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What is the non-local impact of a large-scale destruction of coral reefs?
I'm reading today that the "bleaching" of coral reefs is progressing with unanticipated speed. Bleaching is occurring at a scale which was previously believed to be decades in the future.
Bleached corals, according to the article in the New York Times1, have shed their symbiotic algae in order to protect themselves from toxins the algae produce when the water temperature rises above a certain threshold. If cooler temperatures are not restored quickly, the corals will die. This has happened with many affected reefs in the past and seems likely with the latest wave of bleaching too, given the apparent long-term increase in global water temperatures.
Even if the article does not say so directly it appears to me a distinct possibility that most coral reefs will simply disappear from the planet within just a few decades.
What impact will the disappearing of the coral reefs have on the oceans and the life in them, and ultimately on the whole planet? We know that reefs are the core of a complex and rich ecosystem. Which plants and animals outside the immediately affected areas depend on it? Are there migratory species who lose the reefs as a seasonal base? Which food chains will be interrupted, or over-provided? Do coral reefs have other functions like filtering, causing or reducing turbulence, influencing currents? Have there been studies or simulations which try to assess the global consequences?

[Edit]: I know the question is very broad. I'd be happy about answers to just one aspect. Specifically I'm interested in effects which are not obvious and/or have not been broadly publicized. Links to scientific publications would be awesome. Maybe somebody is working in the field, or knows somebody?
For example, affecting migratory species (fish or birds) may have unexpected consequences in otherwise unrelated parts of the world, similar to the effect of disappearing wetlands on migratory birds.
I also think it's possible that non-reef fish which are important food sources directly or indirectly depend on coral reefs. Are there specific examples?
I'm less interested in answers concerning species just living around the reef because cause and effect (though significant) are obvious.

1Which refers to the original study in this nature article.

Disclaimer: the question is too broad and speculative to some extent, and thus less likely to get complete answer (at least in a single post).
As is already known, thousands (or millions) of species are dependent on coral reefs for their survival and are likely to get extinct (unless they adapt) because of destruction of coral reefs. A short list includes fishes, turtles, sharks, eels, crabs, shrimps, urchins, sponges, algae, and so on1. Now, telling which of them will be immediately affected will be largely speculation, yet the first 5 species to lose the race, as per a speculation, are2:

Butterfly Fish: Species of fish that are obligate corallivores, such as many butterfly fishes (Chaetodontidae), feed exclusively on coral polyps. Obviously, survival would not look good for these fish if their food source disappeared.  Like parrotfish, butterflyfish assist in keeping algae from smothering corals.

Spiny Lobsters: Spiny lobsters rely on coral reefs for protection, especially during their vulnerable molting episodes. These lobsters have a significant role in maintaining a balanced ecosystem. Like sea otters, spiny lobsters are predators of sea urchins, which feed on kelp forests and can destroy them if populations are not predator-controlled. Kelp is important for many reasons, including those listed on OGP’s kelp recipes.

Whales (and dolphins): Many scientific studies have substantiated that dolphins and whales have extreme emotional intelligence. Sadly, their intellect won’t be enough to help these animals if coral reefs are destroyed. Dolphins and most whales (cetaceans) are predatory animals and they are all carnivorous. It’s a fish eat fish world and many fish survive by consuming fish that rely on coral reef habitats. Every species lost will affect another…and another…and many others. So, these come under the indirect adverse effects of coral depletion, since they themselves don't rely on corals.

Whale Sharks: Whale sharks are an important indicator of marine productivity and have a role in the conservation of other marine organisms. Although there has not been adequate research to understand why whale sharks are dependent on coral reefs, it has been shown that decreases in whale shark populations in the late 1980’s and early 1990’s may have been linked to increased rates of coral destruction.

Hawksbill Sea Turtles: Although all sea turtles would be affected by the loss of corals, Hawksbill sea turtles have become critically endangered species and are highly dependent on coral reefs for their food sources, mainly consisting of sponges. Sea turtles play significant roles in their ecosystems in that they help with nutrient cycling from ocean to land, maintaining healthy sea grass beds, and balancing food webs.

Coral reef fishes are in general rather sedentary and territoriality and home range behavior patterns are highly developed. However, many species migrate, often relatively long distances compared to body size and often with spectacular precision. Migrations in reef fishes may be associated with3:

Life history: movements of
planktonic larval stages to reefs or movements of juveniles from nursery areas to reefs
Seasons: precisely timed spawning aggregations drawing fishes to particular locations from wide areas of the reef
Diel patterns: movements to and from feeding or resting areas associated with dawn and dusk.

Another species, which is to be affected, though not immediately, by destruction of corals, is humans(!). As per experts4, coral depletion will bring threat to not only income and economic stability, but also to survival by causing depletion of food and increased risk of coastal disasters, which are likely to kill millions.
Coral reefs also serve many purposes, a few of which are5:

protect coastlines from the damaging effects of wave action and tropical storms
provide habitats and shelter for many marine organisms
are the source of nitrogen and other essential nutrients for marine food chains
assist in carbon and nitrogen fixing
help with nutrient recycling.

Finally, I suppose most of the species will be affected because of depletion of source of food rather than more-than-sufficient amount of something. Also, I was unable to find any simulations of the global consequences of destruction of coral reefs. I hope this much would help!
EDIT: I did some online research, and found lack of research about this topic. But I found a paper regarding relationship between seagrass, mangroves and coral reefs6 regarding life cycle of migratory fishes. From the same:

Coral reefs showed the highest mean fish species richness and were dominated by adult fish, while juvenile fish characterized seagrass beds and mangrove sites...Our results suggest that connectivity of seagrass, mangrove, and coral reef sites at a species and site levels, should be taken into consideration when implementing policy and conservation practices.

It becomes evident from this research that depletion of coral reefs would certainly affect life cycles of these fishes, which include Scarus iseri (Striped Parrotfish) and Lutjanus apodus (Schoolmaster Snapper), which will, in turn, affect biodiversity in seagrass beds and mangroves, leading to further break in food chain in more diverse areas.
Some researches have also suggested that seabirds might also be on a high rank in this list. Seabirds survive by eating fishes, and studies have shown that increasing water temperatures halt their growth while higher sea levels cause them problems in nesting. Now, it has also been suggested that due to coral bleaching, many fish species which live on corals might either die or move to other places, because of which seabirds could also face survival crisis7.
Another point regarding your demand I'm interested in effects which are not obvious and/or have not been broadly publicized, specifically not been broadly publicized, is that it has now become difficult to find such papers. This topic (climate change) has become so much publicized now that all related papers get attention immediately. So, it is quite difficult to find environmental research papers about climate change which hasn't gained much attention. Yet, I'll keeping on adding more research papers as I find some more.

Interesting information in your edit. That's part of what I was looking for. My vague suspicion was that there is such interaction with other parts of the sea, and with food-chains extending elsewhere.

@PeterA.Schneider thanks, I am continuously looking for more such papers, but haven't found any more yet, as I told in answer why. I'll add more when I find more :)


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Blastx: from gi to description
I have done a blastx and use the outfmt 6 option, because I want to work in the tables format. When I do this I get subject ids of the type

sp|Q7XJS0|ASHR1_ARATH, sp|Q39547|CUCM1_CUCME,

et cetera.
However, in this blastx output format I cannot find any option that will give me the descriptions of these blast hits.
Could anyone advice me how I can link these subject ids with descriptions of the sequences, e.g., 'amino acid transporter ANTL1-like'? I'd be much obliged.
j

Does the fasta/gb file from which this BLAST database was built have these descriptions in the header? If not take a look here: https://www.biostars.org/p/110000/

You have to map these ids to a file that contains gene description. Usually the GTF/GFF file for that reference genome would have these descriptions.

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What is the philosophical definition of life?
How does philosophy define life? And how does it overlap and contrast with the concepts and nuances of other sciences such as biology, chemistry, physics and mathematics?

There is no scientific definition that differs from the philosophical definition. You should ask your question on philosophy.SE. If you happen to speak french this book by Bersini is a very good overview of the diversity and difficulties of how to define life

I'm voting to close this question as off-topic because it will be better suited for philosophy.SE

But, this question equally fits in the science section. The philosophy section might argue that it belong to the pure Science section. So, I request not to close but give sometime for other to follow. I just want to hear some thoughts, and might close if it doesn't receive as much attention. Any thoughts?

Nope philosophers will not consider that this is a science question. However, they may consider the question as being too broad such as the post What are the phylosophical implications of the definitions of life?. You should probably start with wikipedia > life

I don't speak french. Hope there is an english version of that book. Also, any personal reviews on that book. I couldn't see any rating or review online. Thanks

@Remi.b: I have read about several topics on wikipedia, as a matter of fact I am an avid wiki reader. The link to the question you posted is closed and marked as broad. But, on my question I think I pointed out specifically - what overlaps and constraints philosophical concepts of life with material science? Isn't that specific?

If it is specific, then it is opinion based as it falsely assume that scientists have a clearly defined concept of life and same for philosophers.

You're asking for the philosophical definition of life. How philosophy defines life. This is very explicitly not a biology question. The philosophy section might argue it belongs in the science question but I don't know on what basis they would do so when the question is so clearly and explicitly restricted to their field.

Isn't every answer an opinion? And if the opinion is shared among large number of people that becomes an answer to that question in that circle. I am not falsely assuming if there is or isn't a clearly defined concept of about anything, not just life. Everything is clearly defined if it makes sense to comprehensive mind, weather that definition is true or not in the real world. Defining something clearly and stating a fact are two different things, isn't it. Wish we had followed on writing an answer, lol :)

Just to add to the conversation, I find the amalgamation of phiolosophy of life and maths in G.H Hardy's "A Mathematician's Apology". And, the answers are in continuum of the imagination not on the discrete elements of classifiable objects.

