What is protein folding and how is it relevant to disease? I am trying to understand what is protein folding and how it could help cure some diseases.

When reading articles about it, it looks like the goal is to find perfect folds for proteins because some diseases are due to proteins that don't fold correctly. I don't understand why do we need to find them in the first place?  Don't correctly folded proteins already exist in the body of people who aren't affected by those diseases? Why do we need to manually find those structures instead of simply "reading" the structure of the correctly folded proteins in the body of non affected people?
In the end, is the goal to find the best structure or to find the folding proecess ? Or both ?

Thank you!

Protein folding is a complex thing. There are huge computer algorithms and huge mainframes which are trying to predict the final 3D structure of a protein.

Knowing the tertiary and the quaternary structure of a protein, allows us to understand why diseases happen. In many cases a mutation of the gene provokes an aberrant protein folding. When the protein is misfolded, it is not able to do its function. This particular condition is called "Proteopathy".

http://link.springer.com/article/10.1385%2FMN%3A21%3A1-2%3A083

If you know the structure of a protein, you are able to design or improve drugs which can directly influence the protein structure and/or function, for example antibody therapies against cancer (Cetuximab-->against EGFR, in colorectal cancer; it is a drug which was very much improved when computers prediction/simulations are used).

https://en.wikipedia.org/wiki/Cetuximab

It is hard to find out a protein's structure - for some proteins it can require years!

So you first go from the sequence of the healthy people, then you sequence their genomes, and you use this as reference for the people with certain diseases. You might find eventually some mutation is in certain loci in the genomes of people with a certain disease. Then you can study the protein structures, so you can design some new drugs which might tackle this protein. If the protein is misfolded, like the tau protein in the neurodegenerative diseases, then is good to study the structure of this misfolded protein so you can design some drugs for these protein too.

So in the end the structure is extremely important, but often times you have to study many stages of the protein folding process to understand the possible final structure that one protein might have in the body and/or in a certain disease.

I hope this can help!


What is the meaning of the following: " completion of open rounds of DNA replication"? I am studying a paper about the relation between polyP granule and cell cycle exit. As the author explained the four general steps for cell cycle exit, the second step is" the completion of open rounds of DNA replication". But I really can't figure out the meaning of this sentence. I hope that someone can explain this to me. Thank you!

From the context of the article I found from an internet search:

Cell cycle exit in bacteria encompass four general steps:
(i) inhibition of inappropriate reinitiation of DNA replication,
(ii) completion of open rounds of DNA replication,
(iii) segregation and compaction of daughter chromosomes, and
(iv) septation.

I would assume that ‘open rounds’ means ‘DNA replication that has already been started’ (‘open’ signifying already started, and a ‘round’ has the sense of one event of a series). ‘Completion’ is obviously ‘finishing’, ‘ending’ — the cell cycle doesn’t end until all the replication that has started has finished.
I have not seen the adjective ‘open’ used in this way previously, and suspect it is uncommon, but as this is not my field I stand to be corrected.


How can highly virulent but uncommon diseases (like ebola) maintain a stable equilibrium? I'm wondering how can very uncommon diseases remain in a relatively stable equilibrium. For example, if it started to spread, the spread could accelerate and become an epidemic. However, if it doesn't spread, why doesn't it wither away?

As I understand, the ebola for example, is highly contagious, nearly always fatal, and kills quickly. So quickly, hat the target has not much time to pass it on to others. If it spread just a little better, it would become an epidemic, just a little slower and it would disappear. How is it possible, that its spread did not change significantly in the last couple of decades? It kills a few dozen, maybe a few hundred people per year, these numbers remain largely unchanged.

Viruses and other disease causing organisms are usually in an ecological steady state in different organism, called a vector.  When they start to infect another organism similar enough that they can reproduce, they may turn out to be more virulent or fatal than is optimal for the organism.

The classic example is the case of influenza outbreaks, the flu virus is causing mild infections in other animals such as birds or pigs and then a human being catches it and it may be serious or even fatal.  This is classically because the viruses lytic cycle (where it reproduces and then kills host cells) is not tuned to the equilibrium ideal for viruses in the new human environment, which is not fatal which gives the virus the best chance of reproduction and retransmission.

In the case of Ebola and Marburg viruses the vector is not known but there is speculation and research going on. So in the extremely rare handful of events where these hemorrhagic fevers have been caught by people they fatal.

Its the non-equilibrium case where the virus is not adjusted to human hosts and adjusted for its vector population where it is usually most dangerous.

If these viruses were allowed to persist they would theoretically come to the point where it wasn't fatal.  The problem being that people would die and there is always the risk that the virus would burn through all possible human hosts before it adjusts...

I want to say that this is all driven by evolutionary forces.  If the environment encourages pathogenic characteristics then human pathogens can persist forever.  Flesh eating bacteria and MRSA and other antibiotic resistant bacteria have found a competitive environment where causing disease and death are the only way to go - hospitals with antibiotics. In the case of Ebola/Marburg, there may be a disease reservoir of monkeys acting as a pool for the high fatality strain.  Anything can happen with the right geography and dynamics.

If you've been thinking to yourself, 'what are the odds that a virus or bacterium would be extra virulent versus not infectious at all?', you are right. One should also note that fatal outbreaks are rare and exceptional.  There are clearly plenty of cases where viruses or pathogens from other organisms can't get any traction at all in humans.  We are practically swimming in viruses and bacteria all the time.


What does it mean for muscles origins and insertions to be the other way around in the right than left limb? Herbert Srebnik writes in Concepts in Anatomy:

  In the right limb, the muscle's origin is proximal to the joint and
  the insertion is distal to it. In the left limb, the muscle's origin
  is distal to the joint and the insertion is proximal to it.
  (The text appears next to an image of the biceps brachii)

What does that mean? What does it tell this paragraph tell me as someone new to human anatomy?

Muscles span joints, and their purpose is to affect movement of that joint. Typically a muscle's origin is the more fixed or stable point of attachment to bone, while the insertion is on the bone which moves when contraction or relaxation of that muscle occurs.

Usually with the muscles of the limbs we think of the more proximal end of the muscle as being the origin, and the distal end being the insertion, because muscle action tends to move bones more distal to the limb joints. For example, for movement of the elbow joint you can typically think of muscles originating on the humerus and inserting on the radius and ulna.

However the nomenclature is somewhat arbitrary, because one can in a sense reverse the origin and insertion by fixing the location of the more distal bone and moving the upper body. For example, by placing your forearm still on the table and moving your upper body, because of the nature of their action in this position you might consider the muscles of the elbow to originate on the radius/ulna and have their insertion on the humerus.

I suspect this is what is described in the book. The biceps brachii attaches to the scapula and radius. Depending on whether it is the forearm or the shoulder moving with respect to the elbow joint, the insertion and origin could be considered at either end of the muscle. It is not that the origin/insertion is always opposite for the right versus left limb.


Difference between autonomic and paratonic movements in plants I can't understand the difference be because both involvery the main cause that is an external stimuli, so how do they differ(

its about the gene that is involved in autonomic movements. while, there is no gene involved in plants for paratonic movements.furthermore, autonomic movements are presents in plants by birth, and paratonic movements are induced in plants by an external stimuli only and not present in plants by birth.


When writing about past research should I use the species name they employed or the modern version? I am currently writing a literature review in which I am talking about the old research on the subject. When this research was carried out the species I'm talking about were classed under a different genus (specifically, it used to be called Vibrio fetus and is now called Campylobacter fetus). What is the correct approach for choosing when to use the older name and when to use the newer name? I see three options, although there may be more:

Always use the modern name.
Use the name used by the authors when discussing their work.
Largely use the modern name but make reference to the fact a different name was employed where it is appropriate to do so.

I'm tending towards option 3, but it's sometimes a bit unwieldy. Is there an accepted convention I should be following?

3. is right thing to do. You can mention in the introduction that "Campylobacter fetus, which was previously known as Vibrio fetus [Ref] ........."

You should not use the old name anywhere again (also for the sake of consistency), once you have made it clear that the species was renamed, in the Introduction.

I don't think there is any written convention like that (As such usage of any obsoleted terms is to be avoided and the standard nomenclature as described by ICZN/ICBN etc should be used).


What is this soil digging insect? It is in Texas(Month: May). Are these flying ants?termites? or Cicada Killers?

Certainly not cicada killers--those have yellow stripes on them, are considerably larger, and also have a very different shape of abdomen. Here's a good pic of one of those: https://bugguide.net/node/view/1721236/bgimage.
They certainly look to have a hymenopteran "waist" so that means they aren't termites, they are some kind of winged ant. Possibly carpenter ants due to the large size (for ants) and the reddish-brown color (like this one https://bugguide.net/node/view/1056576/bgimage).


How does herpes (HSV) infection suppress HIV? HIV compromises the human body to defend against infection. Yet people who are infected with herpes are at less risk of developing AIDS.
How does this work?
This question comes from this paper, which is hard for me to follow since I am uneducated on this field. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1716975/

Alright, having read the citation linked, and doing a little poking of my own, here's my approach at an answer:

Some human herpes virus infections may compete with HIV infection. Essentially, some strains (not the ones you normally think of) infect CD4 cells - the same cells targeted by HIV. These strains down regulate transcription in CD4 cells, which in turn interferes with the HIV infection process. This pertains, it appears most notably, to HHV-7.

However the actual impact on HIV disease isn't clear. Strain competition triggers some fascinating evolutionary pressures, but HIV is notoriously prone to mutation, and competition for CD4 cells might not impact HIV infection on a clinical - rather than microbiological - scale.

Additionally, the two most commonly thought of forms of herpesvirus infection, HSV-1 and HSV-2 are associated with increased acquisition of HIV infection. The clearest reasons for this are genital lesions and inflammation at the site of HIV infection. There's also some interesting dynamics in play for active coinfection, such as the impact of acyclovir treatment for HSV impacting HIV, or HAART treatment for HIV impacting HSV.


