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How do animals end up in remote areas?
I was thinking specifically about random marshy water holes on farmers fields. It seems that you can visit just about any one of these and you will find frogs if you look hard enough.
They usually don't seem to be connected to each other. If it were any other land animal I would figure they walk from one spot to another, but in the case of frogs, I don't imagine their range is very vast. But often these marshy spots can be separated by fairly large distances to a frog.
So this brings me to my question: how do each of these spots end up with frogs in them?  I don't imagine a frog is going to go hopping over a hill to get to a marsh on the other side, is it?

The same with fish - how on Earth do they find their way to isolated lakes?! ! I love this question. +1

I have read that hurricanes can carry animals up into them and displace them. https://en.wikipedia.org/wiki/Rain_of_animals#Frogs_and_toads

First, i would look at statistics:
just because (hypothesis) you visit 1000 watering holes /marshes a year and they have frogs in them it doesn't mean that its a common occurrence; Second, i think froglings (yeah, i know :D ) hatch whenever there is rain, grow, mate and deposit new eggs that survive droughts. Now, these can be relocated by earth movements and birds and wind (i don't think frog rains could help with this level of dispersal).
Basically, they don't end up in remote areas; They were already there in some form.

I think you should narrow down the question (question title) to frogs (if you are mostly interested in those), or a group of organisms with similar biologies. "Animals" is too unspecific, and answers will differ widely between organism groups (e.g. birds, rats, frogs, dragonflies, fish etc), so the question is "Too broad".

You should clarify how great is the distance between two nearest habitats for a certain organism. Frogs can move about in some range. Sometimes their eggs or tadpoles can get washed away with runoff water to land up in distant places.

You would understand it much better when you consider the fact that your question encompasses a geographical aspect more than a biological one, the biological aspect being the creation of a new habitat. Migration/dispersal of offsprings from their parents depends much more geographical aspects such as lay of the land or climate. These links may be of some interest. http://goo.gl/JL1vp3 , http://goo.gl/agcr0d , http://goo.gl/6vb6yp

@Koustav, yes it seems to make more sense being dependant on droughts and floods rather than by glaciation as suggested by MattDMo. Your comment would be better as an answer.

If you are a creation believing person, then the universal flood clearly gives the answer you are seeking about fishes @AliceD

@OneFace - I'm not and if I were, it still does not explain why fishes inhabit new puddles formed after the universal flood :)

This question pertains to organism dispersal, which is a very active field of study with relation to it's impact on conservation efforts. Much of what I will say below has been covered in this wiki.
Definition: From the Wiki

Technically, dispersal is defined as any movement that has the
  potential to lead to gene flow.

It can be broadly classified into two categories:

Density dependent dispersal
Density independent dispersal

The question of frogs and fishes both refer to Density independent dispersal, while an example of density independent dispersal can be the competition for habitat space between big cats and humans (this is a WWF pdf)
From the wiki:

Density-independent dispersal
Organisms have evolved adaptations for dispersal that take advantage
  of various forms of kinetic energy occurring naturally in the
  environment. This is referred to as density independent or passive
  dispersal and operates on many groups of organisms (some
  invertebrates, fish, insects and sessile organisms such as plants)
  that depend on animal vectors, wind, gravity or current for dispersal.
Density-dependent dispersal
Density dependent or active dispersal for many animals largely depends
  on factors such as local population size, resource competition,
  habitat quality, and habitat size.

Currently, some studies suggest the same.
This study in particular studied the movement and habitat occupancy patterns within ephemeral and permanent water bodies in response to flooding. They found that during flooding these frogs moved out to flooded ephemeral water bodies and later on moved back again to the permanent ones.
Other suggested readings for those highly interested in the subject may include this (a phd thesis) and this (a project report)

I don't imagine a frog is going to go hopping over a hill to get to a marsh on the other side, is it?

Why not? In wet weather, the conditions would be just fine for an enterprising amphibian to go exploring, perhaps driven by predators or lack of available resources, not to mention Ro Siv's comment about wind-borne dispersal of animals. Birds of prey may also pick up small animals, fly away with them, then drop them for whatever reason.
You are also neglecting the fact that these organisms have existed for millions of years, and the landscape has changed tremendously in that time, with glacial periods interspersed with interglacials every 20-50,000 years or so. As glaciers melt, large lakes form, and as those dried the organisms were dispersed across the land into smaller bodies of water. Streams and rivers form, transporting aquatic life forms, and may dry out and form isolated ponds, or they may be blocked for any number of reasons (mudslides, earthquakes, volcanic eruptions, beaver dams, fallen trees, etc.). As erosion and landscape remodeling occur, all traces of the original body of water may be erased, except for the wide distribution of similar organisms.

Yes, but marshes have come and gone on an almost yearly basis (or over several years, maybe a decade or so). We're not talking eons here.

@Octopus marshy areas tend to remain marshy areas over the short term (decades to centuries) unless acted upon by an outside force, such as the rerouting of a water supply or human activity. I'm not sure what you mean by coming and going on an almost yearly basis - could you give some examples? Also, as I mentioned in my answer, during prolonged wet weather (maybe over a week or more), frogs and other amphibians could travel relatively long distances with ease. I'm not terribly close to wetlands, yet I often find frogs in my yard during/after a long rain that are no longer there when it's dry.


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Risk of autosomal dominant disorder
What can you conclude about the risk (with each pregnancy) that a couple could have a child affected with an autosomal dominant disorder if...
One parent is affected (heterozygous) and the other parent is unaffected.
I did a punnet square and concluded it was 50 percent because half were Aa and half were aa.
But a classmate told me to line up Aa and aa and conclude that there is only a 25 percent chance that a child is affected because there is only one capital or dominant A and three are "a".  Which do I do?

Your classmate is forgetting that the child will have to inherit one allele (A or a) from each parent. Suppose the dad is affected---so his genotype is Aa. He has a 50% chance of passing the A on to his kid. That means the kid has a 50% chance of being affected.
If your classmate was right, then it would be possible for both the kid's alleles to come from just one parent. You have to pick one allele from each parent.

Agree with the answer by @A.Kennard. Here's a punnet square to clarify your answer further.

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Ebola: cleaning of protective suit
As far as I know, in developed countries protection suits used by people who treat patients with Ebola are disposed of after a shift.
From a rather ambitious costume last year, I still have a hazmat suit like this one and this full-face gas mask.
More out of curiosity than out of real concern, I was wondering whether it would be possible to use this equipment in a potential outbreak of the virus. My greatest concern would be reusing the suit, as it might not be safe after the first use.
Is there a way to disinfect the suit and mask with publicly available chemicals? For example, I could imagine a friend spraying me with a solution of chlorine. Would that be feasible and make wearing the suit reduce the risk of an infection?

You cannot disinfect the filter of a gas mask. If these get wet, they will become more or less impassable for air.

Then the question would be extended to whether wiping the mask with some disinfectant would be enough, instead of pouring something over it.

Disinfection is not so much a matter of the amount of disinfectant used but of the time it has to be active and of the active concentration.

And please remember that the likelihood of a real ebola outbreak in a developed country with modern healthcare system is extremely low. And in the rare event that an ebola outbreak does occur, you're probably better off avoiding physical contact with people than trying to wear a hazmat suit all day.

Notice: the only select agent I've worked with is VSV which was a USDA select pathogen (not as big of a concern for humans).
TLDR:  It would provide some protection, but I would be most worried about a false sense of security.  It would unlikely be up to rated standards, but it would likely be better than a t-shirt.
First let's start with ebolaviruses.
Ebola, like HIV and many other viruses, doesn't do well outside a host.  This might be because the protein structures beneficial in the host are not the same as needed for stability in exposed air and room temperature.  A counter example of a very stable virus would be something like human rhino virus (HRV).  If HRV was compared to be like a rock, ebola would be over cooked spaghetti.
Certainly the virus has to maintain some stability in the environment, otherwise it wouldn't succeed evolutionary.  As I'm sure you've heard on the news, ebola is spread by contact with contaminated fluids.  I would like to point out a wonderful info-graphic that was made for public consumption, especially the image on viral life cycle:

Assuming that you're not going splunking in bat inhabited caves in West Africa, it's safe to assume that what we are worried about is human to human transmission through infectious fluids.  Ebola actual isn't that stable in water, so just soaking a surface in water and a little oil might help you out (if you don't have bleach handy).  I want to be clear that I'm not recommending this, in reality you should just avoid contaminated objects.  I think that we have clearly established that what we're really concerned about is infectious bodily fluid.
This leads me to the wonderful note by Jose Martin-Moreno titled "Is respiratory protection appropriate in the Ebola response?"  I don't think I can express the problem better than he can, so hopefully I will be allowed a substantial quote:

This transmission [of ebola] occurs via close family contact or in
  health-care settings, particularly when placing orotracheal intubation
  or when caring for a patient who is vomiting or bleeding. Ebola is
  rarely transmitted via an airborne route. Although these routes of
  transmission are well known, most agencies, including governmental
  agencies responsible for repatriating western patients, apply
  infection-control measures appropriate for airborne diseases.
  Excessive precautions could offer reassurance to those responding to
  Ebola, yet complete respiratory protection is expensive,
  uncomfortable, and unaffordable for countries that are the most
  affected. Worse, such an approach suggests that the only defence is
  individual protective equipment, which is inaccessible to the general
  population. Moreover, the image of workers with spectacular protective
  clothing might contribute to the panic in some communities. If this
  leads people to flee affected areas it could increase the spread of
  infection.