They ask different questions. Philosophy may ask what is life, is there a purpose behind it, etc. Biology asks how does it work, chemistry what are the chemical reactions that drive it, physics maybe how does physics allow for life and how life utilizes and impacts physics, and mathematics how can life and its components be described mathematically.
It is good to remember that all scientific disciplines branched off from philosophy (and religious philosophy) and that they are interconnected.
This is the answer to the part of your question that includes biology. If you want to discuss the meaning of life philosophically, you are welcome to come to do it on the philosophy page!

There is no difference along the lines of philosophy vs. science. However, there are broader and narrower definitions in biology.
The broadest I know of is "a self-replicating, chemical system (thing) with both exhibits heredity and some form of homeostasis (display internal negative entropy)", and some even argue the last part may be optional.
The narrowest also requires being made of cells, displaying growth, metabolism, adaptation, and response to stimuli. Some argue against these because they are either implicit in the other definition (homeostasis requires a metabolism, self-replication + heredity = adaptation),  that they are unnecessary (cells or growth) or difficult to define themselves (response to stimuli).

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Can a lion be fed cat food?
Is there a correlation between eating raw meat and aggressiveness in felines and canines?
Growing up, I was always told to cook the meat I gave to my dogs and cats so as not to give them the "taste for blood". Is there truth in this myth?
And if that's the case, wouldn't the same food have the same effect on "bigger cats" ? Wouldn't it safer to feed Zoo animals cooked meat ?

I read once (I don't remember where), that captive big cats' food has to be prepared in a way similar to how they would eat in the wild. e.g. cheetahs will only eat extremely fresh meat (in the wild, they have to eat quickly because their kills are often stolen), but leopards prefer meat that's almost rotten (in the wild, they store their kills in trees for days before eating it). In other words, I suspect the reason zoos don't cook meat for big cats is because they want to mimic the animals' natural diet.

I'm voting to close this question as off-topic because it looks pob and better suited for skeptics. Issue with this kind of question is that the answer-er needs to prove or debunk the theory first and then start explaining why; basically a double answer imo. Better split it up I guess; prove or debunk @ skeptics and come back here with a more educated question.


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Correctly depicting spider anatomy
First off, my specific query: When depicting a spider - be it in a picture or in textual/verbal description - should the chelicerae be always be placed so that they project outwards from the ventral side of the cephalothorax's anteriormost part, like in this diagram? Or are there other possibilities (e.g. attached by their basal undersides to the front of the cephalothorax) that are still anatomically correct?
Second, a more general inquiry: Are there any common pitfalls in depiction of spider anatomy that I should be aware of?


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Aging and death of perennials
Perennial plants species generate a new plant annually from the same parent root stock. At the end of the year that new shoot withers and dies, to re-appear the next year. Hence, the above-ground parts of perennials obviously age and die, but what about the rootstocks?
Are the rootstocks from perennial plant species immortal, or do these rootstocks age and die as well?

http://biology.stackexchange.com/questions/13777/cell-life-division-for-immortality-or-reproduction-with-aging/13809#13809 answers the uniucellular question accurately and see Remi's suggestions. I edited the question to leave the rootstock part. That seems to be a valid new question.

Note that you describe herbaceous perennials, as not all perennials die back each year (e.g., evergreen perennials and woody plants like trees and shrubs retain their shoots).

I have a number of rose varieties that have been propagated from cuttings & divisions of plants bred in the 1800s.  And there's an aspen clone said to be about 80,000 years old: https://en.wikipedia.org/wiki/Pando_(tree)

The issue is based on your perception of what an individual ought to be. The concept of individual is actually often hard to apply in biology and therefore is the concept of ageing. In other words, the wish to categorize is a rather human tendency but it may fail to make objective representation of biodiversity. The book The Major Transitions in Evolution Revisited makes a very good job to explain the difficulties to deal with the concept of individual in biology.
You seem to be happy to consider an offspring be a different individual if you can still perceive the parent individual. In bacteria, both resulting cells could be considered as offspring and therefore new individuals. Note however, that asymmetrical division bring some more blur into these categorizations.
Note also that single cell bacteria do age. See the wikipedia article on bacterial ageing. You might also want to have a look at the wikipedia article on biological immortality as well as the posts Why is the Hydra Biologically Immortal? and Do crocodiles age?.

I edited the question - see my comments. Please feel free to revert those changes, but I think the unicellular part is duplicate. Perhaps you can add a sentence on perennials? Up to you.


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How does the body determine where to deposit fat reserves?
People's bodies store fat in similar areas, but often there are subtle differences in which areas are first or slightly more effected. This seems to also be apparent with morbidity, where certain areas are overburdened with adipose while other areas are less effected. What are the factors the determine which areas exhibit build up, while others do not?


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How is the Force of Contraction Applied to the Tendons by the Muscle's Individual Fibers?

Image and question have been updated for clarity!
The image above is a side view of a semi-transparent skeletal muscle. The dark red lines represent individual fibers, the blue lines represent tendons. The pink area also consists of muscle fibers, but it is made transparent for the purpose of the demonstration. Please assume the fibers are properly encased in fascicles and fascia. Tendons connect the muscle to the bones. The bones can move towards the center of the image if pulled. The arrows show the flow of force during contraction along each fiber.
The muscle has grown large enough that the outer fibers protrude around the tendon (where they connect). During contraction, do the protruding outer fibers help pull the tendon towards the center of the muscle like the internal fibers in the middle of the muscle do? If so, how is the force controlled and directed to accomplish this?
It seems there exists athletes with this type of anatomy (such as very large bodybuilders) but the bio-mechanics of this type of anatomy completely confuse me. It would seem the flow of force of the outer fibers would pull the tendon away, unless the force is somehow redirected. Thank you so much for your insight on this!!!

Could you try to clarify this? Is your drawing of a muscle fiber showing a cross section or a side view? My guess based on your quesiton is that it's a side view (meaning contraction is in the same plane as the tendon) -- is that right? If that's the case, knowing that muscles only contract (meaning they are unidirectional in their "tugging" ability), I would suspect your tendon would move in the same direction as the muscle fiber. However, without knowing where your muscle is attaching (i.e., which side is the origin vs insertion) it's difficult to say which direction this muscle is moving.

I recommend thinking about this a little more and then trying to clarify both your picture and what you're asking. Perhaps also provide a reference for your athlete example to help clarify. Thanks.

Sorry about the confusion, I went back and edited the question and image to try and clarify things! I hope the question makes more sense now!


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Are vacuum centrifuges the same as normal centrifuges?
I came across a method that used a vacuum centrifuge:
Carvalho et al. 2012. The diversity, antimicrobial and anticancer activity of endophytic fungi associated with the medicinal plant Stryphnodendron adstringens (Mart.) Coville (Fabaceae) from the Brazilian savannah. Symbiosis 57(2):95-107

Five-millimetre-diameter plugs of each filamentous endophytic fungus were inoculated into the centres of Petri dishes (60 mm diameter, 20 ml PDA). The plates were incubated at 25±2 °C for 15 days. The culture materials from each Petri dish were cut and transferred to 50-ml vial tubes containing 35 ml of ethanol (PA, ≥99.8 %, Vetec, Brazil). After 48 h at 10°C, the organic phase was decanted and the solvent was removed under a vacuum centrifuge at 35°C

I couldn't find information online as to whether a vacuum centrifuge is the same as a normal centrifuge. Is there a difference?

It would be helpful if you shared a link or citation to the study

Also, we would need to know what model centrifuge you have in your lab to definitively say whether it is the same as what is being described.

I presume they're trying to use a non-brand name for what everyone I know calls a SpeedVac.

A "normal" centrifuge = piece of laboratory equipment, driven by a motor, which spins liquid samples at high speed to allow centripetal acceleration to separate substances of greater and lesser density.
Without further information regarding the method you read, a "vacuum" centrifuge might be a reference to one of the following:

Ultracentrifuge

a centrifuge optimized for spinning a rotor at very high speeds.

The vacuum ultracentrifuge was invented by Edward Greydon Pickels in the Physics Department at the University of Virginia. It was his contribution of the vacuum which allowed a reduction in friction generated at high speeds. Vacuum systems also enabled the maintenance of constant temperature across the sample, eliminating convection currents that interfered with the interpretation of sedimentation results

Centrifugal evaporator

device used in chemical and biochemical laboratories for the efficient and gentle evaporation of solvents from many samples at the same time.

The system works by lowering the pressure in the centrifuge system [via a vacuum pump] - as the pressure drops so does the boiling point of the solvent(s) in the system.
The centrifugal force generated by spinning the centrifuge rotor creates a pressure gradient within the solvent contained in the tubes or vials, this means that the samples boil from the top down, helping to prevent "bumping".

"Vacuum Concentrators"

Use a combination of centrifugal force, vacuum and heat to speed evaporation of multiple small samples. They offer maximum throughput required by biology, microbiology, biochemistry, pharmaceutical research and analytical chemistry laboratories

UPDATE: Based on updated info from the OP quoting the method of the paper, it sounds like they're most likely talking about using a centrifugal evaporator to remove solvent.

"Five-millimetre-diameter plugs of each filamentous endophytic fungus were inoculated into the centres of Petri dishes (60 mm diameter, 20 ml PDA). The plates were incubated at 25±2 °C for 15 days. The culture materials from each Petri dish were cut and transferred to 50-ml vial tubes containing 35 ml of ethanol (PA, ≥99.8 %, Vetec, Brazil). After 48 h at 10 °C, the organic phase was decanted and the solvent was removed under a vacuum centrifuge at 35 °C (Santiago et al. 2012)."

from "The diversity, antimicrobial and anticancer activity of endophytic fungi associated with the medicinal plant Stryphnodendron adstringens (Mart.) Coville (Fabaceae) from the Brazilian Savannah." 2012 paper by Carvalho et al.

@Emil Thanks. So follow these steps: 1. Add the pertinent parts of this info to your question (not just in the comments). 2. Go to the references section of  Carvalho paper; Locate Santiago et al. 2012 citation, search for it on Google Scholar, and see if they have more info. Update w/ that too.

