More Frog Development issues

There is this problem that often gets media attention from time to time but particuarly in the late 90's and that is frogs with deformities.

Now this story gives lots of insight into mass hysteria,and science as a way of knowing because it's a mystery with a surprise twist ending.

So in ponds across North America all of a sudden there was an increase in reports of the number of frog deformities. The media quickly picked this up because its disturbing and possibly because frogs look vaguely human with their legs being longer than arms.

There were a number of possibilties that were proposed. One category was genetic mutation. This includes everything to human causes such as mutagens and radiation from various sources one article irresponsibly floats the idea of the ozone layer being responsible. The other was that a negative mutation arose and was being passed around which genetically predisposed some to these mutations.

The second category were environmental disruptor chemicals. This had been seen before with cyclopamine being a naturally occurring plant alkaloid that causes midline deformities in livestock.

There were some environmental correlates that turned up which seemed to initially shed some light but ultimately led scientists down the wrong path. Turns out that deformities were correlated with high numbers of nitrogen compounds. And that these were usually isolated ponds near civilization. Aha! so it must be due to human effects and those damn overgrown golf courses.

The only problem was that raising frogs in high nitrogen tanks didn't cause these deformities in lab experiments. Genetic experiments failed to find any correlates between those deformed frogs and normal ones. For example cloning frogs is really easy and the clones raised in a lab didn't grow up with deformities.

It took a while but the cause for most was ultimately found. It turns out that a trematode worm parasite causes these. At first this would seem to be entirely natural.

However due to complex ecological interactions the high nitrogen compounds caused sudden and unseasonable blooms in algae which lead to increases in snails which hosted part of the trematode worm's life cycle which led to increased parasitism of frogs who acquired these deformites.

http://www.sciencenews.org/sn_arc99/5_1_99/fob4.htm

Mathematics and development

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I have an free app on my i pod touch that generates fractals in response to tilting movements as well as by touch. A while ago before biologists actually knew how development worked they came up with all sorts of elegant mathematical models of how they wished development worked. It turns out that actually the whole thing is a very complicated mess with important things happening both upstream and down stream of genes that everything is made of modified and transposed modules and such.

But now lets look at a beautiful developmental fractal.
cauli.jpg

If you look at this "Romanesco variety" Cauliflower bud. It is a bud with smaller buds running up the side in a spiral which in turn are made of spiral buds and so on. It's buds all the way down. Unlike other aspects of development this phenotype is just the sort of thing you could give to a computer graphics generator and display.

What is really curious is that the whole cabbage brassica alliance was artificially selected from the wild mustard plant. Too bad developmental biologists don't care about plants because heres a case where this pattern could be investigated with many know sister taxa groups that could can find in the supermarket.

The T allele in mice

When you look at wild populations of the common mouse mus musculus there is this area or "locus" on their chromosome where a number of different alleles could be found population-wide. This is called the "T-locus" and the dominant T allele in these populations is very disadvantageous. If a mouse embryo gets two copies of this it will simply die during development during notochord differentiation and all over mesoderm malformations. A male that is heterozygous develops with a shorten tail and/or defects in sacral vertebrae.

It turns out that an allele at this t-locus is able to cheat in order to persist in populations. While there are some genetic conditions where the heterozygous individual has some advantage and then behavior comes in to maintain this heterozygosity this is not the case with the t allele. If you look at male sperm up to 95% percent inherit one but not the other t -allele. This allele is able to repeatedly cheat at the meiotic coin toss and then able to stay in populations despite the clear fitness cost.

Strange Development in Treefrogs.

There's these two species in the same genus of tree frogs in Minnesota and much of North America known by their common name the Gray Treefrog. They are both known by this because for a while the difference wasn't known.

"Gray" is really a poor descriptor of these species because both species can vary over time in coloration from pearl pink to brown to green to gray. Their patterns change to be different combinations of these elements. This is why one is known as
Hyla. versicolor. the other is Hyla. chrysoscelis.

Stranger yet is that versicolor is tetrapolid meaning that it has four of each chromosome instead of the usual two. It looks like versicolor came from multiple separate cases of chrysoscelis having a whole genome duplication in the past and then interbreeding. This is an extremely strong case of speciation in action. Molecular clock dating attributes that the most recent event of duplication that ended up contributing to the species at large was as recent as the end of the last ice age.

They are mostly identical except for this tetraploidy. There is one important difference though that puzzled scientists for a while. The mating calls of the species differ. When you look at what genes are being expressed it doesn't look like there is a significant difference in gene expression that might happen from this. Likewise, their anatomy differences are very subtle and really only come out when you take tons of measurements and average them together.