With that said, all your full face gas mask is going to help with is prevention of fluids from hitting your head.  You could probably take the actual filters out to breath more easily (I find breathing in them a giant pain).  And as @Chris pointed out, they are easily clogged which could necessitate the need to take off the whole mask (which might be doing some good) to prevent suffocation.
Moving to hazmat suit.
It's actually good news that you don't need the air containment of the suit, as that's the hardest element to maintain.  To state the obvious, the main purpose of the suit is to prevent your body from coming in contact with infectious fluids (in this case).  To do that you don't need to be in positive pressure personnel suit (PPPE), or follow BSL4 considerations.  The respiratory concerns from in an BSL4 environment come from other select agents, and the personal working in such a facility are going to be doing very different activities from what you should be doing as person trying to avoid an outbreak (they could be purposefully growing up purified high-titer virus stocks and running around with pointy things as an example).
Here I'm going to run into citation problems because no one (that I could find) has tested the kind of scenario I'm about to discuss, so it should be seen as informed conjecture.  Assuming yous suit is actually an analog of a Tychem QC suit, it's probably not a rated OSHA unit (A-D), but that doesn't necessarily matter.
On it's first use it would likely be sufficient to protect against incidental exposure.  Let's assume for the sake of argument that you didn't run into any Ebola when you used it as a costume, and don't the next time you put it on.  At this point decontamination (decon) isn't the concern, failure of the material is.  In other words, are you sure you don't have any holes, tears or cracks in the material?  I think this is going to be the real limiting factor in the life of the suit.  Using good old fashioned duct tape will be give you a few more uses, but the suits are just not designed to last through prolonged use.
Now let's assume the worst and that you get substantial blood splatter on you (while wearing your suit) from an ebola patient.  And not a little that could easily be wiped of with a spray bottle of 10% bleach and a paper towel (how most decon could be done).  Instead let's assume you're standing next to someone who suffers a traumatic injury on top of having ebola virus disease (EVD).  I'm imagining something like a point-blank shotgun wound or, given the probability of this scenario, a falling grand piano. In this case, you're going to want to decontaminate the suit before you take it off, which is the same thing professionals are going to do.
If you're friends with your local fire department, and you live in an area with a large enough population to have a HAZMAT team, you can probably get them to at least give you a run through of how it's done in ideal conditions.  YouTube videos are also not hard to find, just search JESTC and decontamination.
Presumably you would have a hard time going through several rinse and wash steps, but you would want emulate this as much as possible.  With ebola, you would be fine to decontaminate with a 10% bleach solution (or if you use bargain/cheap bleach 15%).  The trick is that you would want to do it a few times, and with a friend (also hopefully in a suit).  Thus if you got two generic soap sprayers, filled one with 10% bleach, and the other with water, and then alternated spraying your partner with bleach and water, wiping down as you went, you should be able to decon the suit pretty well.  If possible you're going to want to collect all the run off an rinsate.  Again professionals tend to use actual kiddie pools for this.
But just the act of using so much bleach on the suit is going to weaken the fabric, again leading to the principle problem of failure of the fabric. Thus I would be worried that such a suit would provide a false sense of security, leading one to go into dangerous infectious environments when one shouldn't.  Just avoiding and going away from contaminated individuals is going to be the best solution, regardless of a suit.
I considered going into why I think it's highly unlikely that any of the ebolaviruses would evolve to be airborne, but I consider that outside the scope of the question.

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Please identify organ

This is the gut area of an Eastern Grey Kangaroo taken of a property in the Southern Highlands of NSW, Australia. The top red organ appears to be the spleen but what is the elongated tubular organ extending from the spleen? Is it a deformation or the result of disease?

You are aware that all species of kangaroo are protected?

You mean the long red "tube"? At a guess I'd say it just looks like a lobe of the spleen.

Thank you vervet for your response and thank you for clarifying the issue with AliceD. This kangaroo was taken on a cattle farm under the following provision: http://www.environment.nsw.gov.au/wildlifelicences/OccupierLicences.htm

An evidence? http://www.appendicitis.pro/the-sir-frederick-treves/sir-frederick-treves/the-dissection-drawings-of/brush-tailed-kangaroo-gi.html

As far as it can be deducted from the picture you ask about Appendix or just Coecum. This is a normal finding and not abnormal one. (You can see a terminal Ileum as well).
If other pictures were provided it could be possible to give more exact answer.

I don't know if the question is asking about this organ or the extention of the spleen. But in any case here is some information on the kangaroo "appendix": http://onlinelibrary.wiley.com/doi/10.1111/j.1420-9101.2009.01809.x/full It's perhaps more blown up than it would be in a living animal, but that's probably a post mortem change as there's still living bacteria in the GI tract producing gas.

I was under the impression that macropods did not have an appendix


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Understanding David Chalmers claims on direct mappings between our vision and visual awareness systems
I am reading the popular 1995 paper "Facing Up to the Problem of Consciousness" by David Chalmers [PDF] as part of my philosophy course. I am only asking about the relevant vision related claims Chalmers makes, so you need not read the full paper.
In the section 7.1 (emphasis my own):

The properties of this [complex three-dimensional] space can be recovered from information-processing considerations:
examination of the visual systems shows that waveforms of light are discriminated and
analyzed along three different axes, and it is this three-dimensional information that is
relevant to later processing. The three-dimensional structure of phenomenal color space
therefore corresponds directly to the three dimensional structure of visual awareness.
This is precisely what we would expect. After all, every color distinction corresponds to
some reportable information, and therefore to a distinction that is represented in the structure
of processing.
In a more straightforward way, the geometric structure of the visual field is directly
reflected in a structure that can be recovered from visual processing.

"Awareness" is defined (earlier in the same section) as:

...the contents of awareness are to be understood as those information contents that are accessible to central
systems, and brought to bear in a widespread way in the control of behavior. ... Awareness is a purely functional notion,..

So, I believe visual awareness refers to "how visual signals are processed in the brain".
Chalmers gives vision only for example, as he states that "It is also a central fact that to each of these structural features, there is a corresponding feature in the information-processing structure of awareness." - that is - he generalizes these to all perceptions. However, we can restrict our question to vision for now.
Note the phrases I have emphasized in bold. From what I understand, Chalmers is claiming:

direct correspondence, in that 3D structures in real world ("three-dimensional structure of phenomenal color space") form 3D structures in our brain ("three dimensional structure of visual awareness").
the "geometric structure of the visual field" is directly reflected inside our brain in some structure, so that the original geometry can be recovered from this structure.

I wish to ask for biological justification/backing of these claims.
From what I understand, our two eyes receive 2D data, and our brain combines these (slightly offset) 2D images to produce 3D (depth) sensing. Our perceptional ability is severely limited, and it is only because of a lot of "postprocessing" done by the brain that we form our perceptions. This is also the reason why we often perceive motion in changing static images (animation) or are confused by optical illusions (for example, perceing 3d from 2d images on paper, and many more).
My points are similar to the ones raised by Torbjörn Skytt in their paper "The "hard problem" of consciousness is a dead end" (link).
I am not arguing against the claims. But, I am unable to reconcile these claims ("direct reflection" and "direct correspondence") with the day-to-day observations outlined above. Moreover, Chalmers claims that these are "central fact"s, however, I do not find them to be so obvious. If I can get some clear perspective/stand on these claims, it would be helpful.

I'm pretty sure from the context of your quote that Chalmers is talking about color vision here, not depth perception, and it is the information that is three-dimensional, not the physical representation in the brain. In any event, I think you could start with an undergraduate neuroscience textbook, I usually suggest either Purves or Kandel, if you want to know more.

As Bryan alludes to, the 3 dimensions Chalmers is talking about are not height, width, and depth, but hue, saturation, and intensity.

Hey @BryanKrause and mgkrebbs, thanks for the response. Indeed, I completely misunderstood what was being said. I'd be happy to accept your answers if you post them. Thanks.

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What is the rate of mRNA decay in saccharomyces cerevisiae?
I am just looking for a number whether that is a mean or an estimate. I am having trouble finding this value on papers because the papers mention only the methods for calculating such a value. Is there a reason why a reasonable mean is hard to obtain?

It is highly variable. Do you want the range? Did you check BioNumbers?

Here is my best attempt at answering this question:
The median mRNA degradation lifetime is roughly 20 minutes in the case of yeast. Also, the total transcription for RNA pol II in a yeast cell growing in standard conditions is about 60200 mRNAs/h. I am going to go ahead and suppose that the transcription rate is constant throughout time. Thus we have that total transcription rate is equal to 1003 mRNAs/min. Furthermore, I am going to make the rough approximation that all mRNAs live exactly 20 minutes. Therefore, mRNAs will start degrading after 20 minutes. In one hour, 1003 mRNAs will degrade every minute for 40 minutes. It follows that the rate of mRNA decay in yeast is roughly 40120 mRNAs/h.

Now I understand why it is so hard to find a specific number...

in practice nearly everything about the mRNA sequence may cause the rate to vary from mean values.  That includes the sequence itself, the rate of translation, motifs within and outside the coding region that bind to some proteins etc etc.


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How to name such grouping behaviour?
Under which keyword would you try to find out more about the grouping behaviour which looks like this? Does anybody recognizes such behaviour, or know an animal species which uses it?
My tries: threshold group behaviour (threshold here is the group size - if bigger than 5 individuals == stable), or gravitational group behaviour?

After step 6 the group disintegrates (for example due to foraging) and mechanism starts by step 1. Important thing is that the location of forming stable group is always different.

You can check this paper out. I used the keyword "pack size threshold"

Hi @WYSIWYG! Close, but no cigar. Did you know any other examples?

While I don't think it's precisely the behaviour you are asking about, you might also be interested in slime molds (e.g., Dictyostelium or Myxogastria). They start out as motile single cell organisms, have limited 'vision' (chemical cues), coalesce into a large multicellular structure when resources become limiting, and then disperse from (usually) a fruiting body.This is an example of "emergent collective behaviour".
Other searches you may want to try are "Biased random walk models" and "Shoaling behaviour".
Although pretty heavy, these papers may contain a formal mathematical description of the model you are after:

Akira Okubo, 1986, doi: 10.1016/0065-227X(86)90003-1
Angela Stevens and Hans G. Othmer, 1997, doi: 10.1137/S0036139995288976

After reading about emergent behavior and previously shoaling(aka schooling), I don't think those apply. When I answered this question, I original did some digging into schooling as well but concluded it doesn't fit. A discrete agent based model can be represented as a random walk so you didn't add anything new.