@tomd thanks for the info! I really knew little about the history of centrifuges before writing this answer (and now seeing your references). I also found a good "story" that walks through the history of the centrifuge. I'll paraphrase some major quotes from it in a subsequent comment.

"In 1926 Svedberg received a Nobel Prize for the invention of the ultracentrifuge. Svedbergs ultracentrifuge, however, was essentially an analytical instrument. The transition from these analytical instruments to modern preparative ultracentrifuges came through the efforts of Emile Henriot, who achieved high rotation speeds using a bearingless top, driven & supported by compressed air. Edward Pickels & Johannes Bauer build the first high-speed vacuum centrifuge suitable for the study of filterable viruses. Later, Pickels developed the more convenient, electrically driven ultracentrifuge.


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Is a gene located in the sense or the anti-sense strand?
The given image shows a section of a dsDNA.

Suppose it's the blue strand to which RNA polymerase attaches during transcription. The resulting mRNA molecule then codes for a protein $X$.
So, which of the following is considered the gene?
a) The blue strand (anti-sense strand) to which RNA polymerase attaches during transcription and is the one that is technically read by the transcription machinery.
b) The red strand (sense strand) whose base sequence is the same as the base sequence of our mRNA molecule (except that thymine is replaced by uracil).
c) The DNA duplex as a whole, as shown in the above schematic.

As you have recently edited this old question, I assume you are keen to have it discussed. Although I have already answered, I intend to revise my answer extensively Could you therefore clarify two points. 1. Are you asking (a) Whether the term gene, as it is generally used in science (and defined in textbooks, for example), is restricted to one strand, OR (b) Should the term gene which does not normally have this stipulation, be changed or clarified to restrict it to one strand. 2. Are you sure which strand?  The strand actually copied into mRNA is the red anti-sense strand.

(a) is what I intended to ask

I've edited the question to make it more intelligible.

My revised answer specifically addresses point (a) — usage — which the answer you have accepted does not. It provides referenced examples of usage in the full gamut of scientific sophistication. It also demonstrates that the problems of defining a gene are far more numerous than gene overlap.

Short Answer
In referring to genes on a double-stranded DNA chromosome (the situation assumed in this question), the general and scientific usage of the term ‘gene’ includes both DNA strands.
The practical definition of ‘gene’ has come under scrutiny in recent years for reasons that will be discussed, especially in relation to the ENCODE project. However none of the discussions I have encountered considers restricting a gene to a single strand.
General and educational usage of the term ‘gene’
The term gene was coined in 1909 “to describe the Mendelian unit of heredity”, long before it was suggested and established that these units resided in the chromosomal DNA of organisms.
A reputable general dictionary, Mirriam–Webster, suggests a modern concept of the term, comprehensible to non-specialized readers, to be:

a specific sequence of nucleotides in DNA or RNA that is located
usually on a chromosome and that is the functional unit of inheritance
controlling the transmission and expression of one or more traits by
specifying the structure of a particular polypeptide and especially a
protein or controlling the function of other genetic material
e.g. “She inherited a good set of genes from her parents.”

And a similar definition is given to the medical profession in Morton and Spences Genetics for Surgeons.
Despite the knowledge of the complexity of genes that has accumulated in recent years, in two modern molecular biology text books the essential feature of the definition is that it is all-embracing rather than restrictive. Thus, the definition in Alberts et al. — Molecular Biology of the Cell is:

Region of DNA that controls a discrete hereditary characteristic,
usually corresponding to a single protein or RNA. This definition
includes the entire functional unit, encompassing coding DNA
sequences, noncoding regulatory DNA sequences, and introns.

And the definition in the glossary of Lodish et al. — Molecular Cell Biology is very similar.
More recent considerations of the term ‘gene’ in the context of the ENCODE project
There are several features of the structure and the regulation of the chromosomal information specifying proteins that has led to a reconsideration of the use of the term ‘gene’. This in not merely a semantic concern, as the major ENCODE Project, the purpose of which was to provide an “Encyclopaedia of DNA Elements”, had the practical task of naming the elements it describes.
I have found a couple of useful articles by others, considering the problem at length. One is by Smith and Adkinson (2010) and the other is by Portin and Wilkins (2017). A brief summary of the situation that they discuss is that there are two main problems. One problem is the deviation from the ‘one gene — one mRNA — one polypeptide chain’ concept caused by alternative splicing, multiple promoters and  alternative translational initiations sites. A second is the finding of regulation of transcription by sequences greatly distant from the transcriptional initiation site.
The general thinking is to redefine the term ‘gene’ in terms of networks or integrated interactions. Thus, Portin and Wilkins own proposal is:

A gene is a DNA sequence (whose component segments do not necessarily need to be physically contiguous) that specifies one or more sequence-related RNAs/proteins that are both evoked by Gene Regulatory Networks and participate as elements in Gene Regulatory Networks, often with indirect effects, or as outputs of Gene Regulatory Networks, the latter yielding more direct phenotypic effects.

and that employed by the ENCODE project is defined by Gerstein et al. as:

The gene is a union of genomic sequences encoding a coherent set of potentially overlapping functional products

a gene is a genomic sequence (DNA or RNA) directly encoding functional product molecules, either RNA or protein.
In the case that there are several functional products sharing overlapping regions, one takes the union of all overlapping genomic
sequences coding for them.
This union must be coherent — i.e., done separately for final protein and RNA products — but does not require that all products necessarily
share a common sub-sequence

(It is supplemented by an ontological diagram that I shall not reproduce here.)
This is complex, but in relation to the poster’s concern one thing is clear, at no time are the authors concerned with strandedness, and there is no proposal that a gene is confined to a single strand.
Two simple arguments
One might argue that nobody mentions strandedness because everyone assumes a gene is on only one strand. Really? Anyway, I‘ll finish with a couple of mundane arguments that strandedness has no place in defining genes, overlapping or not.

The Transcription Factor/RNA polymerase binding site — the TATA box — is regarded as an integral part of a gene. Both strands of the TATA box are required for binding. Likewise other transcription factor binding sites. Hence the gene cannot be on only one strand.
Single-stranded DNA viruses are found with what are called ‘positive sense’ and ‘negative sense‘ genomes. So clearly among these genomes there are heredity units which read ‘anti-sense’ as well as some that are ‘anti-sense’. On the ‘one-stranded gene’ thesis one of these could not be called genes. One would have to devise some term from them as progenitors of the gene in the complementary strand in the replicative DNA form!

None of the highlighted regions in your figure, is a gene. A gene is a section of DNA which gives rise to a product. Basically, a gene has an orientation (5'→ 3') i.e. it is essentially a single stranded region. However, the strand that mechanistically contributes to RNA synthesis (template) has the reverse-complementary sequence of the gene (in other words, anti-sense). Therefore, a gene, as it is annotated is not a functional entity but a genomic representation of a product. Some viruses (such as M13 phage) have a single stranded genome; for them the transcript is always antisense to the genomic DNA region.
Same section of dsDNA can harbour multiple genes in both orientations and this is clearly seen in viruses which have an highly compact genomes. Other prokaryotic and eukaryotic genomes also have overlapping genes.
Some related posts:

On which DNA strand is TATA box present?
Do transcription factors bind to both strands of DNA?
Which DNA elements belong to the definition of a gene?

Does that mean only the indicated region of molecule A is a gene? Or,
does the Indicated portion of molecule A + Complementary portion
present in molecule B comprise a single gene, such that A is sense and
B is non-sense strand of the same gene?

If the molecules A and B are expressed from opposite strands, then they are considered products of different genes, even if the gene region overlaps.
The situation is more unclear if both the molecules are expressed from the same strand and the transcribed region overlaps. Sometimes they are classified under the same gene (splice variants) and sometimes they are not.
These are some lines from the human genome annotation file which tells the location of genes in the genome (+ and - denote opposite strands):

chr1    HAVANA  gene    1567474 1570639 .   +   .   gene_id "ENSG00000189409.8"; transcript_id "ENSG00000189409.8"; gene_type "protein_coding"; gene_status "KNOWN"; gene_name "MMP23B"; transcript_type "protein_coding"; transcript_status "KNOWN"; transcript_name "MMP23B"; level 2; havana_gene "OTTHUMG00000074713.4";
chr1    HAVANA  gene    1590786 1594063 .   +   .   gene_id "ENSG00000272004.1"; transcript_id "ENSG00000272004.1"; gene_type "antisense"; gene_status "NOVEL"; gene_name "RP11-345P4.10"; transcript_type "antisense"; transcript_status "NOVEL"; transcript_name "RP11-345P4.10"; level 2; havana_gene "OTTHUMG00000185638.1";
chr1    HAVANA  gene    1603429 1604850 .   +   .   gene_id "ENSG00000269737.1"; transcript_id "ENSG00000269737.1"; gene_type "antisense"; gene_status "NOVEL"; gene_name "RP11-345P4.7"; transcript_type "antisense"; transcript_status "NOVEL"; transcript_name "RP11-345P4.7"; level 2; havana_gene "OTTHUMG00000182604.1";
chr1    HAVANA  gene    1604714 1605836 .   +   .   gene_id "ENSG00000269227.1"; transcript_id "ENSG00000269227.1"; gene_type "pseudogene"; gene_status "KNOWN"; gene_name "RP11-345P4.6"; transcript_type "pseudogene"; transcript_status "KNOWN"; transcript_name "RP11-345P4.6"; level 1; tag "pseudo_consens"; havana_gene "OTTHUMG00000182605.1";
chr1    HAVANA  gene    1570603 1590473 .   -   .   gene_id "ENSG00000248333.3"; transcript_id "ENSG00000248333.3"; gene_type "protein_coding"; gene_status "KNOWN"; gene_name "CDK11B"; transcript_type "protein_coding"; transcript_status "KNOWN"; transcript_name "CDK11B"; level 2; havana_gene "OTTHUMG00000078638.4";
chr1    HAVANA  gene    1592939 1624167 .   -   .   gene_id "ENSG00000189339.7"; transcript_id "ENSG00000189339.7"; gene_type "protein_coding"; gene_status "KNOWN"; gene_name "SLC35E2B"; transcript_type "protein_coding"; transcript_status "KNOWN"; transcript_name "SLC35E2B"; level 2; havana_gene "OTTHUMG00000078639.1";
chr1    HAVANA  gene    1634169 1655766 .   -   .   gene_id "ENSG00000008128.18"; transcript_id "ENSG00000008128.18"; gene_type "protein_coding"; gene_status "KNOWN"; gene_name "CDK11A"; transcript_type "protein_coding"; transcript_status "KNOWN"; transcript_name "CDK11A"; level 2; havana_gene "OTTHUMG00000000703.14";
chr1    HAVANA  gene    1634175 1669127 .   -   .   gene_id "ENSG00000268575.1"; transcript_id "ENSG00000268575.1"; gene_type "processed_transcript"; gene_status "NOVEL"; gene_name "RP1-283E3.8"; transcript_type "processed_transcript"; transcript_status "NOVEL"; transcript_name "RP1-283E3.8"; level 2; havana_gene "OTTHUMG00000183552.1";

Not evident in these examples but there are many overlapping genes in opposite strands. Anti-sense lncRNAs would be an example to have a quick look at. See Can both the overlapping genes (in opposite strands) produce proteins? for an example of antisense-overlapping protein coding genes.