Is there a risk of localised die-off when plants bud too early? I've been taking a few walks in the countryside in Scotland and England this winter (end of December 2014). Some parts of England haven't had any frosts yet, which is very unusual, and it's been generally quite warm since summer ended.

My friends and I agree that there's quite a lot of stuff putting out shoots and buds, as if it's April already. I can imagine that this means a lot of small fragile plants could get killed if a hard frost comes in the next few weeks. If so, it seems natural to expect that next summer will be marked by an absence of these plants, and, being dead, they won't put out seeds or otherwise reproduce for next year. In other words, we're expecting some species to experience localised die-off.

Is this plausible or are we just imagining it? If it's actually happening, is it something to actually be worried about? i.e. will a large portion of the seeds/shoots/buds/whatever refrain from growing even if some are being tricked by the mild winter, or will they be cold-resistant if they're coming up now, or is some other mechanism going to make it all okay? Alternatively, is this winter likely to trigger a large ecological change?

I realise this question doesn't single-out any particular species for attention, and perhaps it's too much of an open question for StackExchange's taste, but I'd very much appreciate some insight into how fragile or robust is the distribution of British plant life when the weather is abnormal, as it is right now.

If you're talking about shoots or buds coming out of individual seeds, then those plants are probably doomed. Most seeds are "designed" as one-shot delivery packages. In this case, they'll bud, be killed off by a frost at some point during the winter, and then be spent.

For a perennial plant like a tree that buds year after year, the impact of an early blooming will depend on the species. As per a Q&A from Cornell (Will Warm Winter Wither Plants?, 2007), most plants growing in a temperate climate (like that of Britain) will have experienced warm winters before and will have at least some evolutionary adaptations to help them deal with occasional aberrant weather. For example, even if you do see some fresh buds on a tree this time of year it is likely that the majority of its bud primordia (the parts of the plant that will someday become buds) have not developed. Although you won't see regrowth in the spring of most of the buds that opened early, you will see normal development of the buds that stayed dormant during the winter.

As for the question of wider ecological change, one anomalous year isn't going to make a difference because, as you say, a large portion of the seeds/shoots/buds/whatever refrain from growing even if some are being tricked by the mild winter. However, if a string of mild winters cause significant die-off year after year you would start to see changes in the ecosystem. It works the same way for many with loosing their hair...


When does LH surge actually occur? I’ve seen many textbooks saying that LH surge occurs in the Follicular phase while others say it occurs in the Ovulatory phase.

I’ve tried googling this, only to end up knowing two things:
1) It occurs 2-3 days before ovulation and 2) It occurs in Ovulatory phase.

Doesn’t that two contradict each other?

If you see the hormonal variation graph, LH surge occurs somewhere between follicular phase and Ovulatory phase. This is quite confusing.

So, at what phase does LH surge actually occur?

Some graphs about the ovarian cycle mention only the follicular phase and luteal phase, and the ovulation just as a point in time, not a phase, for example, here:

Source: Differencebetween.com

In this case, the LH surge starts in the follicular phase and peaks at ovulation or shortly before it.

Some other graphs also show the "periovulatory" phase (or "ovulatory phase" or just "ovulation" as a phase):

Source: Nature - Scientific Reports

In this graph, LH surge starts few days before ovulation, so in the follicular phase and peaks in periovulatory phase.

  The first half of the menstrual cycle is comprised by the menstrual
  and follicular phases during which time estrogen levels are low
  (menstrual phase) and rise (follicular phase) and ends with the
  periovulatory phase in which follicular stimulating hormone (FSH) and
  luteinizing hormones (LH) peak.

Now, these graphs are still confusing, but Merck Manual defines the ovulatory phase by the surge of LH and FSH:

  The ovulatory phase begins with a surge in luteinizing hormone and
  follicle-stimulating hormone levels.

In conclusion, LH surge occurs in the ovulatory phase, if the source mentions it as a separate phase, and if not, it occurs in the follicular phase.


How to find conserved residues across species? I want to identify if certain phosphorylation sites are conserved for protein X across humans and yeast. I know from MS data that there are 4 phosphorylation sites in Human protein X. In order to identify if these residues, and therefore potentially the phosphorylation sites, are conserved, is it correct to align both sequences using pairwise comparisons by using software like Needle? Or should I rather perform a bigger alignment and use clustal omega? Are there better approaches?

I'd perform a bigger alignment using clustal or mafft or something. Pairwise alignments will give you a lot of noise from random chance and the set of pairwise alignments will be really large. Multiple sequence alignment will detect smaller conservation signals.

Compare against several species of yeast and maybe other mammals for context. When the alignment is done, perhaps draw it? I like logos for vertically large alignments.


Does breath-holding cause permanent brain damage? My question is: Does voluntarily holding your breath at atmospheric pressure for a few minutes can cause brain damage? I'm talking about periods of time around 3 minutes.

I've read there are some studies showing brain damage in deep-water divers. However, it seems to me as insufficient evidence for breath-holding in general: it could be that frequent changes in pressure are the cause for damage, for example. Or the fact that the person cannot resurface immediately after feeling the need to breathe, which might cause them to hold their breath for a longer period of time than their body allows.

So are there any studies showing results for the effect on the brain in (healthy) humans holding their breath?

In order to reply to your question I (*) need to dissect it into 3 parts.

1 - Can you voluntarily hold your breath so long that damage actually occurs?
There is evidence that apnoe-divers damage their brains while diving. In the above, the marker protein S100B, representing brain, damage was elevated. This marker had been found previously to be increased in stroke and other forms of brain damage. Therefore, it appears that brain damage occurs when trained freedivers hold their breath on average 335 s (range 281-403 s). I could not find published data on whether this results in cognitive changes. Another really interesting study I found was also on US Navy divers but with oxygen supply. Their cognition was tested and transient alterations in affect, visual focusing, and physical activity were temporarily seen for 10 days after diving. Pressure changes might have an impact on top of the lack of oxygen.

2 - To summarize a study from a good previous post, researchers measured oxygen saturation in the blood while subject were holding their breath. Oxygen saturation dropped as low as 75% (see original paper).

3 - Additional studies. A blood oxygen level dependent functional-MRI study in adults and children showed similar activated regions while holding their breath. Breath holding in childrens’ brains causes stronger alterations. Their brains seem to be more vulnerable than adult brains. The insular cortex was identified as a specific region in the brain, being responsible for breathing again after holding breath. These findings originate from a positron-emission study which was able to localize air hunger to the insular cortex. The insula is part of the limbic system which regulates essential tasks in humans including temperature, nausea, and pain. Feeling shortness of breath is important for survival and therefore as shown with PET also located in the limbic system.

(*Note that I'm submitting this well researched answer for Tim, an MD, who took the time to write the text but doesn't have the time to sign up or reach the required reputation limit to post. I only filtered out some medical lingo and streamlined the text. The kudos are his.)


On which chromosomes were the traits studied by Mendel? In his experiment with peas, Mendel mainly studied two traits : yellow/green colours and round/wrinkly shapes.  I've heard that the pea genome is very large and its sequencing is a challenge. However, is there any information about the chromosoms involved in the traits on which Mendel worked ?

The yellow/green color of seeds is on chromosome 1, but the color for for the pods is on chromosome 5. The smooth/wrinkly seed shape is on chromosome 7; however for the pods a similar contrast is governed by chromosome 4. The pea has 14 chromosomes (diploid).

What you mentioned however are not all of the pea genes Mendel studies. He actually studied 7 genes (see table above) but only 4 chromosomes host all of the genes he studied. Mendel was lucky that two combinations don't usually show linkage because of the large distance between them (on the chromosome 1 and 4 respectively). There was one linkage which he should have detected though between plant height and the shape of the pods (both close enough on chromosome 4); apparently Mendel never published anything on that combination though. I don't know whether it was because it befuddled him or he just didn't study it.
Referernce: Blixt, S. Why didn't Gregor Mendel find linkage? Nature 256, 206 (1975). doi:doi:10.1038/256206a0


Using the IMGT/GENE-DB service to find RSS I'm trying to get the data for the Human and Mouse 12 and 23 Recomination
Signal Sequences (RSS), to run a classification algorithm on it. I'm not a
biologist, so I apologise in advance for my misunderstandings and
confusion.

A version of the data is available here, but I thought I would try to
get it from www.imgt.org, if possible. There is also another slightly
different version available for the mouse here.

I'm trying to follow the instructions at IMGT-FAQ to obtain Recombination Signal
Sequences for the mouse.

Here is what I have selected at the search page:

Identification:
Species : Mus Musculus
GeneType: any
Functionality: functional
MolecularComponent: any
Clone name: <blank>

IMGT group: IGHV
IMGT subgroup: any
IMGT gene: <blank>

I'm not clear what "Locus", "Main locus", and
"IGMT group" mean here exactly. Specifically, what is the difference
between "Locus" and "Main locus"?

I think, but am not sure, that IGHV corresponds to V genes in the
Immunoglobulin heavy locus (IGH@) on chromosome 14, where locus here
denotes collections of genes. Clarifications and corrections appreciated.

I would have expected that the IGH locus would correspond to "IMGT group"
entries like "IGHJ, IGHV" etc, and the IGK locus would correspond to IMGT
group entries like "IGK, IGKJ, IGKV", but no matter what I select for
Locus, it does not change the possible entries for "IMGT group".

Running the search gives

Number of resulting genes : 218
Number of resulting alleles : 350

As instructed, I went to the bottom, selected "Select all genes", clicked
on "Choose label(s) for extraction", and selected "V-RS".