There is something that came along that could explain this and if true is a very unexpected way that evolution shaped development. It has been shown that you can use various techniques and make your own separate genesis of a tetrapolid tree frog like versicolor by inducing tetraploidy in chrysoscelis. This has been done much more when comparing the tetrapoid frog model organism Xenopus laevis to a close diploid sister species Xenopus tropicalis.

What seems to happen is that when these duplications happen in the lab there isn't that great a difference in call structure initially, but there is some difference. This could have been explained away with the observation that these man made tetraploids are in fact physically larger than the wild tetraploids. It was found that there is a significant change in cell volume due to these events. Wild type versacolor frogs have a difference but not all that mcuh. In recent publications this difference has been attributed to there physically being more DNA in the cells which bloats the cell at large.


The change in cell volume though differs from tissue to tissue. It has been shown that cells in the respiratory system are exceptionally loosely packed making them larger.
Gerhart et al, found that the wild-type versicolor frogs had more that a 50% lower sounding call compared to our diploid chrysoscelis. The other cells seem to have found ways to epigenetically do some space saving.

Chrysoscelis females do like lower sounding calls because, it is thought, they are an advertisement of body size which is a signal of a successful male. The two species are found along side at it looks like females have evolved some way to be able to discriminate and not simply get wooed into mating with the tetraploid from which they would not get their eggs fertilized.


This cell volume thing could really complicate the difference between how we generally think of phenotype flowing out via the central dogma of gene->rna->protein--(other interactions)---->phenotype.

This is however a good example of how evolution acts on heritable phenotypes. To selection it doesn't matter that this is a ridiculous way of producing a more attractive call, all you need is to express that phenotype and it goes from there. It would be interesting how a species was able to emerge from this tetraploid event and if the call being more attractive happened to also strengthen this speciation event.


Sources;
http://www.jstor.org/stable/1563361
http://rspb.royalsocietypublishing.org/content/268/1465/341.full.pdf
http://onlinelibrary.wiley.com/doi/10.1002/jez.1402100115/abstract
http://www.jstor.org/stable/1563777

There's these two species in the same genus of tree frogs in Minnesota and much of North America known by their common name the Gray Treefrog. They are both known by this because for a while the difference wasn't known.

"Gray" is really a poor descriptor of these species because both species can vary over time in coloration from pearl pink to brown to green to gray. Their patterns change to be different combinations of these elements. This is why one is known as
Hyla. versicolor. the other is Hyla. chrysoscelis.

Stranger yet is that versicolor is tetrapolid meaning that it has four of each chromosome instead of the usual two. It looks like versicolor came from multiple separate cases of chrysoscelis having a whole genome duplication in the past and then interbreeding. This is an extremely strong case of speciation in action. Molecular clock dating attributes that the most recent event of duplication that ended up contributing to the species at large was as recent as the end of the last ice age.

So they are mostly identical except for this tetraploidy. There is one important difference though that puzzled scientists for a while. The mating calls of the species differ. When you look at what genes are being expressed it doesn't look like there is a significant difference in gene expression that might happen from this


Sources;
http://www.jstor.org/stable/1563361

Devo lab pretty worms Pt1

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Well that's the best I was able to get with the first pass. Tomorrow I will try and identify different stages in their life cycles if my dishes haven't dessicated too much.(though hopefully then they would hold still

Themes of Plasticity and Evolution in Salamanders

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So this guy VC Twitty was doing some classical embryology. Back before all the molecular and much of cellular biology; experimental embryology was about moving tissues around and other such macroscopic surgeries. What Twitty (1932) was trying to do is study the proximate details of how eyes, eye muscles, optic nerves, visual centers develop by introducing pathology. Introducing pathology is a classical way to study how a system works, by breaking something and seeing what the effects are. Maybe you'll create some sort of monster you can compare to normal development and the differences might reveal just what sort of mechanisms are at work.

What Twitty did was to take the embryonic patch that would give rise to an eye in a large salamander species and put in on a small salamander embryo of a species in the same genus.

Now before we get to the result; lets think up a few predictions.
I would expected this not to work all. I thought maybe there would be a host rejection of this foreign eye. Or maybe the eye would just shrivel and die. If not that then maybe there would be some effect down the line like the eye would grow too big for the skull and there would be problems.

What actually happened is that the eye grew normally as it would have on the large salamander species and the host (the small one) adapted to live with this eye. Yes the orbit (or the eye socket) increased with size to accommodate this larger eye. The was a debatable amount of vascular increase to supply this eye.
Most surprisingly is that the visual cortex for this salamander grew in response to the larger eye by between 10 and 20 percent. Now it wasn't the brain part that was transplanted. Instead it seems that the brain proliferated brain cells to use the foreign eye.