Bottomline: The definition of gene is constantly changing but usually a gene has an strand orientation. Specifically, if two different RNAs are synthesized from opposite directions but from the same dsDNA region, then they are said to arise from two different genes. (check out this review for some specific examples)

I have revised my own answer and do not address gene overlap. However I am still unclear as to your conclusion. You state "The opposite strand can also sometimes synthesize a product but it is considered a different gene in that case." What is "it" in this sentence? Are you saying that the single opposite strand is the gene, or just that there are two genes sharing double-stranded DNA.

@David I mean that two genes can share the same dsDNA region. I'll clarify this

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


text:
non-coding RNA modelling in silico
I've been trying to model a non-coding RNA molecule which binds to a RNA binding protein. I found the DNA sequence for ncRNA from NCBI. I did not find the RNA seq of the same. Hence my doubt is, whether we should take the DNA seq and convert all the thymidine to uridine and then take that sequence for RNA modelling. Also, I wanted know if there is any kind of splicing occurring in case of ncRNA formation. Thank you in Advance.


text:
What are the chances that the contraceptive pill will cause death of human zygote?
The preventative pill, as I understand it, can cause zygotes to fail to attach to the uterine wall, or pry them off of it.
Ignoring any and all ethical implications, what are the chances that this will occur, provided the woman in question has taken the pill regularly preceding sexual intercourse, comparing with and without barrier method as well, the latter taking into account if it fails.

You should know that there is controversy on when to even define the beginning of pregnancy, therefore there is a really big assumption (and a lot of politics, whether or not you realize or intend that) in your statement "assuming that this qualifies as abortion." I would suggest rewriting your question to "what is the probability that preventative contraceptive pills will interfere with attachment of a zygote to the uterine wall?"

@BryanKrause Done.

Second comment, which I missed at first glance, is in your second paragraph: Why are you referring to a barrier method? I mean, if fertilization doesn't occur (due to a hormone pill or any other method) it doesn't make biological sense to even evaluate the question.

Which pill? What dosage? All barrier methods? Does that include 'soft' barriers like foam and gel? If you don't know what I'm getting at, it's: this is way too broad, unclear, and shows no research whatsoever.


text:
Why does the inside of ear smell nice?
You can judge my habits later, but sometimes I stick my finger in my ear and smell my finger. When doing this, I get a pleasant smell for some reason. I haven't use hair lotion for a long time cause I have like no hair. I suspect it has to do with my headphones since I wear them often, but i have them for more than a year.

Welcome to Biology SE. You could visit the tour-page for basic informations, the help-page for more detailed informations about what could be asked or could not be. For formatting tasks in command prompt, visit this help sub-page. Thanks.

Did anyone else stick their finger in their ear and smell it?


text:
Lab marker for labelling cell culture plastics?
I am a lab manager trying to ask other lab biologists what brand/make of markers their labs use for labeling tissue culture plastics, which need to be repeatedly wiped down with 70% ethanol to maintain sterility. (Most "permanent" markers wash off in 70% ethanol.)
I have been looking for an equivalent to the Sharpie Industrial Extra-Fine point marker, which seems not to be on the market anymore. The supposedly solvent-resistant Fisher extra-fine point marker leaves almost no trace when wiped with ethanol.
Does anyone have suggestions?

I'm voting to close this question as off-topic because recommendations for marking pens can by no stretch of the imagination be considered a question about biology.

I think the question is reasonable because it is asking for recommendations on lab materials which only a biologist would be able to make.

Yes, @David, to clarify: biologists use 70% ethanol to wipe down their cell culture materials in order to maintain a sterile environment, but most "permanent" markers wipe off under those conditions. I am a lab manager trying to ask other biologists what pens their labs use for this biology-specific application.

I agree. This question, though seemingly wayy off topic, is completely valid here. It has the appropriate [tag:lab-techniques] tag. @Ema, to avoid more challenge to your question, perhaps you could edit to add a bit more biology context. I think adding your " I am a lab manager trying to ask other biologists..." sentence from your comment to the start of your question would be good :).

This is hardcore going to come across as a SPAM answer, but I simply did a Google search:
Laboratory Marking Pens from Ted Pella

Statmark Pen™: resistant to formalin, ethanol isopropanol and xylene
Secureline® Marker: water resistant; autoclavable; not suitable below 0°C (32°F)
Secureline® II / Superfrost: resistant to xylene, ethanol, acetone and formalin; service temperature -15°C to 100°C (5°F to 212°F)
You can try a Sample Pack of all 3 for $8 USD to see which you like the best.

@Ema Try them out and let us know how they work! (Alternatively... Has anyone used these that could report on their efficacy?)

I have tried both of those Securelines, but the Extra Fine one doesn't hold up. As stated above, I'm particularly interested in other users' advice on products they have tried and rely on.

@Ema Bummer. Well, don't miss the link in my answer to the sharpies I still found on sale for you! :)

Those are not the correct Sharpie product, but feel free to repost if you find a source for Sharpie Industrial Extra Fine.

@Ema weird. They changed links on me. Now the correct page lists them for sale for $700! 0.o  ... I'll keep my eyes and ears open for ya!

Yeah, I've seen that too... :(

I routinely use 70% ethanol and/or IPA to wipe off plastics written on with Fisherbrand fine-tip marking pens and I find they don't come off easily even after multiple sprays. As long as the marker has had ample time to dry. The sharpie industrial "solvent resistant" markers come off immediately.
So here I have a Corning 250mL bottle, and 3 brands of marker:
Fisherbrand fine-tip marking pen (above)
Sharpie Industrial (above)
Sakura microperm ultrafine-tip
The Sakura markers explicitly state they wash off w/ alcohol but I like the tips for flow tubes and eppendorf tubes. I sprayed the marker with 70% ethanol, let it sit for just a few seconds then used a Kim wipe to clean it off. Fisherbrand, for me, just works the best (excuse my handwriting!).

I've resized the images and put them on less lines so we don't need to scroll for what seems like miles. Feel free to roll back.

Thanks for the input. Unfortunately, I'm in the market for extrafine. The Fisher fine tips work well, but the extra fines come off.

@Ema I see. You might find some luck testing VWR's histology markers, which come as ultrafine and out of necessity have to resist histology solvents. I have not tested these myself. The downside is they apparently don't write well on smooth surfaces, only frosted parts.


text:
How do environmental conditions differ between nitrogen fixing bacteria and denitrification bacteria?
I am currently experimenting with aquaponics and need to better understand nitrifying and denitrifying bacteria.
From my research it seems that both varieties are anaerobic. From an engineering perspective, how would I control the environment such that nitrifying bacteria would dominate a water medium or vice versa? I'm thinking some combination of the following should provide some level of control; pH, temperature, surface area, tds, nitrogen partial pressure, concentrations of fixed nitrogen and types, etc.


text:
Length of upstream and downstream of tss important for gene regulation o
I want to find SNPs in the upstream and downstream regions of transcription start sites of some 42 genes implicated in a disease (on which I am working).
Are there any suggestions on what length should be covered both upstream and downstream? Is there a database which can give the transcription factor binding region of both upstream and downstream regions as a batch query? Or a paper to which I can refer for the search length for looking for SNPs?


text:
What is the name of this series?
My biology teacher used to show us videos (actually animations) on the human immune system. What I remember is that one video was on a virus (represented as a purple colored sphere with spikes) that a woman (who is a part of a music band) inhales in an elevator when a man sneezes.
The documentary shows how the virus travels to her throat and enters one cell, multiplies, and spreads. Then the video shows how white blood cells and T-cells defend the body. In the end, when she drinks coffee, she leaves the virus on a coffee mug and her friend takes on that virus when he drinks from the same mug.
Other videos of the same series include a documentary on fractures, another one on obesity, another one on a disease transmitted when one eats chicken, etc. Can someone tell me what is the name of that series?
I think (not sure) it is a national geographic series?

This question is off-topic as it is not about biology but about a video documentary. This question would be put on hold. In future, if you have such questions please use the chat.

belongs on tv&movies stack exchange

Link to meta; as it serves an educational purpose in Biology I consider it to be on-topic.

The Body Story.
--Have to add some characters for the system to be happy--


text:
MCQ - Events in the Mitotic cycle
The following question confused me at first

However, I presumed that it must be in comparison to meiosis. In that case D would be correct.
However, the correct answer is A.
How can this be? I know that in mitosis it is the chromatids that are 'pulled away' to opposite poles. In meiosis, this is whole chromatids but anaphase still occurs.
I suspect I don't understand the question. Where have I gone wrong in my reasoning?

