(posted in General Biology)

On the other hand, you do still retain a lot of taste ability even with a plugged nose.

Try taste testing a firm raw potato or onion vs. an apple with a plugged nose. 
Our testers had no trouble telling the difference.

Right now we can't make a fetus using two human eggs or two human sperm cells (or the nuclei from those cells).

If we could combine cells from two females, the resulting progeny would all be XX daughters.

(posted in Birds)

A vestigial feature is not necessarily something that is not used.  Typically, an organ will be classified as vestigial if its original use or size has been dramatically reduced. 
Hoatzin chicks have claws that extend past the feathered portion of their wings.  However, as their wings grow, they cover the claws.  Adult hoatzins have fairly typical looking bird wings.  Think about the wing/body ratio of a baby bird compared to a adult bird, the wings get a lot bigger compared to body size as the bird gets older. 

I link to a figure from a Nature article that shows drawings of fossil hands as well as a hypothesis as to the evolution of the development of reduced digits in birds and therapod dinosaurs.

http://www.nature.com/ncomms/journal/v2 … 37_F1.html

Adding animal DNA to a newborn would be very unlikely to generate any large changes in body type. 
This is because most of the DNA that is involved in building a body plan (like types of limbs and numbers of limbs) is used in building the body plan during gestation - so before birth. 

Besides this, we don't quite know enough about development and genetics to convert body parts to other animals body parts.  We can change a fly wing into a haltere (tiny fly wing-like structure) or a haltere into a fly wing but we can't change either into a bird's wing or even a dragonfly wing.

Cladogenesis is the typical way we think of an evolutionary tree.  In cladogenesis, we get a new species by an ancestral species splitting into two daughter species.
Anagenesis is a little different.  In anagenesis, the new species comes about from many changes accumulating in the ancestral species over time.  In anagenesis, speciation doesn't occur via "splitting", but rather the accumulation of mutations and new phenotypes in a single lineage.

As a long-time yoga practitioner, I would like to chime in that results of yoga vary greatly based on the type of yoga.
Gentle meditative yoga is thought by many people who practice it to be good for stress and anxiety relief.

On the other hand, more physically taxing forms of yoga exist including vinyasa and ashtanga yoga.  Both of these involve cardio, strength training, and flexibility training.  Many practitioners of these types of yoga follow a standard cardio/strength type regimen.  Practice begins with movement-based stretching as a warm up then continues through a couple rounds of higher intensity interval training (HIIT).  Core and strength training is integrated into this or follows it.  Practice ends with static stretches and a mindfulness exercise.
Newer "yoga fusion" exercise like Piyo focus more on core and strength training as part of a HIIT regimen. 

Tl;dr:  Typically sports training involves strength training and HIIT cardio training.  This can also be accomplished with sepcific types of yoga practice.

External and internally develping sexual characters have linked but distinct developmental pathways.
Typically the internally developing sexual characters (testes or ovaries) will determine the secondary sexual characteristics as well as the shape of the external genitalia by secreting hormones that affect the rest of the body.

There are a couple of known human variants that make a "mismatch" between external and internal characters.

One is congenital adrenal hyperplasia.  This affects chromosomally female individuals and causes a masculinized external phenotype.   While the genitals still look essentially female, the individual can have some secondary male sexual characters like thick body hair.

Dr. Wynick already mentioned the possibility of hormone secreting tumors and androgen insensitivity.  Any inability to produce or respond to testosterone and it's derivatives can give a female (or feminized) external phenotype even with internal testes.

A parasitic twin of the opposite sex can act similarly to a hormone secreting tumor.

One final way to get a sexual characteristics mismatch is with a chromosomal translocation.  In this case, the affected individual is chromosomally female (XX) but has a small portion of the Y chromosome on one of the Xs.  If this Y chromosome piece contains the SRY gene this can lead to a sexually mosaic phenotype.  In some cells the translocation X will be the Barr body (turned off) while in others the normal X will be the Barr body.  Cells with the normal X turned off can act as "male" and will promote testes development.  In some cases these individuals can have a gonadal mosaic.

I need to note that none of these things (with the possible exception of an extremelly rare parasitic twin) will lead to both types of external genitals.  There is a single external genital field in the developing embryo and this can make male genitalia, female genitalia, or "in between" genitalia (most rare).