I got

  Number of results=98

The first few results were

>X02459|IGHV1-4*02|Mus musculus_BALB/c|F|V-RS|395..432|38 nt|NR| | | |
|38+0=38| | |
cacagtggtgcaaccacatcccgactgtgtcagaaacc

>X02064|IGHV1-54*02|Mus musculus|F|V-RS|295..332|38 nt|NR| | | | |38+0=38|
| |
cacagtgttgcaaccacatcctgagtgtgtcagaaatc

>M34978|IGHV1-58*02|Mus musculus_A/J|P|V-RS|554..560|7 nt|NR| | | |
|7+0=7|partial in 3'| |
cacagtg

Ok, now I'm confused. The lengths of the RSS should be 28 or 39. but I
counted lengths of 4,7, 31, 38, and 39. Are the results here not supposed
to contain the 12 and 23 RSS?

So, I must be misunderstanding things here. Possibly many things. Any
explanations and clarifications are appreciated.

I'm not clear what "Locus", "Main locus", and "IGMT group" mean here
  exactly. Specifically, what is the difference between "Locus" and
  "Main locus"?

From the same site:

  A locus is a set of IG or TR genes that are ordered and are localized
  in a same chromosomal location, in a given species. […]
   A locus comprises the genes of different groups which participate
  potentially to the synthesis of a polypeptide of the same 'chain
  type'.

Main locus should have been Locus minus the orphons:

  A chromosomal orphon set is a set of IG or TR orphons (genes outside
  from the main loci) belonging to a same group and localized on the
  same chromosome in a given species.

However the Main Locus and Locus have the same options; Options for the Locus should have been chromosomes. They must have made a revision in the site but forgot to change the help. I tried setting all the options except any in Locus and selecting all for the Orphons; it yields no result. It works only if you set any in Locus. So it seems Locus option is useless; you can set the Locus as any by default.
 For confirmation it is best to ask the authors.

From the changelog:

  16 April 2012

  Update of the IMGT/GENE-DB Query page:

  The search criteria are organized according to the axioms IDENTIFICATION, LOCALIZATION and CLASSIFICATION of IMGT-ONTOLOGY.
  Addition of new search criteria:

  MolecularComponent (IDENTIFICATION)
  Locus (LOCALIZATION): includes main loci and chromosomal orphon sets
  Main locus: "all" value allows to search genes of all main loci.
  Chromosomal orphon set: "all" value allows to search genes of all chromosomal orphon sets

For details on the IMGT classification you should refer to this paper.

Fixing a Locus option does not change the IMGT dropdown box option but the results are different. If you try your example and set Main Locus as IGH and IMGT Group as IGKJ you would get no results. It is just a problem of the web interface. Apparently the search works fine.

Running the search

I searched with the exact same criterion as you mentioned and did not get any sequences smaller than 38nt. There must have been some bug which seems to be fixed.


Which aspects of renal physiology are standing in the way of an artificial (mechanical) kidney? Scientists have been able to create artificial organs with varying degrees of success.  The mechanical heart (in its various forms, e.g. ventricular assist) is able to sustain life for some period of time.

Efforts to grow whole organs in the lab will probably ultimately lead to a more pragmatic solution.  What aspects of the renal physiology are standing in the way of an implantable mechanical kidney (fashioned more so from tubules and membranes than simply being a shrunken down dialysis machine)?

The problem is that real organs are just damn complex - yes the kidney's prime role is just to be a filter, but in order to do so it must be plugged in to a dozen regulation mechanisms - osmotic balance, ion management, protein management and a plethora of more subtle ones. Moreover it is a part of body, so it must also follow all the standard protocols to live with immune system, obtain necessary resources to its function and maintenance, cooperate with nearby tissues...

Currently we only have rough knowledge about major processes, deciphering them all is a work for many, many years (if it is not futile at all).  Finally, our technology will be long not capable of implementing all those protocols; in peaks of perfection we can serially do simple parts in 100nm scale (microprocessors), while this is a scale of a complete molecular device.


Can a human survive without ACE2? I guess not, but it was discovered in 2000 so I don't know if we know enough about it. Are there people without ACE2 (angiotensin converting enzyme 2)?
It seems mice can survive, but that's not a proof on humans: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4829150/

No obviously inactivating variants are found in this gene, which provides at least negative data (humans generally seem to have at least somewhat functional ACE2). Exome sequencing across >200K humans has found a series of variants, mostly low-frequency, in the population.
Some of these variants may affect gene function, but it is not clear how, and none of them are obviously complete loss of function variants (e.g. nonsense mutations).
A more complete analysis of the data, including e.g. CNVs, might be necessary to fully address this question.


Is curling the fingers considered digit flexion? Is curling the fingers considered finger flexion and straightening the fingers considered finger extension? I feel like this is correct in everyday language, but I am not sure if it is correct in anatomical terms.

In the vertical plane, bending of the fingers is indeed referred to as flexion, while straightening is called extension. In the horizontal plane, spreading the fingers is called abduction, and approximation is called adduction (Fig. 1).

Fig. 1. Finger movements and terminology. source: US Dept. of Veteran Affairs


What gives observable light its colors? I know that difference between different colors of light is difference between their wave length but I don't know what gives beautiful colors (like rainbow colors) to different wave length of observable light?

What makes our eyes to see different wavelengths of light as different colors?

Remark:
I've meet someone which he was color blind, he was not able to see rainbow colors.
So the process that gives color to light must be in our eyes and brain.

Three different types of cones in the eye are sensitive to three different, contiguous and slightly overlapping, sections of the visible spectrum. The nerve signals from these three different types of cones are interpreted by different sections of the brain as cyan, magenta, and yellow, from which all the discernible colours are composed. This forms the familiar Colour Triangle.

The sides of the Colour Triangle bulge slightly (I believe) because of the slight overlap in the sensitivity ranges of the three cone types.

Colour blindness occurs when someone is born with only two (or rarely one or none) different types of cones, instead of the usual three. This causes an inability to detect one of the thee sub-spectra.


Can I drink warm/hot tap water? I live in Canada and tap water is drinkable, as a matter of fact, the government puts a little bit of flouride in the tap water so it cleans your teeth.

My wife and mom always tells me not to drink the tap water when it's warm/hot.

Is there something in the water that's bad for the body or is this a myth? (bacterias in warm/hot water vs cold)

Added info: The water is heated in the water heater which is in the basement of my house. It is a new water heater, only a year old. My house is built 7 years ago, which for a house it's not old. I don't know about the pipes though

This actually depends on how your tap water is warmed.
If you have a personal water heater, which is connected to your tap with non-corrodable pipes, then there is essentially no difference.

However, if the heating comes from a common source, then it would be very difficult to verify that the heater-tap connection does not contain any corrodable pipes. In this case, it might be better to not use the warm water for direct drinking, especially if the building is old.

A 7-year old house should not have lead pipes installed, since the Canadian Plumbing Code has banned lead pipes since 1975. As such, I believe that your warm water is safe to drink.

  The National Plumbing Code allowed lead as an acceptable material for pipes until 1975 and in solder until 1986. All provinces and territories use the National Plumbing Code as a basis for their own regulations.


Will the increase in atmospheric carbon dioxide lead to larger insects? From my understanding, the increase in atmospheric carbon dioxide will also increase oxygen levels. That makes me wonder if in the near future insects will grow larger than they are today, since their maximum size is limited by how deeply oxygen is able to diffuse into their body.

There is the supported theory that insects during the Paleozoic period were larger in size because of the increased oxygen content in the air.

The study adds support to the theory that some insects were much larger during the late Paleozoic period because they had a much richer oxygen supply.
The Paleozoic period, about 300 million years ago, was a time of huge and abundant plant life and rather large insects - dragonflies had two-and-a-half-foot wing spans, for example. The air's oxygen content was 35% during this period, compared to the 21% we breathe now, Kaiser said. Researchers have speculated that the higher oxygen concentration allowed insects to grow much bigger.

This article is based on a paper published in the American Physiological Society:

It is because when the oxygen concentration in the atmosphere is high, the insect needs smaller quantities of air to meet its oxygen demands. The tracheal diameter can be narrower and still deliver enough oxygen for a much larger insect, Kaiser concluded.

There are similar papers that investigate the relationship between oxygen and maximum potential size, such as this article published in Nature (1999):

The tendency of some animals to be larger at higher latitudes ('polar gigantism') has not been explained, although it has often been attributed to low temperature and metabolism. [...] We have analysed length data for 1,853 species of benthic amphipod crustaceans from 12 sites worldwide, from polar to tropical and marine (continental shelf) to freshwater environments. We find that maximum potential size (MPS) is limited by oxygen availability.

Another paper published in Proceedings further supports this theory:

[...] A variety of recent empirical findings support a link between oxygen and insect size, including: (i) most insects develop smaller body sizes in hypoxia, and some develop and evolve larger sizes in hyperoxia; (ii) insects developmentally and evolutionarily reduce their proportional investment in the tracheal system when living in higher PO2, suggesting that there are significant costs associated with tracheal system structure and function; and (iii) larger insects invest more of their body in the tracheal system, potentially leading to greater effects of a PO2 on larger insects.

The question you propose is very interesting, although I am sure it would take thousands of years for these insects to adapt to this oxygen level change (which in itself, to reach prehistoric levels, would take a long time) and in turn become larger.
This article, based on the original APS paper, seems to think larger insects could appear in the future if the limiting factor (in this case low oxygen levels) is removed.

Image from Biotic interactions modify the effects of oxygen on insect gigantism (PNAS, Chown 2012).


What are chemical candidates for replicator molecule? I have read Selfish gene by Richard Dawkins and idea is that at random some molecule was synthesized that had a property if there is enough 'materials' to construct copy of itself - it would. And then it made bunch of it's copies and then copies started mutating and eventually we got to DNA in us.

In his book he never says what actual molecule is original replicator.

What are chemical candidates for original replicator molecule?

There is no accurate answer  , as you say we talk about candidates . there is lots of strong theories about the origin of self replicators . RNA world was a strong candidate since latest experiments that suggest there is a good chance that some molecules that have simpler structure than RNA , could have a chance to do self replications .
    there is also strong theories such as :

1.Prions that delivered by space objectives and Meteorites .