I believe it is a type of fission-fusion society or even some hybrid with agent based modeling.

In ethology, a fission–fusion society is one in which the size and composition of the social group change as time passes and animals move throughout the environment; animals merge (fusion)—e.g. sleeping in one place—or split (fission)—e.g. foraging in small groups during the day. For species that live in fission–fusion societies, group composition is a dynamic property [fission-fusion society].

A classical example is the Bonobo or pigmy chimp.

Bonobo - Pigmy Chimpanzee
Sociobiology
The Social Behavior of Chimpanzees and Bonobos


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Does sociality evolved before or after the ability of motility?
According to book Life Ascending: The Ten Great Inventions o Evolution.
(Lane, N.;2010),

Motility has indeed transformed life on earth in ways that are not
  immediately apparent, from the complexity of ecosystems.

As I understand it, when animals had begun to actively use their bodies to locate resources and thus left the sedentary way of life the amount of information they received has increased exponentially. It induced the rapid evolution of additional physiological, morphological and behavioural adaptations such as specialized brain regions enabling spatial memory, vision or cognition.
Was sociality also additional adaption induced by motility?
Is sociality as a life strategy present only in mobile animal species, or they exist also a social sedentary organisms?
Working definition of sociality: Forming of animal group where information transfer enable cooperation among individuals.

I think a working definition of sociality would be useful, since the question covers a large range of organism types.

Hi @fileunderwater. An edit was made, I hope this definition of sociality is sufficient.

@LadislavNado The question is interesting but it indeed deserves some definitions to be correctly addressed. Would you consider multicellular organisms to be a society of cells? The concept of motility also needs a working definition. For example, sponges are motile in the sense that they have cells with flagellates (and they can follow a chemical gradient). Bacteria are motile as well.

Do you restrict your question to animals or do you welcome consideration from other clades? Note that plants produce GLV (Green leaf volatiles) to warn other plants from predators which really seems to be a cooperative action.

I'm going to hazard that primordial sociality by this definition and this question proceeded primordal motility in cells.
Algae started to form physically attached groups like these filaments, giving them some of the advantages of higher organization.

Its easy to see how this is a relatively simple adaptation - just have proteins or carbohydrates on the cell surface that stick together.  This might also have evolved from large cells compartmentalizing since we're talking about very ancient stages of life on earth.


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Are platyhellmintes and annelids segmented?
Are the organisms of platyhelminthes unsegmented worms or segment? And what about those belonging to annelida?
I guess Platyhelminthes are unsegmented and annelida are segmented but i am not sure about it?

Welcome to Biology.SE. A title should be a short version of the content and not just the field of interest. You should use the tags to indicate the field of interest. Also we expect from an OP some effort to answer its own question. Your question is answered by the first sentences of the respective wikipedia articles. I edited your question. Feel free to roll back if you don't like the edit

Here are the first sentences from the wikipedia articles for platyheminthes and annelids:

The flatworms, or Platyhelminthes, Plathelminthes, or platyhelminths (from the Greek πλατύ, platy, meaning "flat" and ἕλμινς (root: ἑλμινθ-), helminth-, meaning "worm")2 are a phylum of relatively simple bilaterian, unsegmented, soft-bodied invertebrates.
The annelids (Annelida, from Latin anellus, "little ring"),2[n 1] also known as the ringed worms or segmented worms, are a large phylum, with over 17,000 extant species including ragworms, earthworms, and leeches.


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What is this plant?
It was found in Eastern Pennsylvania (in the United States) in a deeply wooded area.

Those are the fruit clusters of a common "wildflower" that often grow in wet areas, called Eastern Skunk Cabbage or Symplocarpus foetidus.  Initially (early Spring), it's not bad looking (and some species - such as the western skunk flower - are even pretty):

But after a while, the spathe (sheath) dries up while the seeds grow in the spadix (the fleshy thing in the middle with the little 'flowers') grow, leaving the swollen spadix (fruit):

The tip off, though, is the characteristic new growth, very skunk-cabbagey, so I would guess those fruits are from the previous year (?).

Eastern skunk cabbage is notable for its ability to generate temperatures of up to 15–35 °C (27–63 °F) above air temperature by cyanide resistant cellular respiration in order to melt its way through frozen ground, placing it among a small group of plants exhibiting thermogenesis.

This allows it to flower through melted ice or snow. Also:

It's a member of the arum family.
It depends for fertilization on bugs that like carrion.
It's virtually impossible to dig up a well-established plant because the roots pull the plant down deeper into the soil every year (it has contractile roots).
It was widely used medicinally.

Skunk Cabbage (Symplocarpus foetidus)

Some types can also be mistaken by the uninitiated for rhubarb, which it definitely is not :)

@MattDMo - Eeeeewww! The smell should be a tip off, no? I mean, they produce chemicals like "putrescine" and "cadaverine". I'll take rhubarb! (Now that I think about it, I can see a tiny resemblance maybe.)

it was a long time ago; I was young and innocent :) I'm not even sure if it was "true" skunk cabbage, but that's what someone else called it after I tried nibbling on a leaf stem and almost threw up. This was in central Pennsylvania, not far from where the OP found the specimens in the question.

@anongoodnurse Putrescine and cadaverine to attract flies? I have also noticed that flies get attracted to spermine/spermidine. I just left a solution (with some sugar) in an open bottle to see and in some days it had maggots. Tried this twice (not enough replicates :P).


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Lotka-Voltera predator prey model isocline?
In lotka voltera predator prey model, why do we get a straight isocline with variable prey/predator population for single value of corresponding predator/prey?
I understand that we get the prey isocline by the equation

N1=prey population ; n2=predator population
What I don't understand is why we are getting variable prey population on isocline for same value of predator population. Shouldn't the prey population be also constant?

PS: I picked the graph image from the internet so the symbols are different. Sorry.

Welcome to Bio.SE! What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!

@theforestecologist  Sorry  for the trouble, It was my first time posting a question.

I dont understand exactly what you are asking. Are you wondering how the prey and predator populations can fluctuate with a "fixed" isocline? Or if the prey population is stable while the predator population is stable ("...getting variable prey population on isocline for same value of predator population"), which isn't the case? Can you please clarify.

@helppp thanks for the updates! You've improved your post :). However, I, too, am confused regarding exactly what you're asking about. Please use fileunderwater's comment as a guide for further improving your question. You're getting closer to an answer -- just a few more clarifications and we'll see if we can help you out!

@fileunderwater Yes I don't understand why prey or predator population fluctuates with a "fixed " isocline? If we are saying that rate of change of prey population is 0 for the isocline, then how come we are getting a line parallel to prey axis?

To me, it is still a bit unclear exactly where your confusion lies (also reading your comment to the other answer). Is it the meaning/interpretation of the isoclines that is the problem, or the dynamics with fluctuating populations of both predator and prey (except at the isocline intersection)?

I think your issue is mainly with the interpretation of the isoclines.
If you assume this standard predator-prey model:
$$\frac{dN_1}{dt} = rN_1-pN_1N_2$$
$$\frac{dN_2}{dt} = apN_1N_2-mN_2$$
you get the isoclines:
$$ N_2 = \frac{r}{p} $$
$$ N_1 = \frac{m}{ap}$$
with the first isocline referring to prey and the second to predators. These isoclines mean that the population growth rate of prey and predators (respectively) will be zero exactly at these isoclines (as well as at the point N1=N2=0). Since the isoclines, for this partuicular model, are fixed values and not functions of N1 and/or N2 they will be strait lines. Also, in a sense, you should view the isoclines as the borderline case where population growth rate shifts between a positive and a negative value (ie a growing or a decreasing population). The isoclines are not giving you the population size of the prey at a certain predator population size (which you seem to be implying with "...why we are getting variable prey population on isocline for same value of predator population"), but the locations in the plane where the population growth rate (for either prey or predators) is zero.
A graphical view of only the prey isocline (with some color coding) can be:

This means that the prey population (blue) is growing (arrows to the right) below the blue prey isocline, so there if a "flow" to the right there, while it is declining at predator population sizes above the isocline (arrows to the left). So basically, for all predator population sizes (N2) below isocline the prey population will grow, and for all N2 above the isocline the prey population will decline. In reality the rate of increase/decrease differs depending on how far from the isocline you are (so arrows should be of different lenghts), but to simplify the issue and to show the general principle I'm just showing the direction of flow here.
The same picture for the predator population is:

Here the predator population (orange) is declining to the left of the orange predator isocline (arrows down) because there is too little prey to sustain the population, and increasing to the right of the isocline (arrows up).
If you combine these you get this, with the black arrows showing the overall direction of the combined population trajectories:

I hope this clarifies the issue a bit. Otherwise, please comment and hightlight what parts you find unclear.
Also, the dynamics of this Lotka-Volterra model also means that populations that start exactly at the intersection of the isoclines (i.e. both N1 and N2 will lie at that point) will stay there, since that is an (unstable) equilibrium point. Populations that are started anywhere else in this plane (except for cases where N1 and/or N2 is zero), will follow an oscillating population trajectory, that will not change if there isn't any external pertubations (environmental changes, input/output through immigration/emmigration etc). Therefore, the combined trajectories of N1 and N2 will form an ellipse in the plane, until they are perturbed (by something outside the current model), when they will then settle at a new ellipsis. For examples of the ellipses, see this phase-plane graph from Wikipedia, with initial values as points:

However, also note that changing the model, i.e. to include a logistic component to the prey population, will completely change the population dynamics.