(posted in Plants & Fungi)

It's just water than has algae growing in it.  Algae is photosynthetic, so it will pull carbon dioxide out of the atmosphere and release oxygen.

Generally a haplogroup is a set of alleles along a particular chromosome.  So if you share an entire chromosome with your sibling, you would have the same haplogroup for that chromosome.
When talking about human population genetics, it's usually referring to either a mitochondrial haplogroup or a Y-chromosome haplogroup.
These are useful for thinking about human migration patterns because there is no recombination along mitochondrial DNA or Y-chromosomes. That means that you have the same mitochondrial sequence as your mom and your siblings.  If you are an XY male, you have the same Y-chromosome sequence as your dad and brothers.

Even though there is no recombination, rare mutations do occur.  If they get inherited, then these mutations can define a new mitochondrial or Y-chromosome haplogroup.  Since the mutations are rare, humans in the same haplogroup share a common ancestor.

(posted in Fossils)

Scientists usually don't use carbon-dating for most fossils since it's half life is fairly short in comparison to the fossil record.  Instead, fossils are dated using a variety of radio-isotopes including Potassium and Uranium.

The half-life of radio-carbon is about 5700 years and it can be used to date once-living material that is up to 50,000 years old.  It can be used to date things older than it's half life  because a half-life is the time it takes half the radio-carbon in a sample to decay into Nitrogen.
So if you start with 1000 atoms of radio-carbon, after 5700 years you will have 500 atoms of radio-carbon and 500 of Nitrogen.  After 11,400 years you will have about 250 atoms of radio-carbon.  After 17,100 you will have about 125, and so on.

The decay of radio-carbon itself is constant, but the amount of available carbon in the atmosphere has changed over time.  For that reason, scientists calibrate these measurements using other measures of available carbon.

For fluorescent capillary sequencing, the majority of the DNA travelling through the acrylamide in the capillary is amplified insert fragments, not intact plasmid.
The inserts are amplified using PCR (http://tinyurl.com/pkz86vz).  The reagents used cause termination of the PCR reaction at random points, when that happens a fluorescent label is incorporated into the gene fragment. 
The "promoter" is actually a single stranded DNA primer.  It usually is designed to bind to plasmid sequence so you amplify the entire piece of insert plus a little bit of plasmid. That is helpful because you can use the same primers to sequence any insert in a particular plasmid, you don't have to have any information about the gene sequence.

(posted in Evolution)

The timetree site has really fantastic trees that use both fossil and molecular evidence:
http://www.timetree.org/book.php
The consensus on bat origination is somewhere around 84 million years ago.

I leave out the dregs of a glass of red wine, a large glass works best.  I consider this semi-humane because at least the flies go out with a big whollop of ethanol.  I also consider it easy because it means I can leave my clearing up for another day.

I'm not sure what your question is here?  I highly doubt a Cardiologist can answer a question about fossil heart tissue.

There are a couple of different levels of biology that you are talking about here.
At the biochemical level, yes there are some "types" of mutations that are more likely to happen, for example deamination of methylated cytosines to make a thymine.
At the genome level, there are also "hotspots" for mutation.  For example, additions and deletions to microsatellites. 

These types of mutations might be "evolutionary dead ends" meaning that either they produce an inviable or infertile phenotype or they are somatic mutations only and do not get passed down to progeny.
But usually mutations don't have any effect on phenotype or fitness at all, in which case they are neutral mutations, or a very very small effect on phenotype or fitness, in which case they are nearly-neutral mutations.  These kinds of mutations can persist in a population. 

When mutations do have a larger effect on phenotype, there still might not be selection against the new phenotypic variation.   The phenotypic abnormalities that you mention - like change in heart size or organ deformity - might be regulated by a very large number of genes.  Its possible that a single mutation in one of these genes would have only a nearly-neutral phenotype and thus it could potentially persist in a population.