What twitty was trying to originally was create a chain of failures to see how these things work but instead found a remarkable capacity for the salamander to deal with changes that would never happen in nature. It seems that it is possible to change one single thing dramatically and still have a viable organism.

I'm no expert but this ability inspires me to ask some broader evolutionary questions. Say that we were to get a "hopeful monster" or a sudden developmental change due to mutation. It would seem that some may not require mutations to other parts of anatomy because by itself there may be enough plasticity.

Say there was a naturally occurring mutation that cause larger eyes in a salamander. It may be possible for the salamander to not only get larger eyes but see better in the same generation. This makes for some interesting fodder to ask questions with regards to natural selection. Maybe there are times when having larger eyes that don't see any better wouldn't
be selectively advantageous. But if your able to take a full step towards better vision then maybe this hypothetical gene could get passed around.

Further follow-up experiments have confirmed Twitty's results.

What I would really like to do is take this established case and maybe start testing salamander vision. I would like to know if in someway there is better vision. Is this a usable proliferation in the brain or just a poorly integrated bundle of nerves?

Cross section of development

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3290643292_73ccd8a24b_z.jpg

This plate is in Anthropogenie by Ernst Haeckel

Plasticity of Sex in Frogs

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A researcher: Tyrone Hayes at the University of California Berkeley was doing research on the environmental impact of herbicides

http://www.pbs.org/wnet/nature/episodes/frogs-the-thin-green-line/video-agricultures-effect-on-frogs/4848/

The video shows how experimentally genetic male frogs can be changed into females by exposure to a commonly used herbicide.

That this is possible probably seems very strange to those who don't know volumes about biology but this is not without precedent. There is the charnov-bull principle of sex determination that shows that some reptiles change sex while in the egg due to the ambient temperature because the physiology of the different sexes have different survival rates dependent on temperature Amphibans have long been known to be very sensitive to chemicals. I have heard it said that this is due to their thin and porous skin.

In fact back in the days before instant pregnancy tests they would take blood or urine from a woman and inject it into an african clawed frog Xenopus laevis and if it developed eggs then that means the human woman had these reproductive hormones at high levels and was likely pregnant.

Still, this is very striking because we usually think of sex as something set in stone.

This brings up some ecological questions such as what ecological effects this will have.
It is generally said that females are the limiting sex and that as long as there are a few males around the population can continue to survive. This probably does matter on the mating style. Amphibians for example often use the "big bang" method where there are just a few nights where actual mating takes place. Since it takes a while for sperm to mature it might not be possible for one male to fertilize more than one female's clutch of eggs.This will is just the sort of thing that produces interesting population genetic scenarios.

Also, maybe this could illustrate the Baldwin effect. Perhaps if males are largely turning into females that there could be a selective advantage to decreased sensitivity to whatever environmental factors are affecting sex ratios.

It should be said though that if you search for information on atrazine you will find astroturf, google bombed links and such sponsored by agribusiness-- reminiscent of big tobacco and climate deniers so be advised.

First thoughts on Evo-Devo

Now that I am finding myself entering into the upper division biology classes I often find that things I was told in 1000 and 2000 level courses are contradicted in later courses. I keep coming across misconceptions that are an artifact of how biology is taught both in coursework and textbooks.

For example I was told thorough the most memorable mnemonic ever made the "ABC's" of animal behavior according to Tinbergen. Under this scheme of thinking there are two divisions of biological thought of what sorts of questions can be asked.

Animal
Behavior
equals=
Causation (What are the physiological causes?)
Development (How does the behavior unfold given the environment?)
Evolution. ( when did the behavior enter a given clade and how is it distributed or modified?)
Function (How does the behavior lead to increases in reproductive success?)

It is said that C and D are proximate which deal with individuals and populations and such.
It was also said that E and F are ultimate causes that deal with populations through time and things like selective pressure. In the lab sections when writing up those lab reports we were asked for sections relating to these four questions(above) in such a way that
the evolution section could only relate to comparing sister taxa and that causation had to just talk about the physiology that say causes a refrigerated nerve to generate an action potential. It was so tightly

Classically there was little attempt to try to explain either C or D in terms of E and F. But I always thought that was a mistake to ignore the middle ground. Now much of this was due to the limitations in technology.

Evo-devo is interesting in that it tries to explain how "evolution is the control of development through ecology". I can see why evo-devo is resented. For the longest time biology was about
naming things, shoving frogs in pickle jars, and just creating volumes upon volumes of facts. From my understanding; that's the point of a synthesis-- to create a new explanatory framework form which things in one field can be applied to others.
I really can't see why there's so much pushback.

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