Cell cycle can be divided into two phases:
1. Interphase
2. M-phase(Mitotic phase)
Note: M-phase can also mean Meiotic phase but it is not the full form of the acronym.
So M-phase in mitosis has four phases:

Prophase
Metaphase
Anaphase(your answer)
Telophase

A mitotic cycle:

The rest of the options:
B. Cytokinesis

Cytoplasmic division begins during or after the late stages of nuclear division in mitosis and meiosis.

Your question doesn't seem to consider cytokinesis as a part of M-phase (i.e to be occurring during the late karyokinesis). So it has to be ruled out.(Making some assumptions as this is a key to reaching the single correct answer in MCQs, if not this would have had two right answers.)
C. DNA replication - happens in S-phase of interphase
D. Interphase (certainly not the one)
Source: ncert


text:
Is the promoter region of a gene transcribed?
If the RNA polymerase attaches to the promoter region of the gene, would it form the initial mRNA segment by reading the promoter region or would it slide across the DNA then read the adjoining region? Or does the enzyme span so long that its certain region attaches to the promoter while its adjacent region starts reading the DNA to form mRNA?
Does the RNA polymerase read DNA base pairs and add the complementary RNA base pairs one by one? Or, does it read groups of base pairs just like tRNA which reads triplet of bases?
Is the terminator region transcribed as well before the process of transcription ends, or does transcription end immediately after the RNA polymerase reaches the terminator region? If the latter is the case, how does transcription end just by the polymerase reading the terminator region?
So, should the promoter and terminator regions of a gene be considered parts  of the gene or separate entities?

In genomic annotations, genes are considered to begin at the first base found in a sequenced transcript, and end in the last base of a sequenced transcript.

Too many questions, too little effort.

would it form the initial mRNA portion soon after attachment by reading the promoter region?

The RNA Polymerase binds to the promoter, however since it is so large the front end of it hangs off the end of the promoter.  When Transcription begins the promoter is not included, as the transcription process occurs at the front of the polymerase.

Also, does the RNA polymerase read DNA base pairs one by one and add the RNA base pairs to the chain one by one?

The RNA polymerase adds nucleoside triphosphate (NTP) one by one.  As the picture shows below, there is only room for one NTP in the active site and once the correct NTP is placed it is added to the RNA chain.

How does the process end just by reading the terminator region?

The question of termination is dependent on the cell.  Prokaryotes terminate in either a Rho independent or dependent process.  Independently, a hairpin occurs in the RNA that breaks off the transcript, dependently, a Rho factor binds that causes termination.  Eukaryotes are less well known, but it is generally believed that after the poly-A site there are also factors that bind and induce termination.

So, should the promoter and terminator region of a gene be considered parts of the gene or separate entities?

This question is slightly more about definitions that biology.  The Oxford Engligh dictionary defines a gene as "The basic unit of heredity in living organisms".  Since the promoter, non-coding, and non-translating regions are still paramount in getting the protein made, I would argue that they are still part of the gene and the larger hereditary unit.


text:
Why do plants not have fat cells, and store their reserves in vacuoles instead?
Why don't plants have fat cells, but instead store reserves in vacuoles. And vice versa, why do humans feature fat cells instead of depositing storage molecules in vacuoles?

Short answer
Parallel evolution can generate similar traits in unrelated organisms based on unrelated structures.
Background
First off, the question is based on a few misconceptions:

First, you are making an apple-and-pear comparison; Fat cells are cells - vacuoles are organelles. Fat cells store fats in liquid droplets, called adiposomes, which are lipid-rich cellular organelles that regulate the storage and hydrolysis of neutral lipids and are found largely in the adipose tissue. Vacuoles have a variety of functions, namely 1) contribute to the rigidity of the plant through hydrostatic pressure; 2) store nutrient and non-nutrient chemicals and 3) break down complex molecules. The latter two functions are quite reminiscent of the function of lipid droplets in animalia.
Plants do not store energy reserves in fats like animalia do. Instead, plants store starch, which is not a hydrophobic lipid, but a hydrophilic glucoside polymer.

Apart from these specifics, the question can be tackled more generally - unrelated organisms can solve the same 'problems' (like storage of energy rich compounds) through parallel evolution (wings in bats and birds for example). Why does a bat wing contain fingers and a bird's wing doesn't? Because they developed the ability of flight through different, parallel adaptations.


text:
What do animal cells store pigment in?
So I know plants store pigment in chloroplasts, chromoplasts, etc., but what do animal cells store pigment in? For example, is there like a chromoplast for melanin in the human body?
I tried Googling my question and didn't find anything, but maybe I was looking at the wrong sources.

I read through the article you linked and it didn't seem to have an organelle or something that contained melanin. I've never heard of melanine, but maybe it's a variation of melanin.

You want to read the Wikipedia page on Melanosomes.

Cool, I did. That was really helpful, thanks!

Melanine is produced and stored in melanocytes. They contain melanosomes that are organelles that store melanine.


text:
Artificial Hormones of human body
Can hormones of human body created artificially even i mean the hormones just consisting of bio chemicals and nothing else?

Human insulin was the first hormone to be artificially made by recombinant DNA technology and marketed  by Elli Lily.

Do u know why only insulin is possible until now not other hormones?

Other hormones have also been made using rDNA technology. Some of which I'm aware of are HCG and GnRH used for Induced breeding of fish. Now humulin synthesised is not exactly the same as natural human insulin it varies in certain amino acid sequences.

Its just out of curiosity that can new hormones be created for the body in order to perform new functions ?


text:
Are Raf, MEK, and ERK MAP kinases?
I am trying to make sense of this diagram.  Can Ras activate RAF or MAPKKK, or is RAF a MAPKKK, making MEK a MAPKK, and ERK a MAPK?

Mitogen-activated protein kinase (MAPK) is a generic name for a family of different but related enzymes involved in this specific signalling cascade. RAF is a MAPKKK, MEK is a MAPKK and ERK is a MAPK. This is evident in the Nature article from which your image is apparently adapted:

Activated RAS triggers the activation of the MAPKKK RAF. Activated RAF then phosphorylates the MAPKK MEK (MAPK and ERK kinase) on serine residues leading to its activation. Subsequently, activated MEK catalyses the dual phosphorylation of the MAPK ERK.


text:
What is the specific role of the cerebellum when it comes to 'coordinating movement'?
In elementary biology (high school level in the UK - A levels), we are told that the cerebellum is the part of the brain that 'coordinates movement'. Literally nobody takes the time to explain what the word 'coordinates' encompasses. Hence, I do not know the specific role of the cerebellum in coordinating movement.
For example, one very daunting thing that we are told is that the frontal lobe contains the 'primary motor cortex', which supposedly contains motor neurons that connect to the spinal cord and brain stem and can send nerve impulses that enable movement in the body. Where is the distinction between such a role and the role of the cerebellum in 'coordinating movement'?

The principal function of the cerebellum, which was detected years ago, is to calibrate detailed movements rather than initiating movements or deciding which movements to execute (Ghez et al, 1985). This was concluded by observing the changes which occurred after damaging cerebellum. Animals and humans with cerebellar dysfunction show, above all, problems with motor control, on the same side of the body as the damaged part of the cerebellum. They continue to be able to generate motor activity, but it loses precision, producing erratic, uncoordinated, or incorrectly timed movements. Thus, cerebellum helps in coordinating fine-tuned movements and inhibits involuntary movements. Apart from this, fMRI studies have indicated that more than half of the cerebellum is intertwined with association areas (Buckner et al, 2011). But since it is out-of-scope here, I'll leave it at that much.
See it like this:

For a more detailed mechanism and circuitry of the cerebellum, you can have a look at this interactive page from the University of Texas. @FilipeRocha have also come up with some fine details in their answer.

References:

Ghez C, Fahn S (1985). "The cerebellum". In Kandel ER, Schwartz JH. Principles of Neural Science, 2nd edition. New York: Elsevier. pp. 502–522.

Buckner RL, Krienen FM, Castellanos A, Diaz JC, Yeo BT (2011). "The organization of the human cerebellum estimated by intrinsic functional connectivity". J. Neurophysiol. 106 (5): 2322–2345. doi:10.1152/jn.00339.2011.

When attempting to execute a movement, a signal is not only sent from the motor cortex through the spinal chord and to the muscles, but also one is sent from the same motor cortex to the cerebellum, containing the information of what is the intended movement (this happens via the cortico-pontocerebellar tract, and enters the cerebellum through the middle cerebellar peduncle, in case you are familiar with some neuroanatomy).
At the same time, the cerebellum is receiving information about the current position and forces of the body, called proprioception, through signals that come from proprioceptors located on bones, muscles and joints, which travel up the spinal chord (through the spinocerebellar pathways) and enter the cerebellum (through the inferior cerebellar peduncle). The cerebellum then processes both pieces information - intended movement and current mechanical state of the body - and sends out a signal back to the motor cortex (via the superior cerebellar peduncle) containing information that will improve the overall execution of the movement, by correcting and smoothing out with how much force, how much time and to what extent each component of the movement should be done.
The cerebellum is also implied in the learning process, not only movement-wise (learning to ride a bike or swim), but also cognitively.
To learn more:
http://www.brainfacts.org/brain-basics/neuroanatomy/articles/2012/the-cerebellum/
https://www.youtube.com/watch?v=mpO4lTDr1to&index=21&list=PLp9HSlEm97VXyQ32Uwjfz3dpmQ8nl63zJ


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Are SNPs and alleles the same thing?
It seems to be quite difficult to find an answer to this. Are SNPs the same thing as alleles?