The assumption that variation in organ size is unlikely turns out to be incorrect.
A quick google search showed me an old paper looking at heart diameters in humans.  It looks like there is a great deal of variation in heart size!  Normal heart diameters ranged from 9-18cm for adult men and 7-16cm for women.  This is a two-fold difference in heart size in healthy adults.
You might be saying to yourself - well some people are bigger than others and that could account for the difference.  Well lucky for us, the authors also measured the cardiothoracic ratio and got a similar two-fold difference between smallest and largest.

http://circ.ahajournals.org/content/35/4/724

It does matter who is doing the caretaking - cukoo birds can invest more into larger numbers of eggs, choice of egg laying site, and larger eggs since they do not invest in parental care.
On the surface, this seems like it would be straight r-selection.  But keep in mind that there are several species of nest parasites and they experience different selective pressures.
In at least some species, nest-parasite eggs hatch earlier and the chicks are larger than the non-parasitic eggs. That means more investment into egg nutrients for the cukoos, which is K-selection.
In some ecosystems, the cukoo might experience high host acceptance, in which case it might have selective pressure for larger high-quality eggs.  In other environments, there might be a high rate of host rejection of the parasitic egg.  In which case there could be strong selective pressure for a larger number of low-quality eggs.

The simple answer is two fold:
1) Prokaryotes have evolved to levels of high complexity - our remote ancestors were prokaryotes, one lineage went eukaryotic, evolved multicellularity and over time evolved complexity.
2) Unicellular prokaryotes are extraordinarily successful. They make up the vast majority of species and cells on the planet. They typically have fast reproduction and have evolved the ability to exploit an enormous range of ecological niches.

But there is another question you are getting at:
Why do membrane-bound organelles seem to be a prerequisite for complex multicellular individuals?
The hypotheses I've seen for this typically hinge around signal transduction and metabolic scaling.
Prokaryotes are size limited due to the smaller amount of membrane space for metabolism.
Prokaryotes lack some mechanisms for signal transduction since they are missing membrane-bound organelles (the golgi and ER) that process proteins for multiple signal transduction pathways.
Small size and less ability to communicate with other cells may be limiting prokaryotic cells to a solitary or simple communal lifestyle.

Since it's only a genetic clone, it would be the same chromosomal sex as its parent (not necessarily gender).

I can't speak to this directly, but yes often trace fossils appear before body fossils.  My understanding is that: 1) There are just so many more traces that organisms leave behind than actual tissue.  If I walk in a mile of mud I will leave behind a much larger area of footprints than I will leave skeletal remains when I die.  So paleontologists are much more likely to uncover trackways than body remains at any stratum.  2) Trackways may be more likely to be preserved than bodies - no predators are attracted to trackways as a food source, bacteria don't eat trackways.  So trackways may have a better chance at being fossilized.

I'm not an actual paleontologist, though, I just pretend to be one for a couple weeks a year when I lecture on the fossil record.  Maybe a specialist can confirm or correct my suppositions?

Just reading the abstract and not the paper, it looks like you are drawing conclusions that go far beyond the authors'.
They are saying that intrinsic reproductive isolation (e.g. not due to external factors like geographical changes, migration, etc) isn't the only thing that drives speciation. 
So you can't use a species propensity to evolve reproductive isolation as a predictor for speciation.  These two things happen at different rates due to other factors helping to drive speciation, like geographical speciation.

(posted in Mammals)

As far as I know, most of the research on pangolin scales is in the biomaterials field.  I don't know of any gene expression studies on pangolins.

Since you asked about eye evolution (my speciality!) I thought I'd link to a very nice paper written for college and high school-level students by two of my colleagues.  It explains both the molecular and morphological basis of eye evolution:

http://link.springer.com/article/10.100 … ltext.html

(posted in Evolution)

I think you are misunderstanding the reference.  The reference discusses a single person with a different number of chromosomes than the majority of humankind.  That will make it potentially more difficult for him to make viable offspring with wild type females. 
But that does not speak to the evolution of chromosomal rearrangements in general.  Imagine that the man in the article has 10 children all with hybrid cells that have extra chromosomes.  Now if he lives in a small community, a couple generations down the line some second cousins with these hybrid cells could marry and start to produce children with the higher chromosome number. 
If there is not strong selective disadvantage this would not become fixed in the population unless by random chance.

However, there is a chance that a rearrangement would produce an advantageous event.  In that case, the progeny of the man would outcompete the wild type people and, eventually, the chromosome number could become fixed in the population.