I am going to try and cover the math with a few more words, to show that your intuition is in fact, correct (which with math, is not always given).
In the differential equation you wrote $$ \frac{d N_1}{dt} = r_1 N_1 - p_1 N_1N_2 \;\;\;\;\;\;\;\;\;\;\;\;\;\;\;\;\;\;\;\;\;\;\;\;\;\;\;     (1) $$
the numbers $r_1$ and $p_1$ are simply constants that give a strength of coupling, between the change of a variable (the left-hand side) and how this change is computed (the right hand side).
Would you set $p_1=0$, then the resulting solution of (1) would be an unhindered exponential growth. If we go and increase $p_1$ to $p_1>0$, then we increase the "efficiency of conversion from $N_1N_2$ into negative $N_1$", or more simply put "the predators become more efficient at hunting".
Hence, intuitively, as the predators become more efficient, by increasing $p_1$, the prey population cannot grow exponentially grow to infinity any more. It must now level off (as the solution of (1) will show you, if you keep $N_2$ constant, see also the logistic function "In ecology: modeling population growth").
And the stable value towards which it is leveling off, is given by the requirement $\frac{d N_1}{dt} =0$, which leads us to the isocline $0=r_1-p_1N_2$.
Now, coming back to your question, it is important to notice that by requiring $\frac{d N_1}{dt} =0$, we have already set $N_1=const.$, we just have no means yet to compute this value.
 So the prey population is in fact constant! And the predator population that can live off this unknown value is given by the ratio of prey multiplication vs. hunting efficiency, which is the isocline.
As a last comment, it is strange that an equation for $N_1$ turns out to give us the most  information about $N_2$, but that's how it often is with coupled differential equations.

Okay, that does clear up a few things.  But shouldn't a fixed predator population of N2=r1/p1 correspond to a fixed value of prey population, so instead of a line we get a point ?

@helppp Could you post the link where you've got the image from? Then I could check with their variable namings. The way I see it the line means exactly that: For one particular N2, there is one constant N1. However, now if we change N2 to some other number N2', then N1 has also to change, in a correspondingly linear fashion, along the isocline.

here you go: http://nre509.wikidot.com/lecture-15-nov-4

Why are you bringing the logistic function into this? The prey model in the Q is not based on the logistic, and the levelling off in the logistic model has nothing to do with the isocline in this Q.

@fileunderwater: Because when keeping $N_2$ constant, this is a logistic DEQ. It helps develop what you expect from a solution. The first term is an enxponential growth, the second one an exponential decline. If the logistic level-off is actually reached, depends on the ratio of the coefficients.

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


text:
Why do some people have cold hands and some have warm?
I've known people who have warm hands even in the most chilling weather and also those having cold hands in a relatively hot climate. Why does this happen?

Although there is certainly something to this phenomenon regarding circulation and other factors, I think it's important to note that this is very relative: the people with cold hands are people with colder hands than you and the people with warm hands are people with warmer hands than you in either circumstance.

@SanjuktaGhosh Homoeopathy "medicine" is not in any way empirically more effective than a placebo. I used quotations because sugar pills are as effective, and sometimes more so than homoeopathic treatment. If hot hands are used as a diagnostic tool in homoeopathy, it doesn't mean that symptom has any biological or medical underpinning.

@James I won't argue, it being more effective or not as compared to placebo. I have been taking them since time unknown(before I could have any expectations). I often wonder how it works actually (I believe it does). Well, it was a comment, just trying to add an information which can be considered not constructive,the science behind it is unknown( with a bit of research I have done). Hence I delete.

@SanjuktaGhosh A meta-study in 2002 found that there was no consistent evidence that homoeopathy is effective above placebo level. The controversial journal of homeopathy remains in dispute. No article I know of outside this journal has found evidence in support of homoeopathy. As for understanding homoeopathy, it is extremely diluted medicine. There is no mechanism by which it works without fundamentally misunderstanding physics.

@James I won't blame either you or @ SanjuktaGhosh for this...homoeopathy is still the first choice for many in (at least) India. And people (don't know why) don't like homoeopathy being called as pseudoscience... :/

@another'Homosapien' Probably because the only way that homeopathy has any chance of working (and the only way for homeopathy peddlers to get anyone to buy their goods) is via a placebo effect; the more people understand that it is pseudoscience, the less effective the placebo effect will be.

Though I haven't heard of people having warm hands in cold temperatures (unless your using a hot pack or something), there are biological explanations for cold hands.

Having cold hands even when you're not in a cold environment is
  common. Often, having cold hands is a part of your body's natural
  response to regulate your body temperature and shouldn't be cause for
  concern.
But if you have persistently cold hands, particularly if accompanied
  by color changes, it could be a warning sign. For example, having cold
  hands could mean you have a problem with the nerves or blood
  circulation or a problem with tissue damage in your hands or fingers.
  If you are outside in extreme cold weather and you have cold hands,
  you should watch for warning signs of frostbite.
  - MayoClinic

Other than frostbite, there are also reports of the Reynaud's disease.
Sources:
Clinic
CNN

Hi, GH05T, and welcome. A mostly copy/paste text doesn't make for a high quality answer on SE sites. Paraphrases of relevant information with quotes as necessary, plus references are much more in keeping with the SE model. Just letting you know, not trying to offend. Thanks, and again, welcome.


text:
Why are turtles classified as reptiles and not amphibians?
I understand that turtles are reptiles because like all reptiles, they have scales on their body. But turtles (specifically sea turtles) live on both land and water, very much like amphibians. Also, don't sea turtles have more of a moist skin unlike reptiles? So is there any anatomical difference which makes turtles different from amphibians?

Once upon a time, taxonomists argued endlessly about things like this. These days, classification is done by sequence, which takes precedence over anatomy or behavior.

1 sea turtles have scaly skin 2 amphibians were defined by having to lay eggs in water, which sea turtles most definitely do not. Classifications have changed since then but even using early definitions it doesn't work.

In addition to @Gerardo's answer:
Reptiles
The term Reptiles as used in popular language does not represent a monophyletic group. When using the term Reptiles, one is typically thinking of turtles, snakes and lizards but excluding birds and mammals (and a few other things not worth mentioning). There are two clades (monophyletic groups) whose name sounds like Reptiles and whose meanings are related; Reptilia and Reptiliomorpha.
Reptilia
Reptilia is the clade that @Gerardo discusses in his answer. Reptilia includes turtles, crocodilians, snakes, amphisbaenians, lizards, tuatara and birds.
Reptiliomorpha
Reptiliomorpha is a clade that includes Reptilia, Synapsida (mammals and close relatives) and a few extinct lineages.
Visualizing the tree of life by yourself
There are two good online resources: tolweb.org and onezoom.org.
Onezoom.org is better updated and has a nice pleasant look. However, I often find tolweb.org more convenient for investigating the true meaning of a specific clade.
Further reading
You might want to have a look at Understanding Evolution by UC Berkeley. It is a very introductory course on evolutionary biology and it includes a part on the phylogenetic tree.
I also strongly recommend having a look at the related question If dinosaurs could have feathers, would they still be reptiles?

Thank you. These sites you mentioned are very helpful and informative.

Turtles are not amphibians because they have (largely) non-permeable skin whereas amphibians can absorb oxygen through their skin. There are also differences in their reproductive cycle: turtles are amniotes, so they produce eggs that must be laid on land, whereas amphibians - like fish - are not and must lay their eggs in water.
Since the categorisation pre-dates the development of cladistics, and the group normally called reptiles are not monophyletic, I don't think cladistic based answers are a good answer to this question. It is the morphology and physiology that matters.


text:
What is this flying insect?
This insect was captured in Australia near Canberra. It has a very hard exoskeleton and is over an inch long. It seems to have 6 wings - 2 large pairs and one very small pair. I did not see a stinger - however I have no idea.

I believe this is the Hairy Flower Wasp, Scolia soror. I don't know what you mean when you refer to six wings, however. Like all other wasps, this species has four wings.

he might be referring to the beetle-like carapace as another set of wings.


text:
What's the difference between male and female?
As long as we only look at humans the differences are clear: males have chromosomes XY, produce sperm and don't get pregnant. Females have chromosomes XX, produce egg cells and bear babies. But when you consider other species, things are more complicated: in birds, it's females who carry the Y chromosomes. In pipefish and sea horses, it's the males who get pregnant. So maybe the only reliable criterion to tell if an animal is a male or a female is looking at its reproductive cells, and decide if they look like spermatozoa or egg cells. But then there are male and female plants, where none of the methods above applies.
So how do you tell, in general, who's male and who's female in a species? Or is the distinction arbitrary?

Sexes (male and female) are generally defined in terms of Anisogamy, which means that there are size differences between the gametes (i.e. the reproductive cells that fuse at fertilization). The sex with smaller gametes is defined as male and the sex with larger gametes is defined as female, and individuals that can produce both types of gametes are called hermaphrodites. This is the case in both animals and plants (plants have pollen vs. ovules and microsporangia vs. megasporangia), and the definition of sexes is therefore not dependent on chromosomal makeup as such or which sex that carries the young. Actual sex determiniation in a particular species is often based on chromosomal inheritance though, but other systems also exists (e.g. environmental cues or sequential hermaphroditism). Anisogamy also comes in several different types, where animals generally have Oogamy, where males have small mobile spermatozoa and females large stationary egg cells.
More generally, Anisogamy is a special case of mating types in sexually reproducing organisms, where fertilization (on syngamy) generally can only occur between gametes of different mating types. In for instance fungi, gametes of different mating types are of the same size (isogamous) and they are therefore only labelled as mating types (e.g +/-) and not different sexes. Functionally, if we are simplifying the issue, male gametes can be viewed only as carriers of genetic information, while female gametes also contain the nutrients necessary for the early development of a newly formed embryo.

In general, It's pretty much the reproductive cells with plants and animals.  The male's unique cells (sperm, pollen) fertilizes the female's unique cells (egg, ovule).  The resulting offspring develops and hatches from within the female's egg/ovule.  Now whether that egg/ovule stays put, gets ejected, hides in a flower, or transferred to the male (like your seahorses)... that's just rearranging the furniture after it's been designed.

You may think of the penis and vagina as well. In animals, males certainly have penises and females have vaginas, huh? As it turned out, this is not always the case. In This Insect, Females Have Penises And Males Have Vaginas. You can read more about it here.

So as fileunderwater answered, the criteria for differentiating between male and female is the size differences between the gametes. The sex with smaller gametes is defined as male and the sex with larger gametes is defined as female.


text:
What is this beetle?
During a pit stop on the road from North Carolina to New York (somewhere in Delaware) I found the following (dead) insect in the car park:

As you can see from the quarter next to it (25 mm diameter) it is rather large - maybe six centimeters, including the "horns".
What was it?