Alleles are variations of a same locus that codes for a protein (gene). These alleles can come in different forms, one of which is SNP. For example, sickle cell anemia arises from an allele of the beta-globin gene which has had a change from A to T.
Meanwhile, for the ABO gene that determines your blood group, the O allele has a missing nucleotide (G) that leads to a frameshift in the gene and a loss of function.
So alleles are caused by SNPs, but can also be due to deletions, additions, insertions and other genetic changes.
Note that SNPs not always lead to new alleles. Sometimes they occur in non-coding areas and nothing happens.
Edit:
SNPs do not need to be gene specific, but this was for simplicty.
@Artem added nicely to the answer, I'm quoting it here:
"Single Nucleotide Polymorphisms (SNPs) are Single Nucleotide Variants (SNVs) at a population allele frequency greater then 1%. Alleles are any variants of the same position of DNA, which includes SNVs, insertion/deletions, or structural variants and at any frequency." - @Artem

Allele doesn't have to be in the coding region

I have two comments:

An SNP is just a substitution, correct?
AN allele can be more generally defined as a variation in a section of a gene, correct? I assume that that's why @student states that alleles can happen in non-coding regions of the DNA, and that makes sense now that we know that these sections are actually useful.

@Mathematician SNP is also known as substation. 2. Yes, but that doesn't have to be in a gene coding area. Anywhere in the genome is okay.

Please add some references to your answer.

What is the basis for  assertion by @Artem that SNPs have to occur at a frequency of greater than 1%? It may be a general agreement in the field — I don't know — but if so a reference is needed to back this up.


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How does the immune system distinguish between commensal and pathogenic bacteria?
There are billions of bacteria living harmlessly in our gut, and in fact most are helpful to us, aiding digestion, producing vitamins and maintaining gut health. The immune system is able to suppress immune responses against these organisms, avoiding killing such beneficial microorganisms in this way. However, it is still able to detect and mount an immune response against those microorganisms that are or would be pathogenic. How does it distinguish them?

This can be a good reading.


text:
Antibiotic resistance of Staphylococcus epidermidis and S. warneri
I am looking for information regarding the antibiotic resistance of S. epidermidis and S. warneri, specifically against penicillin, ampicillin and tetracycline but to no avail. Are there any good websites with databases where this information is shared?

Here some studies concerning the antibiotic resistance of Staphylococcus epidermidis and Staphylococcus warneri:
Antibiotic resistance patterns of coagulase-negative staphylococcus strains isolated from blood cultures of septicemic patients in Turkey - Koksal, Yasar & Samasti [2009]
The abstract of the study above reads as follows:

The aim of this study is to determine antibiotic resistance patterns
  and slime production characteristics of coagulase-negative
  Staphylococci (CoNS) caused nosocomial bacteremia. A total of 200 CoNS
  strains were isolated from blood samples of patients with true
  bacteremia who were hospitalized in intensive care units and in other
  departments of Istanbul University Cerrahpasa Medical Hospital between
  1999 and 2006. Among 200 CoNS isolates, Staphylococcus epidermidis was
  the most prevalent species (87) followed by Staphylococcus
  haemolyticus (23), Staphylococcus hominis (19), Staphylococcus
  lugdunensis (18), Staphylococcus capitis (15), Staphylococcus xylosus
  (10), Staphylococcus warneri (8), Staphylococcus saprophyticus (5),
  Staphylococcus lentus (5), Staphylococcus simulans (4), Staphylococcus
  chromogenes (3), Staphylococcus cohnii (1), Staphylococcus schleiferi
  (1), and Staphylococcus auricularis (1). Resistance to methicillin was
  detected in 67.5% of CoNS isolates. Methicillin-resistant CoNS strains
  were determined to be more resistant to antibiotics than
  methicillin-susceptible CoNS strains. Resistance rates of
  methicillin-resistant and methicillin-susceptible CoNS strains to the
  antibacterial agents, respectively, were as follows: gentamicin 90%
  and 17%, erythromycin 80% and 37%, clindamycin 72% and 18%,
  trimethoprim-sulfamethoxazole 68% and 38%, ciprofloxacin 67% and 23%,
  tetracycline 60% and 45%, chloramphenicol 56% and 13% and fusidic acid
  25% and 15%. None of the strains were resistant to vancomycin and
  teicoplanin. Slime production was detected in 86 of 200 CoNS strains.
  Resistance to methicillin was found in 81% of slime-positive and in
  57% of slime-negative strains. Our results indicated that there is a
  high level of resistance to widely used agents in causative
  methicillin-resistant CoNS strains. However fusidic acid has the
  smallest resistance ratio, with the exception of glycopeptides.
  Additionally, most S. epidermidis strains were slime-positive, with
  statistically significant (p<0.001) association between methicillin
  resistance and slime production.

The other two studies contain information on the aforementioned strains with regards to penicillin susceptibility.
Antibiotic-resistant Staphylococcus epidermidis in patients undergoing cardiac surgery - Archer & Tenenbaum [1980]
Clinical significance of Staphylococcus warneri bacteremia - Kamath, Singer & Isenberg [1992]
In addition, I would recommend to acquaint yourself with Google Scholar for these kind of questions. It normally makes for a good starting point.

Link-only answers are generally not acceptable on Stack Exchange sites. The link may change or become unreachable in the future, and without a summary of what the link contains this answer would be useless. Please summarize what is in the link (don't just copy and paste) and use the link solely for reference. If you remove the link and the answer cannot stand on its own, it is not a good answer.

Fair point @Chris. I will amend my answer at the earliest convenience. I may have been lead astray/tempted by O.kth question for a website / database. However, I agree with what you say in your comment.


text:
Can an exotic species be also endemic?
While talking about the evolution and conservation of dingoes in Australia, someone asked an interesting question:

Can I define the dingo as an endemic species?

That question, despite apparently simple, deals with some terminological conflicts and I must confess that I was not able to say yes or no at the moment.
The context:
As everybody knows, the dingoes (Canis lupus, but for some people Canis dingo1) were introduced in Australia by human beings, between 4,000 and 12,000 YBP. That being said, it's acceptable to define the dingo as an invasive, exotic species. Using Campbell's2 definition:

Invasive species: a species, often introduced by humans, that takes hold outside its native range.

However, some researchers argue that the dingoes, being isolated in Australia for a relatively long time, have a unique genetic profile. As this is controversial, let's suppose, just for the sake of the argument, that they do have a unique, distinctive genetic profile (and that they became a distinct species).
That being the case, the dingoes may be defined as endemic. Quoting Campbell again:

Endemic: referring to a species that is confined to a specific, relatively small geographic area.

I have taught biology for many years and I must confess that, for me, endemic and exotic were always opposite, mutually exclusive terms. However, in this case (and many others), it makes sense to say that the dingoes are exotic and endemic.
Maybe one can say that, from the moment the population became a distinct species on, it stopped to be exotic and started to be endemic, which would keep the two terms mutually exclusive.
My question
So, my question is: can a given species (or population) be defined as exotic  and endemic simultaneously?
PS: I'm not asking for opinions, which would make this question off topic  for SE Biology. I'm asking for rules and guidelines in the use of the terms, preferably with references.

I think this partially depends on the timeframe. Endemism is usually divided into paleoendemism and neoendemism (see e.g. Kier er al in PNAS for use of both terms). Here, neoendemism is referring to the result of recent adaptive radiations that have led to new endemic species. This is then in contrast to paleoendemism, which refers to previously widespread species that are now confined to isolated areas.
Neoendemism is clearly related to your question, but whether dingos should be labelled as neoendemic depends on if it can be seen as a unique subspecies. If it is, it might be more suitable to view it as neoendemic and not exotic (nothing prohibits neoendemic species to be ecologically "problematic" to the previous fauna though).
In the literature (from what I've seen), neoendemism is usually used to describe historical events though (the result from adaptive radiations etc), so timeframe is obviously important (see e.g. Mishler er al, 2014). Even so, all taxa that has led to neoendemic species (through adaptations to local conditions) was by definition exotic at one point in time (e.g. when the most recent common ancestor of the Galapagos finches colonized the Galapagos islands). The same goes for the relatively recent adaptive radiation of Drosophila on Hawaii.
To me, neoendemic and invasive are not mutually exclusive terms, while the division between neoendemic and exotic may depend on time since colonization and whether the population now forms an independent taxon (e.g. subspecies) instead of a subpopulation still connected to its host population. I cannot find a reference or definition to support this interpretation right now though.

Thanks for your answer, I appreciate that. My problem is exactly the beginning of your last paragraph ("To me, neoendemic and invasive are not mutually exclusive terms"). So, you would say that (supposing they are a separate taxon) the dingoes are neoendemic and invasive, right?

@GerardoFurtado I would say; it depends. In the strict sense (and most common use) only non-native species can be invasive. However, in a looser sense also native species can be seen as invasive (or weedy, pests etc) in particular ecosystems that aren't their normal habitat (maybe due to land use changes). Therefore, there is a spatial aspect to 'native' - a species can be native to a geographic region (eg Australia) but also to a particular ecosystem within that region. So to some extent it is a matter of scale.

In this case (IMO), it is reasonable to see Dingos both as native (if they are indeed seen as a separate species) as well as invasive, since they are still new to the ecosystems they are expanding into (both from an evolutionary and ecological perspective). You will probably not find a definite answer though. Purists might still feel that only non-native species can be invasive. But then you are back to the question of whether Dingos are native or not (which depends on species status and to some extent  timeframe)


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Why are all human beings not black in color?
Archaeologists and historians strongly claim human beings originated from the African continent, where the default color is black for humans.
Why are all human beings not black in color?

First let's look at the difference between light skin and dark skin: darker skinned people have higher concentrations of melanin than those with lighter skin. Africa is located around the equator, a place where the sunlight is very intense. Melanin protects the skin against harsh, damaging rays, which is very beneficial in Africa. But a high concentration of melanin also decreases the skin's ability to produce vitamin D3 (1). Vitamin D3 is a vital nutrient to many physiological processes. Deficiencies in vitamin D3 has been known to cause things like rickets and osteomalacia (2).
So in Africa, having a high concentration of melanin in your skin conferred a great fitness benefit: you could go outside without getting cancer. But when humans relocated to places farther from the equator with reduced sunlight, having a high concentration of melanin in the skin actually became harmful because it would make darker skinned people more likely to have vitamin D3 deficiencies. Given this change in the fitness conferred by the trait of dark skin, individuals with lower concentrations of melanin in their skin were more likely to survive and reproduce in these new conditions. After many generations, the allele(s) that cause lighter skin became more common than those that cause darker skin.
Hope that was helpful!