(posted in Evolution)

For vertebrates, tails are extensions of the spine.  To have two tails means that the embryo was exposed to a teratogen or has a major mutation that affects its head/tail axis, or that it is the result of incomplete division of conjoined twins.

This developmental anomaly almost certainly would have other detrimental effects.

(posted in Evolution)

I'm with Corwin.  If it was alive today we would almost certainly call the ancestor of humans and modern monkeys a "monkey."

(posted in Evolution)

It is true that a lot of energy is wasted in sexual reproduction trying to find and attract mates, producing extra gametes, maintaining complex reproductive structures. 
However, sexual reproduction allows for shuffling of genetic material and, thus, increased variation in the population.  If a population is genetically homogenous - say all decendents of an asexually reproducing mother - then any environmental event that selects against that particular genotype can wipe out the whole population quickly.  When there is genetic variation then that same environmental event would only select against the one genotype, leaving the others free to continue the species.

Paleontological work is still ongoing, so it is current research.  New species are uncovered in the fossil record every year.
Phylogenetics also helps uncover species and species relationships every year as does general exploration and observation of the natural world.
Here are the "Top 10" new species discovered in 2012:
http://species.asu.edu/Top10

But back to your question: When and where do we see actual speciation occuring.  Well, this is a little bit of a hard thing to watch in the wild since speciation events occur over geological time scales - thousands and millions of years -  so obviously most of these are impossible to watch unfold.  However, we do have great examples of speciation that appear to be currently happening or have happened very recently.  For example, cichlid fish in African lakes came from a common ancestor about 4-5000 years ago but now look very different and do not appear to interbreed.
In the lab, breeding and selection experiments have generated new species of bacteria (the Lenski lab has watched bacteria evolved the ability to eat citrate, something their recent ancestors could not do) as well as fruit flies (Dodd lab, for example isolated fruit flies and observed speciation).
Here is more information:
http://evolution.berkeley.edu/evolibrary/article/evo_45

Postdocs in the US earn about $35-60,000 a year depending on the field, grants, and whether your position includes teaching (these seem to pay on the higher end in my experience).

For PhDs in the US, herpetology is not a field I see a lot of research stipends for (though of course there are a few!). 
Typically here you would have to work about 20 hours/week as a teaching assistant (TA) to earn a stipend that can vary from $13,000-$30,000 per year depending on the institution and whether you are working summers. Your tuition and fees are covered by your institution or department.

If you don't TA then your program will cost you money - US students at a private institution will pay upwards of $50,000 a year in tuition and fees.

Exercise has been shown to enhance cognitive performance:
http://www.sciencedirect.com/science/ar … 2210002782

One regimen I have seen a few times is regular exercise (increases aquisition) and exercise just before the exam (increases recall).

Ok I didn't see this before but I think I know what he is talking about.
1) The two molecules represent any two of the five proteins. So they want to calculate the probability that the phylognetic tree of any two proteins would be identical if the proteins are only different by chance (and not the product of common descent).
2) All possible trees that terminate in 11 descendents just means that they figured out all the possible ways that 11 organisms could be related.
This number is the same for any group of 11 organisms. Here is an image of all the ways three organisms (I, II and III) could be related:
http://biology.duke.edu/rausher/trees3.jpg
There are three ways.
For four organisms there are 15 possibilities.  For five there are 105, and so on.

So all Dawkins is trying to show here is that there are an incredible number of ways 11 organisms can be related to each other. The chance that two proteins would give the same relationships tree if common descent were not true is vanishingly small.

4. Get some light exercise just before the exam.

It can be either, really, depending on what you are interested in.  If you are looking at the genetic and/or environmental basis for a particular trait, then your phenotype is what you can observe about that specific trait. 
However, your phenotype in general is everything observable.

I would like to note that this includes behavior (what you do), not just how you look.

Krebs cycle mostly generates NADH for oxidative phosphorylation.  Since oxidative phosphorylation requres Oxygen you will get a build up of NADH if you run the Krebs cycle in anaerobic conditions.

I agree with the above!  If you can't stay around your University over the summer, try contacting professors at other Universities, especially small Colleges with active research programs.  Let them know what you are willing to do and what your coursework has been so far.