Looks like it must be a male Dynastes tityus (Linnaeus, 1763).
There are photos for comparison, and a full description with maps and some interesting notes on habitat and behavior, on the University of Nebraska State Museum Generic Guide to New World Scarab Beetles

FWIW, my searchpath on this was 1) "huh, that looks like a scarab", 2) google image search for scarabaeidae+delaware

Looks like you are exactly right. Thanks a lot for your "searchpath" information as well.

Thanks for posting the lovely photo! The scale is a nice touch, too.

It was an iPhone 5, and the light was fading. I was quite surprised just how good it came out... you can see my reflection in the carapace (do you use that word for beetles?). I am a physicist, not a biologist - I would never think of taking a picture like this without some way to determine the size...

Having learnt the correct name, I googled some more. The common name is Eastern Hercules Beetle, it can grow up to 60 mm in length (so this was a big one), and it is "among the largest and heaviest beetles in the US". It even made it onto a US postage stamp in 1999


text:
Antibodies stored in freezer instead of fridge
Someone from my lab put the box of antibodies in the freezer instead the fridge.  Can I hope that they will still work?

Depending on the type of protein and cryoprotectant (eg glycerol), freeze-thaw cycles may or may not damage proteins.

No way to tell until you try them! If they're in glycerol you have a good chance. We normally store our antibodies in the freezer.

@anael Have you read manual for that antibodies? Unless they are home-made, there should be one available. If home-made, then ask person who made them.

Most IgGs should be fine when stored in the freezer.

Freezing at -20 or -80 in small aliquots is the optimal storage
  condition. Ali-quoting minimizes damage due to freezing and thawing,
  as well as contamination introduced by pipetting from a single vial
  multiple times. Aliquots are to be frozen and thawed once, with any
  remainder kept at 4 degrees C.
Enzyme-conjugated antibodies, should not be frozen at all and should
  instead be kept at 4 degrees C. Freezing and thawing will reduce
  enzymatic activity in addition to affecting the antibody binding
  capacity.
Antibodies of the IgG3 isotype are unique in their tendency to form
  aggregates upon thawing and should always be stored at 4 degrees C

Personally, I store antibodies I use at -20 (they are in PBS), and they work fine for the first freeze thaw cycle. I have never tried more than one freeze thaw, so cant comment on that.
http://www.abcam.com/ps/pdf/protocols/antibody_storage.pdf

You don't specify which temperature of freezer you're talking about. Antibody can be stored at -80 for long time, but needs to avoid freeze and thaw process. Some people store aliquot of antibody in -80. Another way is to dilute antibody in Glycerol, make 50% dilution. You need to mix well, and then store at -20.


text:
What neurons make up the CNS?
I generally see it written that there are three types of neurons, classified by projection: (1) sensory neurons, (2) interneurons, and (3) motor neurons. Now, in the CNS, I don’t think there would be sensory or motor neurons, seeing as they connect the PNS to the CNS. Does that mean, then, that all the neurons in the CNS are interneurons? I remember my biology teacher telling me not all neural pathways involve interneurons, so that suggests to me that the CNS consists of other neurons as well. What neurons would these be, if they are existent?

There are probably thousands if not more neuron (cell) types in CNS...this 3 level classification is very simplifying. What level of biology are you learning?

Short answer
Sensory neurons are invariably considered to be located in the periphery. Interneurons and motor neurons are part of the CNS.
Background
There are various classifications possible to categorize neurons.
One classification is the one you mention (Furness, 2000), which is a broad classification based on where the neuron projects to. It divides all neurons in:

Sensory neurons (feed information to the central nervous system (CNS));
Interneurons (are stimulated by sensory neurons and/or other interneurons);
Motor neurons (feed information from the CNS to the periphery).

Sensory neurons are invariably considered to be part of the peripheral nervous system. Their cell bodies are located in the periphery. Their projections may feed directly into the brain. For example, olfactory sensory neurons directly project onto the olfactory bulb in the brain.
Motor neurons include the motor neurons controlling muscles. Their cell bodies are located in the spinal cord, which is the CNS, but not the brain. Here the terminology becomes confusing, as this functional classification uses overlapping terminology with the projectional classification. That's why I, personally, prefer to talk about efferent fibers (away from CNS) and afferent fibers (to the CNS). Especially because motor neuron implies something motoric. In case of neurons driving glandular secretion this is counter intuitive. Efferent and afferent fibers are essentially the same names for motor neurons and sensory neurons. One way or another, motor neurons controlling muscles have their cell bodies in the spinal cord and hence are part of the CNS.
Interneurons are invariably located only within the CNS. Interneuron is also a confusing term, because often they are implicitly considered to be inhibitory. Often they are, but they don't have to be. In the classification scheme discussed, most CNS neurons can indeed be classified as interneurons. For example in the neocortex, 70–80% of the neurons are excitatory pyramidal cells, while the remaining 20–30% are inhibitory interneurons (Markram, 2004). The spinal cord also contains interneurons.
In all, most interneurons are located in the CNS, but not all CNS neurons are interneurons, because motor neurons are part of the CNS too. I agree with 243's answer that the classification scheme is most appropriate for the relatively simple neuronal circuitry characteristic of the spinal cord.
References
- Furness, J Autonom Nervous Syst (2000); 81: 87–96
- Markram, Nature Rev Neurosci (2004); 5: 793-807

For example, interneurons account for 20% of neurons in neocortex (1)(2). I think that the classification, mortar-, sensory- and inter-nerons, comes from the simplest neuron circuits like spinal reflex.
In human brain, their thoughts and experiences modify such simple neuron circuits, suggesting existence of other neurons affecting the simple circuits. It should be noted that many neurons in CNS spontaneously fire(3). If interneurons spontaineously fire, your leg spontaineously move unconsciously. Some other neurons secrete hormones in brain, called neurosecretory cells cells(4).

Inhibitory interneurons make up 20-30% of the cortex see your ref 2


text:
Blood as newtonian flow and Poiseuille law
For a prep exam:
A healtly pacient has a carotid with the following characteristics:
intern ratio: = 2.8 mm,
2 = 89 ,
1 = 90 ,
 blood = 3.5 cp,
=10.0 cm.
Using the following equations calculate:
$$V(r)=\frac{P_1 - P_2}{4 \mu L}R^2 [1-(\frac{r}{R})^2]$$
$$V_{max}= V(r=0)$$
$$\overline{V} = \frac{Q}{A}=\frac{1}{2}V_{max}$$
$$Q=\frac{\pi(P_1 - P_2)}{8 \mu L}R^4$$
where P_1 and P_2 are the mean pressure to in and out the vase, R is ve vase radius, L is the length of the vase segment and $\mu$ is the viscosity of the fluid.
A healthy patient has a carotid withe the following characteristics: intern radius R = 2.8 mm, $P_2$ = 89 mmHg, $P_1$ = 90 mmHg, $\mu_{blood}$=3.5cp, L = 10cm.
Using the previous equations calculate:
a) Mean velocity on the carotid artery Rta: 0.372 m/s
b) Maximum velocity Rta: 0.744 m/s
c) caudal on the carotid artery Rta: $9.16x10^{-6} m^{-6}$
I have tried to solve this problem but when i try to replace changing the units to the adecuate I have not the correct answer

could you please elaborate on how you went about solving it

I'm voting to close this question as off-topic because it is better suited for physics.SE.


text:
Why isn't speciation a negative feedback loop?
To rephrase my question more articulately:
Speciation begins when two groups within a species starts to become reproductively isolated, and is complete when the two groups can't interbreed (for the purposes of this discussion). But then how is this possible when any time a reproductively-isolating mutation occurs in a member of that group, the member carrying that mutation could no longer breed with the other members? Therefore, speciation is theoretically a negative feedback loop. In this context, how does speciation occur?
One of the mechanisms documented by James Patton is chromosome evolution, where changes in chromosome number and shape occurred in pocket mouse and reproductively isolated the different species-complex (https://www.jstor.org/stable/2406859). But then the question still remains that the first mouse to have a different number of chromosomes would not be able to have offsprings because there are no other members with the same number of chromosomes as it does.
unless the genetics of reproductive isolation is continuous i.e. a gentically reproductively-isolated member of a species could
A. mate and have offspring with the general population but with greater cost, for instance, hybrid offspring could be at higher risk of dying in utero or be at higher risk of becoming sterile.
B. hybrid offspring, will go on to produce more offspring, still at higher cost, unless they do so with each other AND with the general population. creating a subpopulation that mates more successfully (i.e. at lower cost) with each other than with the general population.
But I have not found any articles saying reproductive-isolation is continuous rather than binary.

Most things in biology are continuous. Sometimes they appear to be binary due to thresholds, but it's rarely true. I would suggest reading some more about the genetics of speciation, e.g. https://www.sciencedirect.com/science/article/pii/S0960982206026649. Incomplete reproductive isolation is quite common; for example, there are various examples where offspring are sterile when male but fertile when female (e.g. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2776091/). Also remember that genetics can act indirectly through behavior, which is notoriously sloppy. Or simple geographic isolation!

Concerning the continuous vs. binary question with regards to speciation, I think the concept of Ring Species may be enlightening

This is getting clearer, but is still very awkwardly worded. ——— In addition, there is an expectation that users will do research before posting, so I encourage you to check out some of the online resources available for learning more about evolution. For example, this a useful introduction to evolutionary theory from UC Berkeley.