T.L. Clemens, S.L. Henderson, J.S. Adams, M.F. Holick, INCREASED SKIN PIGMENT REDUCES THE CAPACITY OF SKIN TO SYNTHESISE VITAMIN D3, The Lancet, Volume 319, Issue 8263, 9 January 1982, Pages 74-76, ISSN 0140-6736, http://dx.doi.org/10.1016/S0140-6736(82)90214-8
http://www.everydayhealth.com/drugs/vitamin-d3

You can see the same effect at work in India (and I think in Australia).  The people who are native inhabitants of the southern part of India are quite dark, northerners not so much.

@jamesqf lets discuss about Africa only.

@rjames  For Suppose, I moved to Himalayas/Ice regions, but doesn't it make my skin white naturally, Still I have to choose artificial methods like plastic surgery etc to change my color.

@user11287 Evolution occurs over many generations. It takes a long time for changes like that to occur.

@user11287: Limiting the discussion to Africa only would ignore much relevant data.  For instance, while the southern Indians are dark-skinned, they aren't otherwise (judging from those I've met, anyway) like Africans in appearance.  I'll also note that when I live in northern winters, most of my skin is pretty pale, but it turns brown in the summer.


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Why are some animals so much more intelligent than others?
From what I found many biologists state that animals living in large social groups (elephants, primates, cetaceans etc.) have a tendency for improved cognitive abilities. Yet at the same time there are solitary animals with (suspected) high intelligence such as octopuses and plenty of social animals that fail our cognition tests.
What evolutionary pressures pushed certain animals towards such intelligence when their environments are so different while other animals in a similar environment show no exceptional cognitive skills?

When asking "how does intelligence evolve?", I personally think the first step is to recognize that intelligence is an umbrella term for a whole lot of cognitive abilities which is directly a hint that one ought to expect a whole of selective pressures may affect everyone of these abilities. For example, long winters will select for good spatial memories in lineages that hide food during the bad season. I therefore think the question is quite broad.

I agree that intelligence is a broad term that is hard to measure and sometimes we get too subjective about it.  It is not determined by IQ tests.

I'll admit that intelligence is pretty much impossible to exactly define but still, some animals exhibit superior self-awareness and abstract thinking (passing mirror test, tool usage). This question is more about the different levels of sentience among animals than just capacity for memorizing.

@KoenvdH Minor clarification- Do you mean sentience, sapience, or both?

@HarrisWeinstein Please do correct me if I'm wrong but i thought sapience is considered exclusive to humans?

@KoenvdH Not in definition, and there is evidence that various animals (e.g. dolphins, octopuses, etc.) have cognitive abilities that especially push them towards this. I'll grant that we seem to be ahead of the pack.


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Explanation for hyenas asymmetric legs length
Hyenas seem to have disproportionately short hind legs. It may be the opposite, maybe the front ones lengthened to raise their heads even higher than their already long necks do. In any case, this trait is not seen in any other cursorial animal (that I know), asymmetry is not a good Ally in the long run. So why?

This website along others claim (without reference) that it is to allow to see further (like gorillas if I am not mistaken). Do you not believe this could be a sufficient reason?

First most animals have limbs of different lengths. consider a house cat at full extension its hind limbs are much longer than the forelimbs.
The relative length of the limbs means almost nothing functionally, it is the relative length of the gait, or the distance the limbs can swing that is important, a longer less flexible limb may swing the same distance as a shorter but more flexible limb. Source
When the limbs have very different gaits you end up with hoppers or so called pendulum runners like rabbits and kangaroo or they do not fully utilize the possible arc of one limb like gorilla this second one pops up when ground travel is not the primary means of locomotion. Hyena do fall in either category their limbs are close enough for a normal gait.
Hyena limbs are not as different in length as many people think, the massive neck and shoulder muscles make the front limbs look taller than they are in many photographs, but yes they are longer. The heavy musculature plus the longer forelimbs are all adaptation to make the animal stronger with more leverage, better able to rip apart a carcass and crush bones. They do not need the massive hind limbs of the large cats becasue they do not "pounce", you see the same adaptation in the so called "Fanged Cats" or saber tooth cats they have massive forelimbs. More importantly the massive muscles on the shoulder and neck make the forelimbs less flexible so to get the same arc swing out of the limb, it has to be longer.

Thank you very much. I found very interesting that of the pendulum runners. I had already realiced that ther lococmotion is very different and a "pendulum" absolutely matches. Your explanation of the different limb lenght to compensate lack of flexibility is perfdect.


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Mass production of bacteria
Is there a way to mass produce a certain species of bacteria?
Answers I am looking for should not involve a Petri dish: I am only interested in protocols involving, perhaps, more efficient mediums to grow the bacterium-in-question.
Is it done with any yet? In a factory or where etc?
How is it done?

The fed batch culture is a means of bacterial production that is used in industrial setups. Nutrients are fed into the chamber with controlled ideal conditions for growth of a particular species of microorganisms.
Upon reaching the desired yield temperatures can be increased (depending on the species of bacteria) to facilitate spore formation for eventual harvesting.


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Biomedical consensus on human aging and lifespan
Medical technology is improving quickly. Unless there is a global disaster and human progress is set back significantly, e.g. by an asteroid or a global nuclear war, there will come a day when humans can live indefinitely. This does not mean infinitely- people will still die in vehicle accidents, get murdered, etc. Also, at least at first, access will be prohibitive due to costs and possibly outright selection/rejection of patients.
Based on trends in the progress of biomedical research, what is the consensus in the biomedical research community for approximately what year will the average person vs. a very elite person be able to get treatment to live indefinitely?

This question is being voted to be closed as "primarily opinion based" because 1. your premise "...there will come a day when humans can live indefinitely" is strictly opinion and not currently substantiated by any major research that I know about, and 2. your question about the consensus of the biomedical community (which there likely isn't one due to there being no way for us to know) will likely only lead to answers "almost entirely based on opinions, rather than facts, references, or specific expertise".


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Why doesn't life produce diamond, graphene, nanotubes, etc? Could it?
It seems that life is really good at assembling carbon into extremely complicated molecules (e.g. DNA). Graphene is stronger than any materials currently used by biology. Diamond is harder than any biological materials. Do we know about some inherent difficulty that prevents this? Is there any reason to think that humans will never be able to genetically engineer say, bacteria/fungi/ourselves, to produce diamond, graphene, carbon nanotubes, etc?
I'm looking for specific metabolic hurdles that would make this difficult or impossible. (For example, enzymes/proteins can't do that for this reason, or ATP metabolisms don't have enough energy to form the needed bond.)

well, life, meaning humans, are capable of producing artificial diamonds, i.e. https://en.wikipedia.org/wiki/Synthetic_diamond I would suggest you look into energy required for creating diamonds (3000 deg C, 3.5 GPa) versus energy biology is able to apply in biochemical reactions

Possible duplicate of Why do some bad traits evolve, and good ones don't?

as aaaaaa stated, diamond require high heat/pressure to create. Zoological bodies/tissues can't do that. Also, you should review production techniques for creating graphene and try to imagine how a biological organism could accomplish a similar task

Although your post is interesting, your main question, " Is there any reason to think..." qualifies this question as being primarily opinion-based (i.e., "answers to this question will tend to be almost entirely based on opinions, rather than facts, references, or specific expertise."). I would suggest editing your question to avoid closure.

Biology does not have too many uses for super hard but brittle materials like a diamond. The hardest biological materials are also very tough as well since they need to form complex shapes for maximum utility. Limpet teeth are the hardest biological material known but are also incredibly strong, stronger than steel, not super brittle like diamond1.
As for graphene, the big problem there is reactivity; graphene is a great substance except it is pure carbon and has a huge surface area. If you put it in a solution full of carbon reactive chemicals, it starts doing weird things, and it has particularly weird interactions with cell membranes. Structurally, it is far more trouble than it is worth in something made of cells2.
You also have to remember that, in evolution, it is generally about "good enough", not perfection. Making a pure carbon structure would be an incredibly costly process in a biological (and thus aqueous) environment.
References:

Extreme strength observed in limpet teeth
Exploring the Interface of Graphene and Biology

Good answer, but could I also suggest the problem of breaking it down again. If a biological structure is damaged, or the organism needs to grow, it has to be able to break down its structure - this could be difficult for a substance as stable as graphene or diamond

I think there are plenty of uses for diamonds. Rodent teeth are composed of a hard, brittle face with a softer, tougher backing structure. The hard face could be replaced with diamond.
Grass grows phytoliths which would be a perfect application of even highly brittle diamonds.
Composite materials are usually combinations of hard, brittle materials with high tensile strength fibers (e.g. reinforced concrete, epoxy fiberglass). Diamond reinforced by carbon nanotubes would seem to be the ultimate expression of this strategy.

considering rodents can already chew through concrete with teeth made of a salt composite diamond is not going to gain them a whole lot. and far more costly to make while not necessarily showing better wear resistance.phytoliths are made from silica which is basically free (the plant absorbs some by accident as it tries to dissolve other useful minerals out of soil. daimond would compete for cellulose and sugar for carbon usage.

diamond by their very structure do not bond well with anything, they are all but useless for composites.

@gilleain: Breaking down a structure isn't the only solution.  Many animals (sharks, for instance) shed worn teeth and grow new ones.  Many arthropods shed their carapaces and grow new ones, snakes shed their skin, and (as I am all to well aware of right now) dogs & horses shed their winter coats.

@John If you google for diamond composite there are a lot of hits including at least one commercially available product called Versimax. My chemistry is a little weak, but I don't think it's necessary to form a molecular bond with a matrix material in order to form a useful composite with it. I don't believe epoxy and fiberglass form molecular bonds.