2.Life's origins may result from low-energy electron reactions in space:

http://phys.org/news/2016-06-life-result-low-energy-electron-reactions.html

first self-replicator recreated in lab:

RNA, or something very like it, has long been a strong candidate as the first self-replicating molecule in the origin of life. This is because it can both catalyse chemical reactions and carry genetic information.
But chemists first needed to explain how a large, complex molecule like RNA could form spontaneously to begin the process. They had done so for some, but not all, components of the RNA molecule.

https://www.newscientist.com/article/2088006-building-blocks-of-lifes-first-self-replicator-recreated-in-lab/

The origin of replicators and reproducers:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1664675/

you can also check the topic :The RNA World and the Origins of Life
from the book :

Molecular biology of the cell by Alberts B, Johnson A, Lewis J, et al.

after all this article was so innovative for me . I think it's a good explanation for self replication of molecules simpler than RNA.

http://www.nanowerk.com/nanotechnology-news/newsid=40896.php

"Maslov and Tkachenko's model imagines some kind of regular cycle in which conditions change in a predictable fashion—say, the transition between night and day. Imagine a world in which complex polymers break apart during the day, then repair themselves at night. The presence of a template strand means that the polymer reassembles itself precisely as it was the night before. That self-replication process means the polymer can transmit information about itself from one generation to the next. That ability to pass information along is a fundamental property of life"


Does the genome make sense without knowledge of the ovum? Much of the literature for laypeople seems to consider (and to spread
the idea) that an animal (or a plant, I guess) is characterised by its
genome. I do not know whether the same goes for more professional
literature. Even on this site, the tag genomes is defined as The
entirety of an organism's hereditary information, which seems to imply
that it contains a description of all that can be be inherited.

It seems to me that attempting to define an animal with the sole
knowledge of its genome (let alone recreate it as envisioned by some people) does not
really make sense, without the complementary knowledge of the cell
structure of the ovum that has to interpret this genome.

This question seems never to be seriously addressed in lay literature.

Is it the case that this decoding machinery evolves much less than the
genome itself? This could be expected, since changing the decoder has
usually more important, global and drastic effects than changing the
genome, which may result in a very localized effect. Hence, changes to
this machinery are less likely to give a viable being.

To refine that question (unless the moderator prefers this to be a
separate question):

Is there any study of the diachronic evolution of that genome decoding machinery in a
given species, or of the synchronic differences between species, which
would probably give a measure of the speed of diachronic evolution of
that machinery?

When two close species cannot mate, is it analysed (for some cases) whether it is due
to difficulties in combining the two genomes, or to the fact that the
ovum of one cannot properly interpret the genome of the other?

Nice question! Let's start by talking about different forms of heritability.

What is heritable?

Here is a list of things that can be inherited. Some of them are only ('mainly' would be more correct that 'only') transmitted to the offspring while others can also be transmitted to any individual in the population.

The term epigenetics is used with several meaning. In its narrowest sense it refers only to modifications (typically methylation) on top of the DNA sequence or on top of histones (histones are proteins around which the DNA is wrapped). In its broadest sense, it refers to any element of hererdity that is not caused by the DNA sequence. In the below list, I will avoid using the term epigenetics.

What can be inherited:

DNA (obviously)

Modification of the sequence of DNA

Methylation on DNA

Modification of (typically) methyl group added on nucleobasis

Methylation on histone

Modification of (typically) methyl group added on (typically) the tails of the histones.

Environment (or rather macro-environment)

The term environment can be used with different definitions. Histone modification is generally considered as being the environment of the genome typically. I will however make a (somewhat) arbitrary distinction between this micro-environment and the more intuitive macro-environment
Individuals affect their environment and therefore can shape the environment for their descendents. An obvious example is a beaver dam which last longer the the life of a single beaver. Two key concepts here are niche construction and Ecosystem engineering. You should have a look at the post Does modern theory of evolution include modification of physical environment?

Memetics (See wikipedia > meme)

A meme is any idea or element of culture that can be transmitted. This type of inheritence is particularly important is species that have high cognitive abilites such as humans.

In this kind of discussion, there is often someone who stand up to talk about plasticity, developmental noise and mutational noise to mess things up. I will just consider them as phenotypic trait and will not much attention to them for the moment (even though part of my research is focused on these three concepts).

Consideration of the non-genetic inheritence in the literature

I like that you noticed that "the tag genomes is defined as The
entirety of an organism's hereditary information". Such definitions are common and grounded in an old view of inheritance. As listed above, there are other things than the DNA sequence that is inherited by the offspring. While all biologists know that, it is true that few really acknowledge the existence of these other forms of inheritence in their daily thoughts.

Some authors have argued that these other types of inheritence must not be neglected. Odling-Smee and colleagues wrote a whole book on the subject (Niche Construction: The Neglected Process in Evolution). Some have even argued that we should rename our theory of evolution to the light of the existence of non-genetic inheritence (see Laland et al. 2015). My feeling is the vast majority of biologist recognize the existence of these types of inheritence but do not consider that it is worth a renaming of the theory of evolution (current named modern evolutionary synthesis). Some would not consider this renaming necessary either because they neglect the important of these other forms of inheritence or because they just don't think it is worth renaming our theory even in the recognition of the importance of these other processes.

Viewing the cell as a decoder can be misleading

In your question, you are suggesting to view the cell as a decoder of DNA. IMO, this is misleading. In this discussion, I will exit science and enter in the realm of philosophy (identity).

What is generally considered as the mechanism of decoding DNA is actually part of our geome itself (consider typically the importance of tRNA and rRNA). If uneasy with basic concept of gene expression you might want to have a look at an intro course such as Khan Academy from the section Classical and molecular genetics to the section Gene regulation.

Also, I would argue that all the elements that are being transmitted to the offspring shall be considered as being the offspring. If it turns out (which we actually pretty much know is wrong) that histone modification explains more in the phenotypic variance than genetic variance, it would intuitively be unfair to see histone modification as just being a decoder of the genome. We would rather be tempting to see histone modification as central and the DNA sequence as a side-effect.

Layman literature

You say "This question seems never to be seriously addressed in lay literature". Richard Dawkins book called the extended phenotype, while maybe not directly addressing your question does a good job at playing out with thee concept of environment vs gene separation. You might want to have a look at it.

Note that the laland et al. 2015 cited above is easy to read and would be a good source of information for a layman.


Is there a record of species kept in zoos worldwide and number of individuals? If yes, can one have access to it? Looking for the number and species of wild cats kept in zoos to assess the potential pool of individuals available for reintroduction programmes.

A potential data source could the data base that stores zoo animal data, where the most comprehensive (to my knowledge) is Species360 ZIMS (Zoological Information Management System). It contains animal records and current breeding programmes, but also information on how to care for animals (best-practices and studbooks).

In your case, the ZIMS for Studbooks module should be relevant, which contains:

  ZIMS for Studbooks improves Studbook Keeper efficiency and record accuracy with suggested animals, notification of records updates, and extensive data quality tools. [...] enabling users to conduct intensive population analysis, improving species and conservation management

However, I do not have access to the data base myself, so I cannot say how accessible the data is. If you are connected to a zoo, teaching institution or research facility you can however apply for access and a membership, but I don't know the specifics of this process (or possible costs). It might be worth checking out either way.


Limited space for animals - how is that bad? I am writing an English paper wherein I have to appeal for change in the way humans treat wildlife. I was initially given a situation wherein I took a ferry in a certain area and saw a dead baby dolphin.

Along the way, I (it is written in second person) apparently notice how little water is now available for the dolphins (due to some bridge being constructed).

What exactly is bad for dolphins (or animals in general) when they have limited space to roam around?

So far I thought of dolphins hitting boats due to the crowded state of the area in question.

The building of a bridge on a river seems like an example of habitat fragmentation. There are a number of reasons why this may be detrimental to the animals.

Reduced resources available. I'm not too familiar with dolphins, but all animals need food, shelter and a place to raise their young. A smaller habitat can't support as many animals due to limited resources.
Isolation from other habitats. The bridge may cut off the dolphins on one side of the bridge from the other side, meaning they can't mate with dolphins on the other side or migrate. The fact that dolphins on one side of the bridge can only mate with the other dolphins that share that size causes a decrease in the genetic variability on both sides of the bridge. Decreased genetic variability means an increase in inbreeding depression and reduced ability to adapt to disease and environmental changes.
The edge effect. This means that areas next to the edge of the habitat (i.e. next to the bridge) will be even less suitable than they were before


How does taxonomy work? The case of the Avian Dinosaurs I recently discovered that the class Aves (or Birds) has been renamed Avian Dinosaurs. My question is when this taxonomic denomination achieved the consensus of the scientific community and through witch process, this change was made.

There was a taxonomic revolution brought about by cladistics https://en.wikipedia.org/wiki/Cladistics. Willi Hennig wrote about it in 1950, but he was an East German, and his work did not gain traction in the West until it was translated into English in the late 1960s. Then it took a while to become consensus. Since then, all taxonomy is based on phylogenetic relationships. So for 100 years, we talked about "Reptiles" and knew what they were. Under phylogenetic taxonomy however, once we understood that birds were descended from theropod dinosaurs, nomenclatural rules require that birds ARE dinosaurs. This makes sense, because a Robin is more closely related to a Tyrannosaurus than a Tyrannosaurus is to an Iguanodon. Technically, taxonomy changes with the publication of phylogenies that make formal nomenclatural changes. Once a peer-reviewed paper is published, the names change. But sometimes phylogeny papers are sloppy, or wrong. So for something as major as Avian Dinosaurs, it would generally take more than just one sloppy paper to change consensus. Scientists now consider birds to be Dinosaurs. The public will continue thinking of Dinosaurs without birds. This is a difference between common names and scientific names. Birds are a subgroup of Dinosauria. Consensus depends on whether you are a scientist or not. Scientists now are at a consensus that Birds are derived from theropod dinosaurs, and therefore, ARE dinosaurs. The consensus of the public will lag behind.