I'd suggest looking at this article, which contains an intuitive model for how hybrid incompatibilities can arise between isolated sister taxa (i.e. populations). This criterion of pre-existing isolation is an important factor in most models.
I think that one thing that is missing from your representation of speciation is that you are assuming that every organism in a species is in one big population. This is not true. Isolation by distance is one of the simplest ways that isolation can happen.
For example, Bateson-Dobzhansky-Muller incompatibilities arise when two isolated populations of the same species each have diverged in two genes. Each change is harmless on its own, but when you put divergent allele from gene 1 from population 1 together with divergent allele from gene 2 from population 2 together, suddenly you get hybrid sterility or lethality.
Of course, the divergent alleles of gene 1 and gene 2 can't arise in the same population, for reasons you point out. Incompatibility can only evolve when these two divergent alleles arise in different populations of the same species.
For a simple isolation by distance model, imagine a river with snails (or whatever) in it. The snails at the headwaters interbreed a little with snails just downstream. Those just-downstream snails interbreed a little with headwaters snails, and also a little with the snails just downstream from them. But by the time you get to the mouth of the river, the connection between the headwater and the mouth-of-river snails is very tenuous. Now, how much of a problem is an incompatibility between headwater and mouth-of-river snails?

Thank you! This made so much sense. Are hybrid incompatibilities the main driver of genetic isolation or are there other equally common mechanisms?

@AnethOthbo I think that part of my argument- which perhaps I should be clearer about- is that reproductive/genetic isolation can be achieved by many mechanisms. Probably the simplest mechanism is geography: if two people live on different continents all their lives, they will never meet and have children. If what you are interested in is cytological/molecular mechanisms of isolation, then yes, hybrid incompatibility is probably the big one.

This isn't a complete or exclusive answer, but inversions can contribute heavily to reproductive isolation.  A crossover within the region inverted in one homologous chromosome of a hybrid, but not the other, will typically mean one end of the chromosome is absent in the offspring, which is generally not a good idea.
Nonetheless, within the same species it is possible to have an inversion polymorphism taking up most of a chromosome.  This means that you have a species which exchanges genetic material normally within most of its genome, but is divided into somewhat isolated populations in terms of that one region.  (The barrier is not watertight, especially with such a large inversion, because a gamete produced by two crossovers within the inversion is perfectly normal)
This review discusses more about the general evolution of inversions and their role in speciation.  (I pulled it out at random; there has been quite a bit published on the topic)

While I certainly agree that inversions are an important example of an isolating molecular change, I think that the OP is asking more about how a reproductively isolating variant (such as an inversion) can arise, if it contributes to isolation- e.g. more of a theoretical and less of a cytological question. That said, your linked Kirkpatrick (2010) reference provides some helpful answers that might be worth highlighting: 1) superiority of inversion heterozygotes, 2) meiotic drive of inversions.


text:
Confusion on polarity and hydrophobicity of Proline, Tyrosine and Cysteine?
I will list here several sources that state differently on the polarity and hydrophobicity of Proline and Tyrosine:
From the article Amino Acid on Wikipedia, it states that Proline is a special case, Tyrosine is hydrophobic and Cysteine is also a special case.
From Khan academy, it also states that Proline is polar, Tyrosine is nonpolar and Cysteine is polar.
However,
From Pearson Prentice Hall's Biological Science, it states that Proline is nonpolar, Tyrosine is polar and Cystein is polar.
From BioNinja, it states that Proline is nonpolar, Tyrosine is polar and Cysteine is nonpolar.
On Wikipedia,
The article Proline supports Proline is nonpolar.
The articleTyrosine supports Tyrosine is polar and hydrophilic.
The article Cysteine states that Cysteine is polar and hydrophobic, AS WELL AS Tyrosine.
To summarize the result, I'll put them in the following table

Please help me to clear out the confusion, why the polarity and hydrophobicity of these amino acid are not agreed with each other?

Cysteine shouldn't be considered polar as the difference in electronegativity is lower than 0.4 between Carbon (2.58) and Sulfur (2.55) or between Sulfur and Hydrogen (2,20). The difference is higher in the C-H bond. That's also the reason why Methionine is nonpolar.

TL/DR: these are borderline, complicated cases. There is no broad consensus on whether cysteine and tyrosine should be considered hydrophobic or polar. Proline is clearly nonpolar though.
The reason for the confusion is that are there several ways to define and measure polarity and hydrophobicity for amino acids. First, the polarity and hydrophobicity of the free amino acid is very different from that of the amino acid side chain in the context of a peptide (protein). I assume you are interested in the latter.
Polarity is rather difficult to define for amino acids. The dipole moment is the usual measure of polarity, but this depends on the molecule's geometry, and consequently is only well-defined for small molecules that cannot "wiggle" around, such as water. Larger amino acids side chains can wiggle quite a bit, and their dipole moment is difficult to define. Instead, polarity is usually given by rules of thumb like "hydroxy groups are polar" and "aromatic rings are nonpolar. But then there are borderline cases like tyrosine that has both an aromatic ring and a hydroxy group.
Hydrophobicity is related to polarity, but it is an experimentally measured quantity, usually determined by how an amino acid partitions between water and nonpolar solvents, or by observing how it orients in folded proteins (towards or against the water solvent). More detailed information is found here. But the results of such experiments don't always agree, and so amino acids which are borderline hydrophobic/hydrophilic can be difficult to classify. For example, for two amino acids X and Y, we might find that X dissolves better in water than Y, so X appears more hydrophilic in this sense; but at the same time, X could also partition better into a lipid bilayer, so in this sense X appears more hydrophobic than Y. In such cases, the various scales of hydrophobicity will differ.
For these reasons, there is disagreement on whether some amino acids are polar/hydrophobic. With this in mind, here's my two cents on the amino acids you mention:
Proline is a bit special in that it does not have an -NH3 group; the amine nitrogen binds to the side chain -- it is more of a "loop" than a chain -- and the peptide bond is different. But this "side loop" clearly has no polar group, and I think there is good agreement that proline should be considered nonpolar. The Khan Academy page is probably mistaken on this one. Proline is intermediate in hydrophobicity.
Tyrosine: As mentioned, polarity of the tyrosine side chain is unclear since it is quite large and has both polar and nonpolar groups. Tyrosine is somewhat hydrophobic, but among the amino acids, it places itself near the middle on most hydrophobicity scales. So tyrosine is a borderline case, which explains why different sources disagree.
Cysteine is special in the context of proteins, since cysteine residues often pair up via disulfide bonds, and this changes its properties. By itself, the -SH group is polar (although less so than an -OH group) so the cysteine side chain is somewhat polar. It is intermediate in hydrophobicity as measured by solvent partitioning. Cysteine was considered hydrophobic based on the observation that cysteine is often found in the interior of proteins, away from the water solvent; but this is largely due to its ability to form disulfide bonds.

Thank you. Very insightful and detailed explanation. Accepted and upvoted.


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Is there anyone discovered new drugs by actively create mutations in drug-producing organism?
Recently I was reading about drug discovery.
As far as I know, there are currently 2 sources of creating new compounds by:

Screening from natural sources.
Synthesizing by add/remove/replace-ing the functional groups of a known compound using chemical processes.

On the other hand, molecular pharming is the process of producing drugs by integrating the drug-encoding genes into bacterial (typically E. coli) genome.
I came up with the idea that if we create mutations in these drug-producing colonies, by UV light for example, eventually by chance we can obtain some new compounds once the mutations occur in the drug-encoding region or related genes.
I want to search in the previous studies for those who has come up with this idea already, I tried with several keywords and there's no luck.
I would want to ask is this idea practically possible? How high is the chance of having new compounds compare to screening natural sources and chemical systhesis? And if someone has already done this study, can you please provide me some references on this matter?

Would you consider the idea of site-directed mutagenesis for creating mutations?

It could be site-directed mutagenesis or any kind of random mutation when exposed to stress. But the product is unknown. Because the use of known mutant strain is not the idea at all.

I'd say this is possible, but not really practical. Mutating genes by UV light is not that hard, it's just the screening for the (new) compounds that makes it difficult. You would probably be better of creating diversity using established chemical methods.
Usually UV mutagenesis is done for whole organisms, but some people probably also tried this for single genes (even though they'd hit the whole genome). This is the easy part; you could get an enormous amount of diversity with very little work. Even though mutations that change enzymatic products are probably much more rare than mutations that change substrate specificity or product chirality, people find those mutations (example from the top of my head: p450 hydroxylation patterns, although they probably used targeted mutagenesis).
Determining if a specific compound is produced by an organism is also not very hard. You break all the cells, put the solution on a column and check with your favorite analytical method whether or not your compound is in there. Checking for new compounds is much harder. You need better analytical methods such as MS/MS as you don't have analytical standards, and the adapted molecule might not even be detectable with the analytical method you used for the starting molecule. We are very good at detecting needles in haystacks, but determining if there is a needle, a stick, or maybe a piece of hay from another species in the haystack is much harder. You'd already have to predict what kind of altered molecules you expect to find.
When you have successfully done all this, you have identified a single new molecule. Nowadays, people use libraries with >100,000 compounds to screen against their disease protein of interest.
The idea of mutating enzymes to produce new products is not that strange, people work on this, publish, find a lot of interesting things and we learn a lot about enzymes. As an approach for drug discovery this approach is just not high-throughput enough.

Indeed, small molecule and secondary metabolite detection has been, and often still is done through both random and rational mutagenesis. UV light is one option, but often it's easier to use slightly more aggressive methods such as ethanemethanosulphate (EMS) exposure.
Streptomyces for example, the model organism for secondary metabolite production has been subjected to all manner of mutagenesis methods throughout the years (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3472513/).
A random mutagenesis approach used frequently these days is genetic rather than chemical, and uses the mobile elements transposons for random insertions. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3416362/)
Much secondary metabolite production these days is done via modification of Non-Ribosomal Peptide Synthase clusters (NRPS). These clusters exhibit something called the 'colinearity rule' (http://www.sciencedirect.com/science/article/pii/S1074552110000499) whereby, the 'modules' that make up the protein complex, play 'pass the parcel' with the growing seconday metabolite, with each module subsequently adding a new moiety - like a conveyor belt. It's possible to therefore predict the molecule an NRPS will make just from the modules and mutations you see within it, whether produced randomly or rationally.
However, it's often the case that we understand the myriad of secondary metabolite molecules that an organism is capable of producing so poorly, that simply screening the wildtype organism turns up hundreds of thousands of molecules before you even need to consider modifications.