(posted in Evolution)

Bdelloid rotifers are evolved from an ancestral sexual species.  The evolution of asexuality in this lineage is thought to have occured about 80 million years. 

I do not know what you mean by "species hybrid event" so I can't answer that part of the question.

There is actually quite a bit of evidence in the literature for some kind of caloric restriction (hypothesized to be linked to glucose restriction) in inhibition of tumor growth.  I would not be at all surprised at a clinician interpreting this as "no carbohydrates." 
What I have generally heard from oncologists is that they recommend limiting simple sugars and processed carbohydrates (sucrose, bread, some sugary fruits) but not vegetables.  However, this may not be the case for all types of cancer and I can't speak to your individual situation!

I'm afraid this review article is behind a paywall but you may be able to access it at your local public library:
http://www.ncbi.nlm.nih.gov/pubmed/21516129

Snakes use sight much the same way we do, though their eyes are not nearly as keen.  Their infrared sensors are a completely seperate sensory system, apparently, much the same way that you get information from your nose about odors and from your tongue about tastes.  These two types of information don't necessarily "compete" with each other, rather they complement each other. 

Some neurons in the snake brain can respond to both infrared and visual information, but others respond only to one or the other.

We already see non-evolutionary responses to higher fitness in humans.  In several countries birth rates/population have been getting lower for many years.  These are countries where individual people have decided that they do not have the resources (time and money) for multiple children.

Another huge factor affecting this is that women are waiting until they are older to have their first child.  This has a giant impact on the number of children they can possibly have and lowers the birth rate overall.

Even though we have used our big brains to build technology to increase our potential fitness (greater access to food and healthcare -> lower mortality rates, higher fertility), we are also using technology to decrease our reproductive fitness (birth control).

(posted in Evolution)

Just to expand a little on the construction of phylogenetic trees.
To create a phylogeny we typically use hundreds to millions of molecular traits. By using so many traits and so many different distinct genetic loci any convergence will be quickly swamped out by good data.

Trees built using morphological characters (like presence of eyes) are more rare nowadays but still very useful when molecular data cannot be obtained. These trees will often be built from tens to hundreds of characters with methods used to find the most "useful" characters. That would preclude convergent (or homoplastic) characters. Thus the tree would use characters like presence of wings and feathers, shape of the pelvis, ability to exchange gas over the skin, etc. to build a phylogeny that includes both parrots and salamanders rather than presence of eyes.

I think you may be misrepresenting what your teacher said. AA, AO, BB, BO, OO are not phenotypes.  A, A, B, B, and O are the respective phenotypes.

What I just saw on the test I graded last week (and I suspect your teacher may have seen as well) was students thinking that type A blood was a genotype, not a phenotype.  Someone with phenotype A can be I^A i^A or I^Ai  therefore you can't just say that their genotype is A. 

Sometimes people for shorthand will say that someone with type A blood can be either AA or Ai.  That is generally considered acceptable but of course if your teacher told you to write everything using standard notation it would technically be incorrect.

After mitosis but before S-phase our chromosomes do not look like the famous X picture, they are composed of one chromatid (but are still called chromosomes). They are condensed "springs" for a little while but then decondense after the nuclear envelope reforms. At that time they look more like thin tangled strings although they still have many proteins associated with them.

Depending on who you ask, you can get different answers to the "n" question. Probably the easiest way to think about it is that n=the number of distinct (non-homologous) chromosomes in a nucleus.
That means that sperm and eggs are each 1n and most cells in our bodies are 2n (we have a copy of each chromosome from each of our parents, one from sperm, one from egg n x 2 = 2n).

After S-phase each one of these chromosomes is now an attached pair of sister chromatids. Some people would argue that since each pair of chromatids is technically a single chromosome, the cell at this point is 2n. For simplicity I say that the cell is 4n - each genetic locus is represented 4 times in the genome.

The earliest vertebrates, Haikouichthys and Myllokunmingia, date to the Cambrian - about 525 million years ago.  They did not have the calcium-based skeletons that we see in many vertebrates today, though.

You can lower your IGF1 levels by going on a vegan (low protein) diet.   

http://www.ncbi.nlm.nih.gov/pubmed/18843793

In this study the vegans ate about 1g of protein for kg weight (still well above recommended levels of at least 0.75 g/kg weight for average adult females) compared to the omnivores who ate about 1.67g/kg body weight.