How does residual chlorine in tap water work? As I understand it, residual chlorine levels in tap water are below 1mg/l in the UK. Most chlorine based cleaning products suggest at least 1% solution to be effective (quite a long way off 0.5mg/l by my maths).

Given that chlorine has a very slight disadvantage to health (albeit a tiny one), if 0.5mg/l is not enough to kill harmful bacteria, why is it there at all? If it is enough to kill bacteria, how does it do it when cleaning products require what seems to be several thousand times greater concentrations to do the same job?

Actually, I think that to qualify this statment, you should use about a 3.33% solution of household (5%) bleach for disinfecting. So that's actually, 0.15% sodium hypochlorite solution.

Also, time and pH are factors. A 0.15% bleach solution will kill many bacteria within 5 minutes. But after a few days, a more dilute solution will also have killed many bacteria.

Also, given that household bleach has a pH of around 11, a 1% solution will have a pH of about 9. The optimal pH is about 6, where all of the -OCl is converted to HOCl which is roughly 80x more effective as a germicide.

So, I realize that 0.5mg/L is still about 3000 times less than 1.5g/L (= 0.15%), and that's the real question. The real answer is that the place where the bleach is added (in a municipal supply) is at the filter, where bacteria collect. Once the old filter has been bleached the fresh water supply is allowed to resume which flushes the bleach along (at tolerable levels). Also, they often use other oxidizing agent which are synergistic with HOCl, so that they can reduce their cost and improve the function.


Do mosquitoes need to pump blood out of the host? Many species of mosquitoes have bloodsucking females.

When they bite a host, do they need to pump? Or does the sheer blood pressure combined with capillary action suffice to make the blood rush into the mosquito's stomach?
If the blood pressure is enough, can the mosquito "explode" or simply die from having too much blood rushing in?

Take a look at Ramasubramanian et al.[1] The authors have some great SEM images of the proboscis and fascicle tip and derive a mathematical model for the "bite" itself.

They mention that there are two types of feeding: pool feeding, where the mosquito creates a hemmorrhage and feeds slowly via capillary action, and capillary feeding, wherein the mosquito taps into a capillary and the feeding process is much faster, as the blood is driven under pressure.

Another source to check, one that the authors above cite, is by Kashin[2]. This only links to the abstract, however.  You'd have to hit the stacks to get the article, I'd imagine.

Edit

This source[3] indicates that:

  "The blood is imbibed by action of the cibarial and pharyngeal pump muscles via the food canal formed by the labrum and hypopharynx. Blood then passes into the midgut."

For @Luke, and others:

All images are from Ramasubramanian et al.[1]

Ramasubramanian MK, Barham OM, Swaminathan V. 2008. Mechanics of a mosquito bite with applications to microneedle design. Bioinspiration & Biomimetics, 3: 046001, doi:10.1088/1748-3182/3/4/046001.
Kashin P. 1966. Electronic recording of the mosquito bite. Journal of Insect Physiology, 12(3): 281-286, doi:10.1016/0022-1910(66)90143-0.
Robert V, Brey PT. 1998. Biting physiology of Anopholes affecting Plasmodium transmission. Research and Reviews in Parasitology, 58 (3-4): 203-208.


What are common causes of unexpected ligation products? I digested two plasmids, one with EcoRI and AgeI and the other with EcoRI and XmaI. Digests looked as expected, so I purified the respective fragments and set up the T4 DNA ligation (AgeI and XmaI sites are compatible).

After E.coli transformation, culture and miniprep from 12 of the resulting cultures, I digested the isolate from the minipreps with BclI to confirm I had the correct product (because there was one BclI site in the insert and another one in 1.4kb away in the backbone). The results of this digest clearly show that there are two different ligation products: four lanes share one banding pattern and the other eight share a pattern which is different from it.

I checked both plasmids for other restriction sites of the enzymes used which I overlooked before, but found none. Because EcoRI and XmaI/AgeI sites are radically different (AATT vs. CCGG), I would exclude the possibility of the insert being ligated in reverse orientation.

Are there any common causes of unexpected ligation variants besides unnoticed restriction sites and reverse ligation?

Could be insert polymerization.  If you have your stretch of DNA like this:

 (5')-AATTagctagcatcgtgatcgacg-(3')
          ||||||||||||||||||||
     (3')-tcgatcgtagcactagcagcGGCC-(5')

And you take that, flip it around, it will ligate onto itself, like this:

 (5')-AATTagctagcatcgtgatcgacg-(3')(5')-CCGGcgacgatcacgatgctagct-(3')
          ||||||||||||||||||||              ||||||||||||||||||||
     (3')-tcgatcgtagcactagcagcGGCC-(5')(3')-gctgctagtgctacgatcgaTTAA-(5')

This is easy enough to check for.  Just calculate the size fragments you'd expect from a vector with two inserts (there'd be an extra BcII cutsite now, and the extra fragment would probably be the size of the insert).  If this is just out of curiosity, and one of your things is the correct size, I'd ignore the ones that didn't work and go ahead with your ones that did.

If you do have a problem with it, or you are getting all your clones polymerizing, you can treat your insert with an alkaline phosphatase.  This will eat off the (5') phosphate that the ligase needs to stick the on to the (3') hydroxyl.  The result is that an insert cant bind to another insert, but once it finds a vector it will be able to ligate:

 insert to insert:    AATTagctagcatcgtgatcgacg-(3') :( CCGGcgacgatcacgatgctagct-(3')
                         ||||||||||||||||||||              ||||||||||||||||||||
                    (3')-tcgatcgtagcactagcagcGGCC  :( (3')-gctgctagtgctacgatcgaTTAA

 insert to vector:    ....ctagct-(3')     AATTagctagcatcgtgatcgacg-(3')(5')-CCGGcgacg....
                      ||||||||||              ||||||||||||||||||||              |||||||||
                      ....gatcgaTTAA-(5')(3')-tcgatcgtagcactagcagcGGCC     (3')-gctgc....

There will be nicks on the top left, and bottom right, but the bug you put it into should clean those up for you.  You can get alkaline phosphatase for fairly cheap from lots of places, NEB is always a safe bet.


Mutation Rate in Multicellular Eukaryotes I always hear people saying that the mutation rate is around $10^{-6}$ or $10^{-7}$. I don't even know if this number is the mutation rate of genes or of a single nucleotides and I actually (almost) never seen a referenced estimation of the mutation rate.

I know there is an impressive variance in mutation rate depending on the species we look at and depending on the genomic region we look at. Various other factors also influence the mutation rate such as ecological factors (thermal stress for example).

In multicellular eukaryotes, what is a good estimate of the mutation rate per nucleotide, per gene and per genome? How does real values vary around these estimates?

The real mutation rate of any organism depends by too many factors both external, like the environment, and internal, like the error rate of the DNA polymerases and DNA-repair enzymes and even from different region in the same genome (the mutation rate of non-coding DNA tend to be higher than the one of actively used DNA).

In general however it is possible to determine an average mutation rate for a given organism and usually it is expressed in mutation per base pair (or single nucleotide) per generation.
If you want to know roughly the mutation rate per gene or per genome you just need to multiply the mutation rate by the number of bases of the gene or genome.

Good papers on the topic are:

  Drake JW, Charlesworth B, Charlesworth D, Crow JF (April 1998). "Rates
  of spontaneous mutation". Genetics 148 (4): 1667–86.

  Ossowski S, Schneeberger K, Lucas-Lledó JI, et al. (January 2010).
  "The rate and molecular spectrum of spontaneous mutations in
  Arabidopsis thaliana". Science 327 (5961): 92–4.

  Nachman MW, Crowell SL (September 2000). "Estimate of the mutation
  rate per nucleotide in humans". Genetics 156 (1): 297–304.

If you want to know about some specific organism you have to dig into the literature...


Long term storage of agarose-ethidium bromide gels that have already been cast I have come up with what I thought was a clever idea: Store the agarose gels I pour, and only cut as many lanes as I need to run later, minimizing wasted agarose (and wasted effort/time) when I need to make many electrophereses using a small number of lanes.

I realized that over time, the EtBr would diffuse out of my gel into the buffer that the gels are kept in. Since I add 2 µl of EtBr to 50 ml gel, and the gels were kept in 400 ml TAE buffer, I added 16 µl EtBr to the buffer, reasoning that now concentrations are equal and no net diffusion will take place.

However, after several weeks, I noticed that the EtBr signal from the gel is severely weakened. What can I do to fix this? I can see the following options:

Use higher concentration of EtBr in the buffer (how much?)
Change buffer weekly, adding fresh EtBr every time
Cover the transparent container with aluminum foil to prevent hypothetical photobleaching

Which one is most likely to solve my problem? Should I just give up, and throw away gels that are older than a day or two (I want to avoid this option, because of the record keeping needed to track when the gel was last made)?

To increase storage life: after gel solidifies, dampen it with running buffer. Wrap the gel in polyvinyl chloride. Place in plastic container with a lid. Store in fridge in dark. It will last for a year as long as you re-dampen it with buffer each time you access it. Don't keep it submerged in buffer as the etbr will diffuse out. this is probably the cause of your problem. Notice when you order precast gels (either agarose or acrylamide) they are sealed and only a small vol of buffer is added to keep it hydrated. Additionally, the etbr and EDTA in the buffer helps prevent most mold growth although I have seen black mold grow a few times at around a year.

You can always spike the buffer with etbr adding it directly to the electrophoresis chamber before you run the gel (etbr doesn't even need to even be in the gel for it to work) although I find you get a little more sensitivity with the etbr in the gel. If you spike it be sure to mix and let it sit for about 20 min for the etbr to diffuse.

If you are trying to cut down on cost you are probably using a higher grade agarose than you really need for the application your doing so I would take a look at that

If you end up needing to store gels for rna work, add plain old Clorox bleach to a final concentration of 1% to your TAE gel just after microwaving. It sounds crazy but it works extremely well. You will completely inhibit RNAse and your rna bands will look nice!!!. The bleach also helps  with storage of the gel.