I think your sources point more towards mutagenesis to produce more of a certain molecule, not towards producing completely new molecules.

I hadn't interpreted the OPs question in that manner, but on rereading I guess that's possibly what he meant. In that case I would say random mutagenesis to produce totally novel compounds is functionally impossible. On average, mutations are neutral, and of those that aren't they're more frequently deleterious than advantageous so you'd need an extremely long time frame and a selection pressure to generate mutations that would stick to be able to produce a brand new molecule. It's simply not feasible to start from scratch.


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Evolution of a Population
Scientists observe a newly established population of sexually reproducing plants growing on the shore of a small island. An observable trait of the plant has two possible phenotypes. It is determined by a single gene, with the dominant allele having complete dominance over the recessive allele. The first generation had 26 plants with the dominant trait and 25 with the recessive trait. The data below is from the first six generations of this population:

Use the data to explain the changes in phenotypic frequency from generation 1 to 3.  I'm not sure how to explain the increase in the recessive trait for generation $2$ to $3$. How would a population go from $p^2+2pq=1$ to $q^2 \simeq .2$?
Do you think this population is in Hardy-Weinberg equilibrium? Support your answer.  No, I don't believe so, since the population seems to change constantly in both the total number in the population, as well as the number of individuals with each trait.
Propose a possible explanation for the change in phenotype frequency from generation 5 to generation 6. Perhaps a climate change or the introduction of some new factor such as a  drought or new preadator?

You should probably take a step back and review Mendelian genetics first. It has to do with the fact that the dominant trait has complete dominance over the recessive trait. This means that while the offspring of a homozygous dominant and homozygous recessive plant will all be genotypically heterozygous, their phenotype will still be of the Dominant trait. So if Red flowers are the dominant trait and White flowers are recessive, then the heterozygous genotype will have Red flowers, and you will not be able to tell genotype from phenotype of thing individual offspring until the next generation.

So let's say that all of Gen 1 is genotypical homozygous. WW for red flowers and and ww for white flowers. To get generation two all of the ww plants will have had to be pollenated by WW plants. This will lead to 100% Ww offspring for those pollinations. There could be WW offspring as well in the mix, but you cannot be certain. The only thing that you know for sure is that no ww pollenated another ww in Gen 1 because you would have seen a phenotypically recessive trait. When Gen 2 breeds, if a WW pollenates a Ww, then the 50% WW and 50% Ww, but still phenotypically red.

If however, two Ww's breed, then the distribution is 25% WW, 50% Ww, 25% ww. As the 75% Red 25% White distribution in the Gen 3, then you can go back and say that all of the offspring from Gen 2 were Ww, so no WW pollenated another WW in Gen 1, besides the fact that no ww in Gen 1 pollenated a ww. I am going to leave you to think about the other questions on your own.


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Why is the DNA helix anti-parallel?
Why is it that DNA strands are running in anti-parallel fashion? Given the chemical base-pairing, they could have been parallel just as well.

How could they run parallel instead of anti-parallel when they need to be complementary to each other, and at the same time have the same structure? Having them parallel and complementary would need them to be enantiomers, and that's biochemically a huge mess. I'm not posting it as answer because I can't really justify it

This is a similar question in Biology SE http://biology.stackexchange.com/questions/27839/why-is-dna-antiparallel-can-it-be-parallel

Parallel nucleic acid double strand is possible but it is not as stable as the antiparallel form (Szabat and Kierzek, 2017). This is because the nucleobases are not aligned in a way that is conducive for the Watson-Crick (WC) type base pairing. In parallel conformation, the bases can form Hoogsteen (HS) and reverse Watson-Crick (RWC) type base pairing (see below).

You can see that these base pairs are not as strong as that in WC base pairing:

No triple bond between G and C in RWC base pairing
GC pair occurs in HS base pairing only when C is protonated at low pH

Formation of parallel helices, therefore depends on the sequence.

In general, the formation of duplexes with parallel strand orientation
  is determined mostly by the sequence context and pH conditions.
  Fragments of RNA or DNA capable of forming a parallel duplex are often
  rich in A and C, which is related to their ability to become
  protonated, in middle acidic conditions.

However, it is not as simple as RNA/DNA base pairing with its complement. Parallel helices would not follow the WC base pairing rules and therefore predicting whether they will form is not that straightforward. However, parallel helices can form in vivo (see references 23–25 of Szabat and Kierzek, 2017).
You can also check out this article by Leontis et al. (2002) for hydrogen bond patterns in parallel and antiparallel helices.

This is more chemistry than Biology.
Both strands of DNA are 5' to 3' direction. Why so? because the direction is determined in terms of the direction in which purine or pyrimidine bases are added.
The four bases that exist in DNA are Adenine, Guanine, Thymine and Cytosine. They are referenced under Purine and Pyrimidine links posted above.
This molecule is added to the end of a new DNA molecule.
It will be added to the 3' end of a new growing DNA molecule.
"Adenosintriphosphat protoniert" by NEUROtiker - Own work. Licensed under Public Domain via Commons.
What is the 3' and 5' end?

The ribose sugar at position two will lose the OH, the 5' position is the one where the long chain of phosphates are added in the top image and this phosphate at position 5' will be bonded to the OH at position 3' seen in the deoxyribose molecule, this reaction will generate a phosphodiester bond.
"Phosphodiester Bond Diagram" by File:Enlace fosfodiéster.png, File:PhosphodiesterBondDiagram.png: User:G3pro (talk)
Original uploader was User:G3pro at en.wikipedia.org
Derivative work: User:Merops (talk)
Derivative work: User:Deneapol (talk)
Derivative work: User:KES47 (talk)
Text tweaks: Incnis Mrsi (talk)
Text tweaks: DMacks (talk)) - File:Enlace fosfodiéster.png. Licensed under CC BY-SA 3.0 via Commons.
And here's the complete reaction

If you have noticed the negative charge on the Oxygen, then you will notice that Oxygen has one more electron to donate for a covalent linkage. So this electron attacks the O-H bond at the 3' OH of the deoxy-ribose sugar to generate the phosphodiester bond.
So the 3' OH is always a requirement for addition of new bases to a DNA strand. The 5' refers to the dangling 5' end of the first Phosphate, while the 3' refers to the 3' OH of the Ribose sugar at the last base of the DNA. The entire reaction is catalysed by DNA Polymerase
P.S. They are not really free, there are many modifications which make them inert.
So that is why DNA is anti-parallel.

This answers why DNA strand have polarity but not why they form anti-parallel helices.

Is there any other way in which DNA polymerase can polymerize the polymerization reaction?

Nucleic acids must be added to the 3' OH forming the phosphodiester bond, which is the basis for 5' to 3' direction of DNA, there must always be a 3' OH to add more bases to which is why a Primer is added during replication, or else DNA will not have been replicated, so is that not reason enough for anti-parallelism?


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Living intermediate species?
Hypothetical question regarding three animals 'species' {A, B, C}.
Are there any examples in nature where {A and B} cannot regularly produce viable offspring, however {A and C} and {B and C} can regularly produce viable offspring.
I imagine that such a situation could arise if {A, B, C} have a common ancestor, but {A and B} are sufficiently different from each other, but not from C.

The hybridization situation you describe could be found in ring species, and is partially related to this concept.
For instance, the three species A, B and C could have partially overlapping distributions, such as:

In such a situation (assuming that the relative distributions have been stable over evolutionary time), A and C might be able to produce offspring, as well as B and C, while A and B might not produce viable offspring if they would meet.
Here is a picture from the wikipedia page for a similar situation, showing interbreeding between seven gull species in the genus Larus:

However, I also know that the ring species concept has been challanged, mainly by the fact that there are very few good empirical examples of ring species. See for instance the nice blog post "There are no ring species" by Jerry Coyne, which may also include a couple of examples of species groups that are relevant to your question.
Also, the hybridization patterns that you describe can be caused by other processes, for instance specific reproductive barriers between groups of species (molecular or behavioural). My answer is therefore merely mentioning one possible explanation for the hybridization patterns you ask for, but there are many other processes to consider.

I don't know what the molecular mechanism behind this phenomenon is but one possibility is presence of a set of lethal mutations that can be compensated in certain crosses.

I don't know either, and it will depend on particular species pairs. My last point is mainly that there exists other examples of the type of hybridization patterns that the OP describes, that doesn't involve ring species. There are probably examples of sympatric species where A+C and B+C can produce viable offspring, but not A+B, depending on specific features of their reproductive barriers.

Re Jerry Coyne's blog post -- What is it about Darwinian Theory that engenders so many dead-end conjectures and false pedagogical stories?

@user23715 Maybe that a naive version of evolution is higher fitness + selection -> perfect adaptation, which easily can lead to pattern-based apparent adaptation (or other "outcome" assumed to be the result of evolution) -> inference assuming selective forces

Maybe it's the underlying theory though and not just a naive understanding of it? See the recent "news" about Great Ape Evolution (Pliobates cataloniae). --- If the underlying theory is sound wouldn't it be driving field and lab work that supports itself instead of "turning it on it's head" as happens so often? --- The Standard Model in particle physics is known to be incomplete yet has truly underpinned the associated research. --- NDE and biology? Meh, not so much.

@user23715 Are you saying that the modern account of evolution has often been turned on its head? If so, when? What about the finding of Pliobates cataloniae do you find problematic (I've only seen a couple of headlines so far)?

The Mods will probably move this to chat but, in a nutshell: What is it about NDE that produces ideas like Ring Species or a proposed "tree" for the evolution of the Great Apes, and yet when field work is done in support of the idea, instead of reinforcing it, the theoretical concept gets "turned on its head"? --- Contrast this with Plate Tectonics, a theory that fruitfully guides field work in geology --- Or the aforementioned Standard Model in physics. These latter two have proven themselves time and again. NDE not so much. There is seemingly nothing about NDE that drives fruitful research.

@user23715 Exactly what are you referring to with "NDE" (not familiar with the acronym)?

Neo-Darwinian Evolution.