I fixed the wikipedia page. Hopefully that will help!  A major fact to note is that the voles include over 150 species, so lots of speciation has happened in this group, possibly some of it due to polyploidy.

In the species with different chromosome numbers in males and females - that can actually be a mechanism of sex determination as is seen in many insect and crustacean species (among other organisms).

Great deep questions!  I can't really comment on the mass extinctions part, but here is some info on the first few questions:
1) Did abiogenesis happen just once? 
We don't know!  What we do know is that if life originated more than once it seems that in the end just one form (what we see now) predominated.  Of course it is possible that there were multiple origins of life and they "combined" to form what we know now as life. 
2) Why is it so difficult to generate life in the lab?
Early pre-life (self-replicating molecules) were really little.  I mean so little we wouldn't be able to see them even with a fairly powerful microscope.  That makes these kinds of molecules difficult to study.  That said, there has been amazing progress in the last 60 years on life's origins.

From showing how the complex chemical building blocks of life can spontaneously form from very simple chemicals that were probably abundant on the early earth:
http://www.chem.duke.edu/~jds/cruise_ch … iller.html
http://www.wired.com/wiredscience/2009/ … cleotides/

to creating simple self-replicating RNA molecules in the laboratory:
http://en.wikipedia.org/wiki/Ribozyme

3) Could viruses or prions be a seperate origin of life?
Prions are proteins that normally are encoded by an animals genome that have misfolded and have gone haywire.   So these are not a seperate origin of life.
Viruses, on the other hand, might possibly be (though this is unlikely).  They are nucleic acid based but have evolved so quickly that at least in some cases their origin is unknown.  Some viruses, however, do seem to carry a signature linking them to known forms of life.

In response to Glorianne - that is not what cellular memory is, this is what cellular memory is:

http://en.wikipedia.org/wiki/Epigenetics

It has nothing to do with personality traits, but rather innate properties of individual cells.
Epigenetics could potentially affect personality, but only when it is affecting central nervous system cells or, perhaps, endocrine cells.
I think in some exceedingly rare cases, such as a glandular tumor, parts of a personality could reside outside the brain - but this is only because hormones can affect the central nervous system.  This has nothing to do with visceral neural networks.

I would like to quickly address your question of compatibility.  If we are looking at the single gene level then there are regions of compatibility between humans and onions.  For example, both species have many of the same genes used in metabolism and quite a few of these are probably more or less interchangeable. 

To directly compare the similarity level between species, we would need to sequence both genomes and then compare genetic regions to each other.  There are some computer algorithms that will do this, but it is not an easy feat when looking at organisms that are so distantly related.  We can also do binding assays - where we look to see how much of the DNA from each species can hybridize to each other.  This gives a measure of similarity as well, though it is not as precise as genome sequencing. 

An animal that scientists often use as similar to humans is the lab mouse.  Even though our chromosomes look pretty different, most of our genes are very similar to each other.  So at the gene level we are compatible, even though at the chromosome level we are not.

Hi Klaus,
We can infer the "history of DNA" by comparing DNA sequences between different organisms.  For example, if we take two species we are pretty sure are very closely related, we can compare their DNA for a particular gene or genetic region and look for differences.  Say we find 5 differences and 500 identical nucleotides.  That would suggest that the last common ancestor had those same 500 nucleotides but we wouldn't know what nucleotides they had at the places that are different.  We'd have to do more work and look at the sequences of more species to figure that out.

By doing this with a lot of species and a lot of genes, we can start to figure out the history of the DNA for that group of organisms.  We can also look at things like "gene order," which is the order of genes on a chromosome, to figure out events that happened in the history of the group of organisms.

This isn't a reference book, but my 5 year old would suggest Dinotopia - it is a fantasy book but is primarily beautiful illustrations of dinosaurs and does use their scientific names.

He also does enjoy reference books like the National Geographic one, so I would heartily recommend that as well!

Probably not - fish scales come from dermal (mesoderm) tissue while reptile scales come from epidermal (ectoderm) tissues and, unlike fish scales are made of keratin. Fish scales are more similar to teeth.