How are we able to selectively inflate our cheeks? First an observation - I noticed that I can not inflate my cheeks with my mouth open. This means that inflating cheeks is not a muscle property and that only pressure of air from lungs trapped inside my closed mouth is responsible for any inflation. Also, once inflated I can move my tongue anywhere and still retain the inflation. This means that tongue is also not responsible for air regulation inside mouth.

Moving on, we all know that we can either inflate both our cheeks, or we can inflate only cheek from one side or we can inflate *portion of face between lips and chin* (I don't know what it is actually called). Put simply, we have complete control over which part of my face would I like to inflate.

I don't understand how this is possible without muscle control? Air has tendency to occupy all space therefore my entire cheeks should get inflated without me having any control whatsoever, but as it turns out I can control and redirect the air to apply pressure only at a particular cheek without any help from tongue. How?

Muscles can only "pull" never "push" - that's just how they are organized at a molecular level. We can only push things because we use joints as levers: if you "pull" on the outside surface of your arms, you can push things out with your hands because that pull acts to extend the forearms.

It's not really possible to puff out your cheeks with muscle, because there is nothing floating in the space outside your face to pull against. Your cheeks puff up a bit when you smile, but I think you will agree that's a completely different type of "puffing" and comes from gathering up a bunch of tissue.

However, it's fairly simple to contract muscles in your face (specifically the buccinator) to prevent a cheek from bulging out by tightening the muscles in the cheek. The air pressure you are producing is pretty minimal, so it doesn't take much strength. The cheek bulges out when the muscles are relaxed, and doesn't bulge when the muscles are contracted.


What is this? Found crawling across ground under oak tree. Six arms waving, I broke off 1 trying to pick it up. Less than 1 inch long Crawled like snail.  No slime trail.  Less than one inch.  Six arms, I broke one off.

That is a Hag moth caterpillar

Don't touch.


Why doesn't cellular, replicative senescence (or the hayflick limit) constrain the normal development of an organism? The wikipedia article on cellular senescence states:

  Cellular senescence is the phenomenon by which normal diploid cells cease to divide. In culture, fibroblasts can reach a maximum of 50 cell divisions before becoming senescent. This phenomenon is known as "replicative senescence", or the Hayflick limit.

My question is, if many cells in diploid organisms (e.g. humans) have an inbuilt limit of the number of cell divisions, how is it that a human can develop from a single celled zygote to a organism comprised of many 10's of trillions of cells - if many cells can only divide 50 or 60 times?

Wouldn't the cells "use up" their available telemeres during development? or is it a simple mathematical relationship, that whilst yes, existing cells are "burning up" their telemeres as they divide during development, but because the number of cells are increasing exponentially they develop all the tissue mass the organism needs before hitting the hayflick limit?
e.g. if cell numbers are doubling during each division phase, it only takes 30 doublings to achieve a billion cells, after 40 doublings you have a trillion cells.
i.e. after 40 or 45 doublings it has developed all the tissue mass of a mature organism, and still has some telemeres left over for additional tissue generation during the organisms lifetime?

You pretty much have answered your own question. It is a math problem. Cells are burning up their telomeres during fetal development onward but the cells are multiplying exponentially in number.

But biology is a bit messy, embryonic stem cells do have telomerase activity and their telomerase are maintain. So the clock doesn't start counting down immediately.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2360127/

Temporal wise hES cells are around 4–5 days post fertilization, at which time they consist of 50–150 cells. https://en.wikipedia.org/wiki/Embryonic_stem_cell.

So you don't quite start with an n of 1 cell. But of an n of 50-150 (in humans)... before you start to see telomere shortening. With that head start those 50 doubling can make a lot more cells. By my guestimate with excel ~1.69E17 cells ~320 tons. More than enough you to last a life time.)


How is oxygen and carbon dioxide exchange mediated by hemoglobin? Oxygen is transferred by hemoglobin from the lungs to tissues, while carbon dioxide is transferred by hemoglobin from tissues to lungs. How is this regulated bidirectional transfer mediated?

Under conditions of high CO2 (in tissues such as muscle) and hence high acidity hemoglobin binds preferentially CO2, thereby mediating CO2 removal. Under conditions of low CO2 (high pH) and high O2 (conditions met in the lungs), it preferably binds O2, thereby releasing CO2. Hence, the specific characteristics of hemoglobin allow for CO2 uptake in the body, and O2 uptake and CO2 release in the lungs. Info from wikipedia on hemoglobin


What evolutionary mechanism caused felines to develop purring? And why can some felines roar while others meow?

It makes sense that the ability to express your emotions improves the quality of the interaction you have with those around you. If a cat purrs those around it know it's feeling good, which can be useful information for future interaction.

I'm sure there have been cats who had a worse life because they didn't bond as well because they didn't purr, and consequently had a slightly lesser tendency to have their DNA end up in the next generation.

This argument goes for every ability to express emotions.


What is the purpose of the adrenal medulla? The adrenal medulla is less of a 'real' endocrine organ like the others in the endocrine system and much more an extension of the sympathetic nervous system. In fact, its chromaffin cells are modified neurons by descent and secrete adrenalin and some noradrenalin upon stimulation by sympathetic preganglionic fibres, effectively turning the medulla into a sort of 'endocrine ganglion' with the whole cardiovascular system as its 'postganglionic fibres'.

Adrenalin in the circulation seems to have pretty much the same effect as all the adrenergic neurons of the sympathetic nervous system (which innervates all blood vessels, organs etc.): arteriole constriction, cardiac output increase, breath rate increase, pupil dilation, glucagon secretion and insulin inhibition, stimulation of glycolysis and glycogenolysis etc.

So what is the purpose of the adrenal medulla, if all of the effects which the endocrine adrenalin produces are essentially the same as those produced by the sympathetic mass response?

I have found the answer to the purpose of the adrenal medulla to be flexibility. Just like regulation for example of gene expression or metabolism occurs on many levels with different speeds and permanences of their effects, signalling needs to be available both quick and short-lived, and slower but with more long-lasting effects. The adrenal medulla provides exactly that.

Sympathetic adrenergic neurons are quick, but as quickly as they release their neurotransmitter, the effect is only of short duration and adrenalin is quickly cleared from the target area. Rather than giving off short bursts of adrenalin, the medulla maintains a constant systemic level of it and in response to stimulation raises or lowers that level. This response takes more time as blood circulates much slower than neurons respond, but its effects last longer.


Could someone entirely absorb smells by smelling? When smelling, your nose detects the smells by absorbing them.

Does this mean that, if you were in an enclosed space, you could smell so much all the smell goes, and there is none of that molecule left to smell?

Would it take so long it would never happen in reality, or does it happen?

On the contrary, your olfactory epithelium - the bit that does the smelling up at the top of your nasal cavity - doesn't absorb smells. The olfactory receptors bind small molecules reversibly.
However, the olfactory epithelium has a coating of mucus, and so small molecules dissolve in the mucus in order to meet the receptors. Molecules will also evaporate off this mucus, but some vanishingly small fraction of the odorant in a room may stay in the mucus of the nose and the upper respiratory tract long enough to be moved by cilia to the stomach.
I think that for water-soluble molecules, the surface area of mucus lining the airways that odorant can reach is a more relevant factor than the number of a particular receptor (which is very low); but depleting a room of an odorant (which is concentrated enough for you to sense in the first place) by breathing would surely take an extremely long time; as the concentration dropped the remaining molecules would become 'harder to catch', and you'd suffocate first in this enclosed space.
Interestingly, hydrophobic molecules that do not readily dissolve in mucus may be bound by soluble 'shuttle'-like proteins which bridge the gap to the receptors: http://www.ncbi.nlm.nih.gov/pubmed/12044155
These odorant-binding-proteins probably contribute to the diversity of molecules we can smell, and presumably also bind odorants reversibly and may release them back in to the nasal cavity.


A cure for radiation exposure? Some of the greatest inventions of my lifetime have been from looking at nature and copying. I found out tadigrades in outer space have the ability to repair their own DNA when exposed to radiation thousands of time higher than what it would take to kill a human being. Can the tardigrade's genome be mapped and the section of DNA responsible for repairing radiation damage be duplicated? Would that be a good thing? Could a stem cell with that section of DNA make our astronauts safer?

Would that be a good thing?

Recent research from the Samson lab at MIT suggests that there are side effects from amplifying the DNA repair mechanism.

Hyperactivity of a base-excision repair (BER) protein called AAG in mice caused a positive feedback loop in DNA repair signaling that triggered macrophages to attack retinal cells, leading to a cycle of increased inflammation, photoreceptor (PR) necrosis, and ultimately blindness.

From the linked paper:

In this study, we demonstrated that programmed necrosis and subsequent inflammation are important mediators of AAG-dependent alkylation-induced PR cell loss in male mice... We showed that PR cells present necrotic morphology and oxidative DNA damage after the induction of PR cell death with alkylating agents; furthermore, we observed that PARylation in the PR nuclei is associated with the release of HMGB1, increased macrophage infiltration, and elicitation of an inflammatory response.

Another research project looked at a DNA repair protein called ATM in mice, where hyperactivity or overexpression may be implicated in Alzheimer's and Huntington's diseases. Knock-down mutants show reduced expression of this protein and reduced neural damage.

Ignoring the larger ethical questions of splicing genes into human beings, and the technical questions of how to get said genes inserted, transcribed, and translated in the right place at the right time in the right way, it would likely require considerable study to see what the systematic effects might be from expression of tardigrade or other organisms' DNA repair genes in humans.

At the very least, these papers suggest that the biology is complex enough that turning up the dial on repair machinery could cause serious health problems downstream, as much as it might confer greater protection from radiation or other environmental damage.


The colour of aquatic plants found deep under oceans I have read that many aquatic plants found in deep oceans are red in colour, however, I do not understand why. As red is the color which gets the least scattered it should be the only light available to them. Thus reflecting red light would deprive them of any light. Yet they appear to be in red color. Why is this so?