@user23715 If you truly believe that "There is seemingly nothing about NDE that drives fruitful research." you must be either ignorant about what is going on in evolutionary research or ideologically blinded. I don't think we will get further in this comment-field discussion though.

"Ring Species" was an idea birthed by NDE thinking. "Ring Species" do not exist... or maybe one example exists. What's wrong with NDE that it promotes thinking like this? --- Compare with the fruitfulness of the Standard Model in physics or Plate Tectonics in Geology. It just seems odd to me that the fundamental theory in Biology doesn't actually produce anything worthwhile. Advances in Population Genetics, Molecular Biology, etc. have all taken huge leaps irrespective of any potential underlying link to NDE. --- Name any recent (50 yrs +-) advance in Biology needs NDE to be understood.

The term that describes this phenomenon is 'clinal speciation', and the easiest examples to point to are all 'ring species'.
Wikipedia mentions four ring species examples. Three are avian examples (Larus gulls, Song Sparrows, and Greenish Warblers), and one is a plant example (Euphorbia tithymaloides).
The classification of the Larus gull complex as a ring species is contested. Liebers et al (2004) argue that the isolation-by-distance model, with genetic contact at all near points of the species' range, is not well-supported by genetic analyses for this species, and that the species' genetic structure is better explained by a series of 'splitting' events associated with long-distance colonisation followed by genetic isolation of the new colony.


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Standard practice for generating rarefaction curves from Next Generation Sequencing data
We have a few million 18S reads from a particular environment. The reads have been clustered into Operational Taxonomic Unit (OTU), and the OTUs annotated against a reference database.
To generate a rarefaction curve, my understanding is that one randomly samples $n$ reads where $n$ ranges (with some step size) from 0 to the total number of reads, and counts the number of OTUs observed at each such sub-sampling.
Which of these two ways, as implemented by sequence analysis suites such as QIIME and mothur, is standard practice? Which would be best to use with the above situation?

Treat the original assignments of reads to OTUs as truth, and when resampling $n$ reads, just count the number of "original" OTUs observed in this sub-sample.
Re-cluster the sub-sampled reads, and then count the number of "new" OTUs in the sub-sample.

My sense from reading through the QIIME documentation is that method 1 is the standard, but I am not sure. I also do not quite understand why method 2 wouldn't be the better way to go, though it would be computationally more expensive.

perhaps related https://www.biostars.org/p/4147/ .. Colwell et al. 2012

The first one is the standard. Rarefaction curves (as they are) only make sense under invariant sets of OTUs. Since alignmnent distances are not metrics (that is they violate the triangle inequality) clusters, defined by an identity threshold, are not some geometrically stable areas in a sequence space, hence they are not invariant under reclustering given a smaller/larger set of sequences.

@ Eli, exactly, but if the point is to say "this is how many OTUs we would have identified if we had this many sequences", doesn't re-clustering make sense? Or is that not the point?

My experience is with 16S, but I can say in that context option 1 is standard. You could try running your pipeline on simulated data so that you can calculate error, and compare methods.

I actually work in the same group as Chris (QIIME author), so I hope this helps: An explanation he gave to us a while back about the basis of rarefaction curves is just to give an indication of whether your sampling is reaching saturated diversity, when comparing 2 unequal samples.
If you compare 2 samples, where sample x has less information (reads/amplicons etc) supporting it, you can't be sure you've sampled all the possible diversity.
Thus, you plot the number of OTUs you see for increasing numbers of reads. If you're saturating the diversity you should see it plateau.
To bring the 2 samples inline with the 'amount of supporting data' they have, you randomly sample the data of the larger dataset, so that it is equivalent to the smaller, and then compare the number of OTUs each is reporting.


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Is nicotine toxic to humans?
More specifically, is nicotine in the concentrations that smokers receive when smoking cigarettes toxic? I know that in great enough concentrations it can be toxic (but then, so can just about anything else, including oxygen) and I know that in plants it is used as a defense against insects and can even be used as an insecticide. However, it has always been my understanding that nicotine is irrelevant as far as the harmful effects of smoking go.
I recently had a conversation with another biologist who had just quit smoking and had done quite a bit of research on the subject. He said that nicotine itself is in fact bad for you and, therefore, that tobacco-less alternatives to cigarettes (such as electronic cigarettes) are still harmful because of the nicotine alone.
Does anyone have any more information on this? Perhaps some references? Or, even better, a detailed explanation of the pathways involved? Again, I stress, not about nicotine's toxicity in general but about its harmful effects on vertebrates (preferably human) at the kinds of concentrations one could expect to ingest when smoking.

This would be such a perfect chance for me to revise our recent lecture on nicotine. I'm under deadline pressure though so just a quick one: Nicotine is a stimulant and next to its effects on the brain (reward cycles, addiction etc) it upregulates the sympathetic autonomous nervous system. This can lead to problems mainly with the cardiovascular (CV) system due to raised blood pressure and cardiac activity. Essentially this shows itself like CV disease. It also raises metabolic rate and decreases appetite. And it protects from Alzheimer & Parkinson. Still not as bad as other stuff in smoke :)

@Armatus, yes it protects from Alzheimer's, but you never remember where you've left your cigarettes :). Joking aside, please take the chance and revise, or at least post some juicy references. This smoker would very much appreciate it.

I think its useful to say that nicotine is not very toxic to humans - cells don't die or get sick for typical smoking habits.  Secondary health effects are possible, but here is a toxicological profiles.
Nicotine is a toxin in large enough quantities and nicotine has an LD50 (lethal dose for 50% of individuals) of 0.5-1 mg Nicotine / kg of body weight.  So even a small spill on your skin of the chemical can be life threatening, but for smokers the nicotine itself is not dangerous.
Individuals who smoke intake about 1 mg per cigarette smoked.  So a small adult (110 lbs) can smoke 25 cigarettes in a short period of time (or all at once!) and just barely get to the bottom end of that limit.  Nicotine is water soluble and clears out through the urine at a fast rate though - half of the nicotine from a cigarette is cleared from  your system within 2 hours, which means that 4-5 pack a day smokers are not really killing themselves (from nicotine).
That being said, children are about 5-10 times more sensitive than adults, so even 5-6 cigarettes in an hour can be toxic.  That's quite a bit of smoking though.
Not all animals have the same relationship to the nicotinic acetylcholine receptors as humans do.  Nicotine is toxic to insects and will kill an insect in a matter of minutes or hours. Rats are about 50x less sensitive than people.
I think its comparable to the question of whether caffeine is harmful to people.  In the amount we consume it, sometimes up to grams a day, there is no obvious common side effect, but you figure that decades later it will show up as a problem - a difficult connection to prove.

I do recall this being used as a method for murder in the novel Random

Nicotine acts as a ligand for nicotinic acetycholine receptors (nAChRs), which are ligand-gated ion channels normally activated by acetylcholine. This family of receptors is expressed in every mammalian cell (Schuller, 2009). A priori, at least to me, I'd suggest that it's a bad idea to chronically introduce a foreign substance that mimics the activity of an essential signaling molecule like acetylcholine.
Directly to your question of toxicity, nicotine appears to be linked to many forms of cancer (Schuller, 2009). Cancer promoting signaling pathways are stimulated as a result of calcium entry through nAChRs. Also, interactions of nAChRs with other signalling systems, such as those based on stress hormones, GABA, and dopamine, can lead to cancer.
Nicotine also has important effects in the brain. Chronic exposure to nicotine induces a homeostatic mechanism that upregulates nAChR expression in the brain to maintain responsiveness to endogenous acetylcholine. This effect partially underlies nicotine addiction (Penton and Lester, 2009). As @Armatus notes, nicotine appears to have some neuroprotective properties against neurodegenerative diseases like Parkinson's (Quik, M., Wonnacott, S., 2011) and Alzheimer's (Mehta et al, 2012).

Schuller, H.M., 2009. Is cancer triggered by altered signalling of nicotinic acetylcholine receptors? Nature Reviews Cancer 9, 195–205.
Penton, R.E., Lester, R.A.J., 2009. Cellular events in nicotine addiction. Seminars in Cell & Developmental Biology 20, 418–431.
Quik, M., Wonnacott, S., 2011. α6β2* and α4β2* nicotinic acetylcholine receptors as drug targets for Parkinson’s disease. Pharmacol. Rev. 63, 938–966.
Mehta, M., Adem, A., Kahlon, M.S., Sabbagh, M.N., 2012. The nicotinic acetylcholine receptor: smoking and Alzheimer’s disease revisited. Front Biosci (Elite Ed) 4, 169–180.

When exploring whether nicotine is toxic to humans, the discussion isn't complete without the inclusion of non-adult humans / humans-in-development. Nicotine is toxic to humans beginning at conception. Nicotine has adverse effects on sperm, making them malformed, less likely to fertilize eggs, and making the embryos they do create less likely to survive. Mohamad Eid Hammadeh, PhD, professor of obstetrics and gynecology a the University of the Saarland, Homburg/Saar, Germany, in an interview with WebMD, is quoted as saying,
"The DNA alphabet of these sperm has one or two letters missing. And this cannot be repaired. When we inject these damaged sperm into an egg cell, the sperm is not capable of fertilizing the cell. And even if it does, the [miscarriage] rate is very high."
This paper talks about the abnormalities seen in sperm exposed to nicotine, whether sperm can recover, and after how long.
This paper links the nicotine consumption of fathers to their children's likelihood of developing childhood cancer, citing one possible explanation that smoking causes genetic damage to sperm cells. The sperm cell mutations then become inborn cancer-causing mutations in the offspring.
They jury may be out on the extremity of nicotine's impact on adult health, but it's clear that it's deleterious to the next generation.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3880486/
Suggesting that the LD50 is an oral LD50 of 6.5–13 mg/kg.

Hi and welcome to the site. While this might indeed be relevant, it isn't considered a useful answer here. Please [edit] your answer and explain the relevant points of the paper here as well as how they answer the specific question asked. For instance, a suggested LD50 is irrelevant unless you also discuss the amount that would be ingested while smoking and what part of that LD50 it represents.