mutation.  If the goal is to decrease the time needed for a plant to bear mature fruit, this mutation would not be ideal, given that disruption of UPB1 activity leads to slowed cell differentiation.


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Can the activity of a specific gene in a cell artficially be increased?
While there are many gene regulation mechanisms from the cell itself, I was wondering whether it is possible to increase the gene activity in a living cell permanently (so that the protein that it codes for is produced in higher amounts) using methods of biotechnology (i.e. no external factors)? Are there any studies or experiments regarding this topic?

What do you mean by "Using the methods of Biology"? Genetic modification? Breeding? Evidently yes in that case.

@David oh I actually wanted to write biotechnology. So yes, this would include genetic modification. Do you know any studies or experiments using genetic modification to increase gene activity?

I don't particularly want to answer your question as I am not an expert in this field, and others can and will no doubt answer now you have clarified it. However there must be dozens of practical examples in modification of crops and lifestock, these based on earlier experiments with simpler organisms.

Do you want to increase telomerase production with CRISPR?

@Sergei I actually just asked general, but that might be an interesting application

There are technologies available for inducing higher (or lower) gene expression in cultured mammalian/human cells as well as in bacteria. The state of the art is CRISPR-mediated gene activation/repression, where you fuse a transcription activation domain to a Cas gene in a CRISPR-Cas system (usually Cas9), and provide a guide RNA to target genes of interest. This Cas gene is made "nuclease-dead" so that it can only target but not cut or degrade DNA (as opposed to natural CRISPR-Cas systems that do both), and serves to bring the transcription activation domain to your gene of interest, which leads to an increase in transcription of that gene.
Check out this paper for an earlier example of such a system in cultured cell lines. The field has advanced quite a bit since then, and people have successfully activated genes in mouse lines

A sequence is executed with transcriptase. To double amount of signaling or some protein production try doubling the sequence occurrence.

If you are after large amounts of a particular protein, search "recombinant protein production". It is a huge field.

It can be done. I've found this article which describes how cou can use a modified CRISPR-Cas9 mechanism to either repress or activate transcription.