They do bond that would be the reason for epoxy as opposed to just just using a bulk filler. you can make composites with only mechanical interaction but biological composites need to be built on molecular level casting and such are not an option. As for diamond composites note they are all either metals or ceramics, not materials known for occurring in organisms and both requiring absurd temperatures.

Biology is way ahead of us in producing stuff with useful properties. Nanotubes are nothing new, some structures in your body are made out of nanotubes, take e.g. your tooth enamel. The nanotubes there can become depleted of minerals after eating foods containing acids, but they'll refill in about an hour's time. This is why your dentist will tell you to not brush your teeth immediately after eating a meal. Empty nanotubes are easily damaged, they won't be replaced so you'll have permanent mineral loss.
Diamonds crystals have no known use for ling organisms and they are also hard to grow in a biological setting. You have to keep in mind here that humans are used to build structures on a macroscopic scale. Machines that we build will have smallest functional parts that are still enormously large when viewed at the atomic scale. This then means that our machines are prone to degradation due the system accumulating damage at scales that are smaller than the smallest accessible scale.
Biological systems don't have this problem because the relevant machine parts here are at the molecular scale. Damage at smaller scales requires bonds between atoms to be broken which requires very high energies. Also the systems themselves are small enough to intervene at that scale. So, the reason why we want to use diamond (a strong material that doesn't degrade) is not relevant for biological systems.
Here we also need to keep in mind that biological systems are constantly at work to maintain themselves. So, it's not like any machine that we build that only very occasionally will need downtime for maintenance and still we'll take it for  granted that it will degrade over time. A biological system will almost immediately fall apart if the internal self maintenance processes were to stop.  It's the equilibrium between breakdown and rebuilding that keeps your body in shape. Increasing the demand for rebuilding by exercising will shift the balance such that your body becomes stronger.

If hard materials weren't useful for biological organisms, they wouldn't make them. Biological organisms do make hard materials - teeth (as you mentioned), scales, bones, claws, pincers, exoskeletons, bivalve shells, diatom shells, beaks, phytoliths, etc. Diamond is highly resistant to acid, which would prevent cavities. Its hardness would greatly reduce tooth wear in herbivores ingesting phytoliths or digging rodents. Diamond faces on compound eyes would reduce scratching.

@hexagon Yes, I agree here, but do note that in biology the stuff that is used is also being manufactured at the same time. So, you're bones are constantly being broken down and also build up. For diamonds to be used would require the machinery to make the stuff from diamonds to be there at work too. We tend to think of the building phase as being separate from just having that stuff after it's being build, it's then a static thing. To appreciate that biology is different, you should watch these videos https://www.youtube.com/watch?v=SNiiLfB8s0s and https://www.youtube.com/watch?v=zkGb12xBKlM

Bones are created that way, yes, but I don't believe that is the case for all hard materials. Exoskeletons are molted. Snail and bivalve shells are shaped to grow indefinitely. I suspect phytoliths never shrink.


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What happens to apetite hormones like ghrelin and leptin when a person in coma?
Don't coma individuals feel hungry? If so, how does the brain senses this condition (as coma is caused by neural death or damage) and switches off gene expression of ghrelin and leptin.
Is there any research done on revealing the mechanism by which apetite hormones expression are shut down during brain death???
Thanks


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Can plants be grown using lights in the home?
Plants need sunlight to grow, mainly the blue and red wavelength of the sunlight . The lights used in homes are also white light, it will also have red and blue wavelength of light.
So , can they be grown in such lights perfectly?

Yes, though you may need special full-spectrum lights.  Ask any operator of a marijuana grow house :-)

Sunlight is about 60,000 lumens per square meter . A 100 watt incandescent bulb produces only about 1,600 lumens.

@Jim Young: People still use incandescents?

@jamesqf. No. But most of us have an awareness of the brightness of a 100 watt bulb. Point is how dim interior lighting is compared to outdoors. The OPs logic is okay, but off by a few orders of magnitude.

It depends on what kind of light you are using. I recently did an experiment on this for my school's science fair and I found that you can use LED lights to grow plants. Nowadays you can actually buy LED lights called "Grow Lights" to grow your plant and the only difference is that Now the current LED lights that are used include four LED lights into groups where each light can produce the correct wavelength that will allow for increased production of growth. For beneficial growth of the cannabis plant for example  you want to use your LED lights directed at 439nm, 469nm, 642nm and 667nm. Link http://easy420grow.com/what-is-the-difference-between-hid-grow-lights-and-led-grow-lamps

Typically, regular incandescent bulbs like the ones you'd use in your house omit orange and yellow light. These wavelengths of light are used in photosynthesis but foliage growth relies more on blue wavelengths of light. Therefore regular lights aren't ideal for the growth of plants. Incandescent bulbs also generate a fair amount of heat which can damage plants when the bulbs are placed too close. Usually supplemental lighting is needed to grow plants with artificial life (eg. fluorescent, grow lights etc).
However, if there is a window in the room, plants generally do well even with just diffused light.


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What is the function of oxyphilic cells in the parathyroid?
Apart from the chief cells, which produce and secrete parathyroid hormone (PTH), the parathyroid gland has another type of cells, which are large and fewer in number, have small, dark nuclei and an acidophilic cytoplasm with many mitochondria. These cells increase in number with aging. As far as I know, we still have no knowledge of what role they perform, or why they increase with age.
Is this true, or are there already some concrete ideas about this?


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How do we know with so much detail the molecular structure and composition of some molecules?
I can't understand how can we get to and be so sure about so detailed information about the molecular structure of certain substances. How do we get this information? What tests are used to such?
Let's take for example somatostatin:

you can see it is a big and extremely complex molecule, and my question is, how have we arrived to this structure? How can we know this to such detail? What tests do we use to know this?

Although this does not answer the general question, I should point out that your example is a polypeptide, so the atom connectivity could be determined mostly from its sequence (AGCKNFFWKTFTSC). That, plus the disulphide bond

@gilleain that is one possibility for my example, in fact. But I'm still curious about a general answer

I'd take a look at this wikipedia page on chemical structure. The take home point wont be whats on the page, but the techniques it references. Sometimes it's a combination of 3 or more different techniques that elucidate the final chemical structure, and all of them are somewhat difficult to understand at first.

Usually X-ray crystallography maybe, have a look at PDB for proteins. It (probably) has info on the original observations of discoverers. Also, many such structures are flexible and the accepted structure is chosen by consensus.


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Digestion of milk in humans
The intial step in the digestion of milk in humans is carried out by which of the following enzymes?
A) lipase.
B) trypsin.
C) rennin.
D) pepsin.
I'm confused between the C and D option. as it's not specified whether they're asking about adult humans only or humans in general (where infancy also included), which between pepsin or rennin will be the answer for this question?
I know that in infants the milk digestion is initiated by rennin and in case of adults due to its absence it's carried out by pepsin. Which is the correct option for that question?

Comments are not for extended discussion; this conversation has been moved to chat.

Short answer
My best bet is D)
Background
A) seems incorrect as lipases break down fats. However, one has to realize there quite some fat in milk (up to 3.5% in untreated milk). Digestive lipases in man are secreted by the pancreas into the duodenum.
B) Might be a correct answer, as trypsin is released in the small intestine and...

[Trypsinized] peptide products are further hydrolyzed into
  amino acids via other proteases, rendering them available for
  absorption into the blood stream. Tryptic digestion is a necessary
  [first] step in protein absorption as proteins are generally too large
  to be absorbed through the lining of the small intestine.

C) Chymosin, known also as rennin, is a proteolytic enzyme synthesized by chief cells in the stomach. Its role is thought to be in digestion is to curdle or coagulate milk in the stomach, a process important in young animals. If milk were not coagulated, it would rapidly flow through the stomach, impairing protein digestion. So this is a enzyme in the stomach and active earliest in the digestive system (answers A and B concern enzymes in the duodenum, which is later down in the digestive tract). However, in humans there is only a chymosin pseudogene present, and since the answer specifically deals with humans, answer C) is incorrect.
D) Pepsin is

...[] one of three principal proteases in the human digestive system, the other two being chymotrypsin and trypsin. [These] enzymes [...] break down dietary proteins into [...] amino acids, which can be readily absorbed by the small intestine. Pepsin [mainly] cleav[es] peptide bonds between hydrophobic and [..] aromatic amino acids [...The other two proteases have different targets].
Pepsin's proenzyme, pepsinogen, is released [...] in the
  stomach [...], and upon mixing with the [...]
  gastric juice, [it is] activate[d] to [...] pepsin.

Here we have the adult equivalent of rennin, also active early in the digestive tract, namely the stomach. So D) is the enzyme present in humans (as opposed to C) and active already in the stomach (as opposed to later in the duodenum in answers A and B). So D is the answer.

https://www.physicsforums.com/index.php?threads/908437/  please do check this link.I agree with your short answer but the reason why pepsin seems to be contrary to what I learnt from the link that I quoted.Have a look at that link and come back here again to let me know your views on that :)

I did. https://www.physicsforums.com/index.php?threads/908437/. Did you?

you say chymosin is present in human infants. But chymosin wiki says humans don't have chymosin.they have chymosin pseudogene. So pepsin is the answer be it be human infants or humans is what I had learnt.

also see this please https://www.ncbi.nlm.nih.gov/pubmed/1455182 this supports my claim of no rennin in humans (infants and adults)

@user129402 - gotcha. This is on humans and they lack the chymsoin gene. Nice thinking!

@AliceD we should also remember that there are many proteins in milk other than casein, which are digested first by pepsin.

von Ebner's glands secrete lingual lipase. Perhaps option $A$) is a good idea?

Additionally, @notherHomosapien's answer here [  https://biology.stackexchange.com/questions/57531/what-inactivates-pepsin-in-infants ] indicates that humans do produce rennin (at least during infancy). Meh, this is confusing....I think I'm going to have to ask this as a separate question. I like how you took apart the question option-by-option in your answer. Good answer! O:)