You're right that certain wavelengths of light are more capable of penetrating deeper depths of water. However, it turns out, blue light typically travels to deeper depths than all other visible wavelengths of light (and red light does not travel deeply at all).

See my previous SE answer for more details about plant coloration due to this phenomenon.

So that leaves the question of why are these plants red?
Plant life itself cannot exist without the ability to photosynthesize, so actually no plants exist beyond a few hundred meters down. And in fact, many of these plants are still green (e.g., see here and here).
However, some red algae represent an example of a red "plant" (not actually a plant, but quite closely related) that can live fairly deep. According to the University of California-Berkeley:

red algae are red, "because of the presence of the pigment phycoerythrin; this pigment reflects red light and absorbs blue light. Because blue light penetrates water to a greater depth than light of longer wavelengths, these pigments allow red algae to photosynthesize.

Interestingly, this 'reddening' phenomenon is shared by many deep sea organisms, though more often for the sake of protection from predation.
Red light does not reach ocean depths, so deep-sea animals that are red actually appear black and thus are less visible to predators and prey.
See this NOAA page for more:

All objects that are not transparent or translucent either absorb or reflect nearly all of the light that strikes them. When struck by white light (containing all colors), a red fish reflects red light and absorbs all other colors.
The deeper you and the fish go, the less red the fish will appear, because there is less and less red light to reflect off of the fish. At 100 meters, red light does not penetrate and, at this depth, a red fish is difficult, if not impossible to see. Instead, the fish appears blackish because there is no red light to reflect at that depth and the fish absorbs all other wavelengths of color.


Physiology of hyperpolarization In my textbook, it is stated that after the closure of potassium voltage-gated channels and during hyperpolarization, potassium leakage channels allow potassium influx passively and this returns the cell to its normal polarised state. I don't understand why will potassium ions enter the cell against its electrochemical gradient ?

My textbook quote :

  during Hyperpolarizatio: The Leakage K+ Channels tend to drive the membrane potential from hyperpolarized state to the resting state as they drive K+ ions inward

I don't get to say this on very many occasions with questions like this...

Your textbook is wrong.

A typical potassium reversal potential in a cell is ~-90 mV. Hyperpolarization through voltage-gated potassium channels can never go more negative than that reversal potential.

An experimenter with access to the cell through a patch clamp electrode could possibly set the voltage more negative than potassium reversal, in which case indeed, potassium would flow against it's concentration gradient into the cell due to the electrical potential. It is not possible to reach those very negative potentials using potassium channels alone.

For a typical cell, the resting membrane potential is more like -70 mV. This resting potential is due to the "leak conductance", which does include potassium but also includes other ions. The ratio of sodium to potassium permeability is typically around 1:20; potassium dominates but you can't just ignore the other ions. A more accurate replacement statement for your textbook would be:

  The leakage conductances tend to drive the membrane potential from hyperpolarized state to the resting state as the net positive flow of ions is inward.

Even at rest, you will always find a slow potassium leak out of the cell. The reason that the cell is at equilibrium at rest is because this leak out of the cell is perfectly balanced by net positive charge flowing in to the cell; this is mostly sodium but can be other ions like calcium as well (note also that that chloride leaving the cell is also a net positive charge in).

Some of the sodium leak current is through specific sodium leak channels, but co-transporters that use the sodium concentration gradient also contribute.

Ren, D. (2011). Sodium leak channels in neuronal excitability and rhythmic behaviors. Neuron, 72(6), 899-911.


Had there been a non-flying pterosaur? Since there are non-flying birds and secondary non-flying insects, it is reasonable to assume there were also non-flying pterosaurs.

Well, according to this source there are no flightless bats, so it isn't an absolute that all flying clades have flightless members:

https://pterosaurheresies.wordpress.com/2011/07/21/meet-the-first-flightless-pterosaur-sos-2428/

  Everyone knows about the various flightless birds: the penguin, the dodo, the ostrich… the list goes on. There are no flightless bats. And no one has ever discovered a flightless pterosaur… until now.

But the short answer to your question is: no confirmed flightless pterosaur fossil seems to have been discovered so far.

The longer answer is: from what I can tell no pterosaur has been found that was clearly flightless, but pterosaur flight isn't well-understood in the first place so there is debate as to how and whether some specimens could have flown. It seems to be the consensus so far that they did fly however (based on the lack of mention of flightlessness on the Wikipedia page, and the last paper I link to in this answer is fairly convincing).

As far as not finding flightless specimen, the above link claims to have found one but the source is not reputable and I found no confirmation of it elsewhere (Wikipedia confirms, and I'm usually all about Wikipedia but here the page has all the hallmarks of having been written by the same person who wrote the blog). The same author argues a large pterosaur is flightless here, but their arguments are quite poor compared to others made in the field and they seem again to be the only ones making them.

Here is a post from Tetrapod Zoology in 2008 imagining what a flightless pterosaur might be like, and also claiming none have been found:

  Long-time readers will know that I am an unashamed fan of both speculative zoology, and of Dougal Dixon’s hypothetical ‘alternative’ animals. Inspired by a comment made here in August by Jenny Islander, I have been having a re-think about the possible evolution of flightless pterosaurs: the fossil record gives no indication that such animals ever existed, and maybe they didn’t, but that hasn’t stopped people from speculating.

A similar quote from the 2004 book "Posture, Locomotion, and Paleoecology of Pterosaurs":

  So far, there is no example of flightless pterosaurs.

The Wikipedia page for pterosaurs makes it clear how hard it is to figure out how pterosaurs flew.

Here is one of the main arguments that the largest pterosaur Quetzalcoatlus northropi was flightless

  The estimated mass for the largest pterosaur known, Quetzalcoatlus northropi, exceeds the previous highest estimates by more than 100%, and it is argued that this extremely large pterosaur is better interpreted as a secondarily flightless form.

And an argument that the largest pterosaurs would have been flightless based on a comparison to modern oceangoing birds:

  Our result therefore casts doubt on the flying ability of large, extinct pterosaurs. The largest extant soarer, the wandering albatross, weighs about 12 kg, which might be a pragmatic limit to maintain a safety margin for sustainable flight and to survive in a variable environment.

This paper summarizes the debates and argues against those assessments (the whole paper is worth reading actually):

  While the conclusions on giant pterosaur flight by Chatterjee and Templin [19], Sato et al. [17], Henderson [25] and other workers using avian analogues for pterosaurs are not without merit, we find that they leave themselves open to criticism by not considering alternative data sources when making inferences about the palaeobiology of extinct animals. Giant pterosaur anatomy, functional morphology and, in the case of Pteranodon at least, sedimentary context all indicate that they were flighted animals and, likewise, clear anatomical distinctions between birds and pterosaurs indicate that only basic mechanical details can be treated interchangeably.


How do marine mammals and penguins maintain bone density? After much searching on Google with no results, I decided to ask my question here.

If I'm not mistaken, swimmers' bone density is less than normal; at least for lifetime swimmers. Astronauts also lose bone mass from the lack of stress (from gravity) on their bones; it stands to reason that being in the water and thus being weightless, would lead to bone loss.

So my question is, how do marine mammals and penguins maintain their bone mass?

I wouldn't refer to it as "bone loss" but more as bone strength. Lifetime swimmers spend a lot of their time in the water. As in water yes they are almost "weightless" and their bone strength will decrease because it has gotten used to the "low" gravity. Now in the case of penguins and other Marine mammals, they have adapted to the force that the water applied to them.

Here is a link to a picture of penguin's flipper.


Time needed for transcription of DNA How much time would it take to complete the transcription of an average-sized human gene?

From Bionumbers, the average transcription rate of RNA Polymerase II is about 3.8 kb/min. Other researchers measured it as 6.3 nucleotides/sec, or 378 bp/min, a 10-fold decrease. In the same paper, however, they measured the maximum rate at 71.6 nucleotides/sec, or 4.3 kb/min. To figure out the differences between the measurements, I suggest reading the paper, but since it's from Nature Publishing Group you'll have to pay for it, unless you're at a subscribing university or institution (or someone posts the paper in the comments <hint hint>).

So, the answer to your question, like most simple questions in biology, is it depends. It likely depends on the size of the gene, its structure, what transcription factors are necessary for the assembly of the polymerase complex, and, last but not least, exactly how and when you measure. Transcription likely initiates in fits and starts, then gets going faster. This is similar to (but not exactly like) measuring the speed of your car from Point A to Point B. Are you starting from a dead stop, or passing the starting marker at speed? Do you have to start the car first, or is it already running? How many turns and other slowdowns are on the road? Do you stop measuring as the car passes the finish marker, or when it comes to a complete stop? All of these things figure into the final answer, and the result given is entirely dependent on the scientists' choices of methodology.

If you are interested in a broader discussion, I got started on this page at Bionumbers.


Why is the administration of exogenous Anti-D not harmful to the foetus? Haemolytic disease of the newborn can result from Rhesus incompatibility in utero.  In this disease an Rh- mother becomes exposed to the antigens of an Rh+ foetus by fetomaternal haemorrhage causing her to mount an immune response against the D antigen.  In her second pregnancy, repeat exposure to the D antigen activates memory cells causing a large production of IgG Anti-D antibodies that cross the placenta adhering to foetal red blood cells, which are then destroyed.
To prevent this, Rh- mothers are normally given exogenous Anti-D at 28 and 34 weeks gestation or after any sensitising event.  The aim of this treatment as I understand it is to 'mop up' any D antigen in the maternal bloodstream, covering it in exogenous antigen so the mother's immune system does not mount its own response.
I had previously assumed that these exogenous antibodies would be IgM to avoid them crossing the placenta, however looking at the summaries of product characteristics for some of the common preparations I see that "at least 95%" of protein content other than albumin is IgG.  I then wondered if the exogenous antibodies had a much reduced half life, however the half life is "about 3-4 weeks."
Why does the exogenous IgG not cause haemolytic disease of the newborn in the exact same way that endogenous IgG would in a previously exposed woman who had not had prophylaxis?  Is it dose-dependent or am I missing something entirely?

I've had a difficult time getting anything definitive to support my answer to your specific question of safety, however, I thought I'd go out on a limb and give you my understanding. A recent review of what is known about this can be found at: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2809506/

I think you are on the right track with your 'dose-dependence' hypothesis. This is exactly what the makers of RhoGAM suggest, saying that the amount of antibody administered at 28 weeks into the pregnancy is sufficient to block any Rh antigen on Red Blood Cells that escape into the mother's blood, but insufficient to cross the placenta and be a problem. At this time the child will be large enough that any RhoGAM that does cross the placenta will not kill enough Red Blood Cells to harm the child.

Mom gets another dose of antibody after the delivery in order to ensure thorough coverage of antigen that results from mixing of blood at that time, however this dose is not a problem as the baby has already left the mother.

By the way, the rationale for the antenatal dose is that post-partum administration alone failed to prevent sero-conversion in almost 2% of Rh- women, putatively due to transplacental hemorrhaging.


Approx 1cm, white and brown insect feeding on fruits, what are they? I found these insects yesterday that were feeding on a guava that I left outside for days. We have a tropical climate here (Mauritius). These insects are about 1 cm long. They have a white abdomen, brown wings, 6 long legs and they have segmented bodies divided into three regions: head, thorax and abdomen. Can someone help to identify them. Thank you in advance.

The picture isn't really focused on the insects. I think those are Crane Flies.  Crane flies have small club like appendages under their wings called halteres,which are used for steering in flight.I dont know the genus or species of these insects. The order is Diptera, the family is Tipulidae. Here are two links.
[https://www.orkincanada.ca/pests/flies/crane-flies/
[https://simple.wikipedia.org/wiki/Crane_fly


Why do predatory mites have to be introduced multiple times? I'm combating spider mite infestation using either Phytoseiulus persimilis or Amblyseius californicus. After extensive study of the literature, I'm still unsure why the producers of these predatory mites suggest that they have to be introduced several times (2-3 times depending on manufacturer). I know that adult predatory mites are very agile and scout for new prey. Phytoseiulus is also known to wipe out spider mite populations. So as long as spider mites are present, why should one introduce them at intervals rather than just introduce a large number of predatory mites at the beginning?

You are right that ideally it should be enough to apply them once, but predatory mites seem to be quite sensitive: If it gets too cold or too hot or the moisture is too low, they might die.
I applied several rounds of predatory mites in non-optimal conditions without any success. They just kept disappearing without any effect whatsoever. Funnily, some small type of Heteroptera came to save my plants. (from nature without my doing)
Next time I would try some Chryson instead.


What is a chromosome? I read the wikipedia article and am confused if a chromosome is the pair of two chromotoids or if each chromatoid is considered a chromosome.

I've heard someone say we have 23 pairs of chromosomes for a total of 46 chromosomes.

I am trying to be precise with my words here.

Even more confusing they always seem to pick this certain state of the chromosoes lifepsan to describe them.

The point at which it replicates to create a pair.

Why not just describe the chromosome before it replicates for simplicity sake.

Would it be correct to say that before the chromosome divides, there are simply 23 of them?

Would it be correct to say that before the chromosome divides, there are simply 23 of them?

No, in a normal, non-dividing cell of the human body there are 46 chromosomes in the cell's nucleus. The 46 chromosomes are separate, but are often considered as 23 pairs of chromosomes.  The two chromosomes of a pair are called homologous chromosomes because they contain very similar, but not quite identical, information.  One member of each pair comes from the mother and one from the father.

Each of these non-dividing chromosomes effectively consists of a single chromatid, but because there is only one, indistinguishable from the chromosome as a whole, it is not talked about.

  Why not just describe the chromosome before it replicates for simplicity sake.

It is often described in that form (as one very long molecule of double-helix DNA).  However, a chromosome is also very commonly illustrated in the mid-replication form where it has two chromatids and takes an X-like shape.  One  reason for this is that chromosomes can be seen in a light microscope only in this mid-replication form, and that is the form in which they
were first observed and first shown to be the basis of heredity (long before they were known to be composed of DNA).


Good book on Origin of Life What is a book that goes into reasonable detail (but isn't textbook-level technical) about the origin of earth and in particular the origin of life on earth? Something intended for a broad audience, but that still covers the biology/geology and does not completely gloss over the sicence.

I would recommend The selfish gene by Richard Dawkins. It is targeted at a scientifically interested audience, but well written and recognized by the scientific community.

http://amzn.com/0199291152


Why do some bad traits evolve, and good ones don't? If a trait would be advantageous to an organism then why hasn't it evolved yet?

Conversely, if a trait is not advantageous or mildly disadvantageous, why does it exist?

In other words why does evolution not make the organism more "perfect"?

This is a general question that would be applicable for any kind of trait. Please keep the answers precise and scientific.

Read this meta post for more information: Questions asking for evolutionary reasons

During the process of selection, individuals having disadvantageous traits are weeded out. If the selection pressure isn't strong enough then mildly disadvantageous traits will continue to persist in the population.

So the reasons for why a trait is not evolved even though it may be advantageous to the organism, are:

There is no strong pressure against the individuals not having that trait. In other words lack of the trait is not strongly disadvantageous.
The trait might have a tradeoff which essentially makes no change to the overall fitness.
Not enough time has elapsed for an advantageous mutation to get fixed. This doesn't mean that the mutation had not happened yet. It means that the situation that rendered the mutation advantageous had arisen quite recently. Consider the example of a mutation that confers resistance against a disease. The mutation wouldn't be advantageous if there was no disease. When a population encounters the disease for the first time, then the mutation would gain advantage but it will take some time to establish itself in the population.
The rate for that specific mutation is low and therefore it has not yet happened. Mutation rates are not uniform across the genome and certain regions acquire mutations faster than the others. Irrespective of that, if the overall mutation rate is low then it would take a lot of time for a mutation to arise and until then its effects cannot be seen.
The specific trait is too genetically distant: it cannot be the result of a mutation in a single generation. It might, conceivably, develop after successive generations, each mutating farther, but if the intervening mutations are at too much of a disadvantage, they will not survive to reproduce and allow a new generation to mutate further away from the original population.
The disadvantage from not having the trait normally arises only after the reproductive stage of the individual's lifecycle is mostly over.  This is a special case of "no strong pressure", because evolution selects genes, not the organism. In other words the beneficial mutation does not alter the reproductive fitness.
Koinophillia resulted in the trait being unattractive to females. Since most mutations are detrimental females don't want to mate with anyone with an obvious mutation, since there is a high chance it will be harmful to their child.  Thus females instinctually find any obvious physical difference unattractive, even if it would have been beneficial.  This tends to limit the rate or ability for physical differences to appear in a large & stable mating community.

Evolution is not a directed process and it does not actively try to look for an optimum. The fitness of an individual does not have any meaning in the absence of the selection pressure.

If you have a relevant addition then please feel free to edit this answer.


Why are market squid attracted to fishing lights but also avoid naturally lit surface waters during daytime/full moons? Squid fishermen use really bright lights (which can be seen from space!) to attract squid to the surface at night, but a lot of squid also naturally avoid surface waters that are lit during the day (by the sun) and at night (by full moon). As far as squid are concerned, what is the difference between the bright artificial lights and diffuse light that naturally occurs?

Despite many sources stating that the lights attract the squids, the explanation given here is much more logical. Squids feed of small fish, crabs and shrimp, which in turn feed on plankton. Zooplankton is known to migrate vertically during the day (up at night, down during the day), which has also been reported for squids, probably following their prey.

The reason for this migration is that zooplankton feeds on phytoplankton, which can be found at the sea surface, where it gets most of the sunlight. During the day the zooplankton stays in deeper waters, because at the surface its easier to be spotted by predators. It's safer to move up during the night to feed. Other predators feeding on zooplankton follow, including the squids.

The vertical migration might be coordinated by an internal clock rather than light. It would therefore not be inhibited by the bright fishing lights. The squids don't seem to respond to the light, but rather to their prey.

Therefore, rather than attracting the squids directly, the fishing lights will attract phytoplankton, which attracts zooplankton and small fishes, which attract squids.


DIfference between diversification and differentiation In Adaptive dynamic :

what is the difference between Ecological Differentiation and Ecological Divergence ?

As already said in a comment: I would guess that ecological divergence emphasizes on the process of speciation by niche differentiation while ecological differentiation emphasizes on the process of niche differentiation due to overlapping niche of non-necessarily closely related species.

But looking to some articles, it seems that they use both term without making any difference. As found on this article for example.

Therefore, I would rather advice to no consider too much difference in meaning between ecological divergence and differentiation. But take time to define accurately the words you're using, especially if you talk about cases that fall on the border of two concepts!


What is the name of this species which I found in an Epipremnum (Money Plant)? I found a very rare specie (at least from my knowledge of species and research) today in a money plant (Epipremnum plant) in my kitchen garden. This caterpillar was on it. Please help me with the name of this species and any information about it.

The caterpillar in question is a kind of hawk moth caterpillar, most easily noticed by the pair of "eyes" on the thorax. From my experience with hawk moth caterpillars though, they generally have multiple sets of eyes, and so, this one was somewhat difficult for me to ID (not to mention a location has yet to be provided).

Looking at the OP, other defining features include: unique pattern on thorax; repeating triangular pattern on dorsal; a single tail; stripe along each side of the abdomen; overall coloration.

That being said, I believe this caterpillar is of the genus Eupanacra, and is most likely of the species E. elegantulus.

Such well defined patterns on the OP suggests full maturity. Consider the following instar sequence, and notice how the emergent patterns converge to the OPs.

images source

After undergoing pupation, the caterpillar will transform into the following:

And then, here's a distribution map.

source