Monday, December 22, 2008

Phylogenomics suggest ratites lost flight multiple times

ResearchBlogging.orgRebekah Wukits discusses recent findings about ratite evolution for Bio 135.


Ratite evolution has been debated for centuries. Some of the earliest evolutionary biologists questioned whether or not ratites had a linear evolution or if the major groups had had independent origins. Richard Owen proposed that living ratites had much more in common with other flight capable groups while being united by the “arrested development of wings unfitting them for flight”. In 1951, two ornithologists, Mayr and Amadon, stated that, “the present consensus is that the main groups of these birds are of independent origins”.


Traditionally, ratites have been considered to be monophyletic, or ascending from a common ancestor. They are placed in the major group Noegnathae, with the flight-capable tinamous as a sister group. Since the extinct tinamous were capable of flight, it has been thought that the ratites lost flight once in their history, then diversified. Unfortunately, simple geography contradicted this theory. All living ratites (rheas, cassowaries, emus, ostriches and kiwis) are isolated on different southern continents.  Rheas are found in South America. Ostriches reside in Africa. Emus and cassowaries are found only in Australia and kiwis can be found in New Zealand. Extinct species of ratites follow the same pattern. Moas were also found in New Zealand, and elephant birds lived in Madagascar. The question became that if flight was lost once early in ratite evolution, how did they become so spread out and isolated? The perfect answer seemed to reside in the theory of continental drift. Ratites came from a single ancestor, lost flight and were then isolated when Gondwana broke up.


Though most of the recent studies of morphological and molecular ratite characteristics have supported the monophyletic theory, many still debate it. Rarely challenged is the fact that adaptations to a cursorial lifestyle, one that is adapted to running, can lead to convergent evolution, and can be misleading when basing phylogeny on morphology. This led scientists to do further phylogenomic studies in order to test the prevailing theories. These studies include data taken from genetic loci that represent the entire avian genome. In this particular study, data was taken from 20 loci that are dispersed widely throughout the avian genome. The data set included all living ratites and eight outgroup taxa. Previously done similar genetic tests have supported ratite monophyly, however these tests were more sophisticated and advanced and supported a different conclusion.


The results are as follows: analysis of the data strongly supports placing the flight capable tinamous within ratites and ostriches as the sister group. If this new phylogeny is correct, the single loss of flight in ratites is unlikely. In order for all ratites to have lost flight in a common ancestor, the tinamous would have had to regain flight at a later time. It is much more likely that flight was lost multiple times do to convergent evolution than to have gained flight in the earliest ancestors, lost flight in the common ancestor of ratites, than gain flight again in tinamous.


It seems more likely that ratites descended from a single ancestor, than diversified when gondwana broke up. Flight was lost in each family and convergent evolution occurred due to similar environmental conditions. Flight is very costly both energetically and morphologically. Ratites had little pressure to fly and since these features are costly to maintain, they became reduced over time.  The theories of this paper seem concrete however more study is needed. Their own genetic studies produced conflicting results. Placing tinamous within ratites has great implications for their evolution and dispersal. This idea needs to be further developed and supported.


Reference:


J. Harshman, E. L. Braun, M. J. Braun, C. J. Huddleston, R. C. K. Bowie, J. L. Chojnowski, S. J. Hackett, K.-L. Han, R. T. Kimball, B. D. Marks, K. J. Miglia, W. S. Moore, S. Reddy, F. H. Sheldon, D. W. Steadman, S. J. Steppan, C. C. Witt, T. Yuri (2008). Phylogenomic evidence for multiple losses of flight in ratite birds Proceedings of the National Academy of Sciences, 105 (36), 13462-13467 DOI: 10.1073/pnas.0803242105

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Wednesday, December 10, 2008

Studying the Flamenco Dance of the Jumping Spider

If you were intrigued by the video you saw in class of the mating dance of jumping spiders, this will show you a bit more about how one can go about studying such fascinating complex behaviors.







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Why Sex?

Apropos of the recent steamy discussions in class about sex and evolution, Sonica Sangha shares this video she found on the PBS website:



[via Evolution: Library: Why Sex?]


And as a bonus, here's a behind-the-scenes video podcast accompanying the wonderful PBS Nature series "What Females Want and Males Will Do" which aired last spring. Click on the show titles for more fun video clips and information from the PBS Nature website.




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Wednesday, December 3, 2008

Modeling the emergence of multi-drug resistant TB hot zones

ResearchBlogging.orgRebecca Freeman submitted this essay for the Evolution class.



According to the World Health Organization (WHO), a “hot zone” is an area with >5% prevalence (or incidence) of Multi-Drug Resistant Tuberculosis (MDRtb). Sally M Blower and Tom Chou have been using a mathematical method to track the emergence and evolution of multiple strains of drug resistant tuberculosis, but they have now developed a new, more complex mathematical model. Before this model, there was only a two strain model, meaning it was only relevant to individuals that can be infected with a wild type pansensitive strain or a drug resistant strain, but there are many more strains then this. There are a resistant strains only to one drug and some resistant to multiple drugs. This means there is a multitude of strains in these hot zones and there was a need for a better way to track this (Blower and Chou 2004). Blower and Chou realized that a more complex mathematical model is necessary to capture the complexity of the epidemiology of the hot zones, and the evolution of hot zones was very unclear



Understanding drug resistance is important to understanding the, and Blower and Chou explain the evolving of resistance very well. They give three processes that are involved in generating drug resistance: Transmission of drug resistant strains to uninfected individuals, which is transmitted resistance; Conversion of wild pansensitive cases to drug resistant cases, which is acquired resistance; finally, cases where they have drug resistant strains and it becomes resistant to more antibiotics during treatment, which is amplified resistance. What everyone has had to do in the past is just study acquired and transmitted resistance, and now with the new model, they can incorporate amplification resistance. This was a big problem because it has been shown that inadequate treatment of DRtb can result in the amplification of drug resistant strains, which may be an important process of MDR epidemics (Blower and Chou 2004). So this is where Blower and Chou came in. They created a model, the call the amplifier model, that enables the tracking of emergence and evolution of MDR strains, the transmission of these strains and the amplification of these strains during repeated episodes of treatment.


Blower and Chou are really studying the effects of inadequate treatment programs, and how this may lead to a higher prevalence in MDRtb. One problem that this research cannot completely take into account yet is the transmittance ability of MDRtb compared to pansensitive tuberculosis. This is an area that is hazy right now, and so this cannot completely be incorporated into the model. Amazingly, they have measured a general fitness of MDRtb vs. pansensitive tuberculosis, by calculating the treatment fail rates and treatment cure rates of the each category of strains.



The authors were very clear with the purpose of the model. Even though the mathematical model is very complex, the idea and how they explain it is easily understandable. They use R0 to stand for the average number of secondary cases caused by one infectious case in a population where treatments are available. Their model breaks this up into four categories of strains: The wild type pansensitive [R0(1)], which is sensitive to all drugs; Pre-MDR [R0(2)], which is sensitive to one of the main drugs used to treat tuberculosis; MDR [R0(3)], which is resistant to both of the main treatment drugs; and post-MDR [R0(4)], which is resistant to both of the main antibiotics and others as well (Blower and Chou 2004). With the information gathered from over 30 years of date they constructed likely evolutionary trajectories of hot zones, and with this they also took into account low cure rates vs. high amplification probabilities in many areas. They also tried to incorporate which strains are more transmissible, but as I said before this was not really possible with their model and there was a large degree of uncertainty.



The results of their model matched the WHO predictions well, but there were some distinct differences, and I think these differences are what make this research so important. By using all for types (R01-4) they found great variability in incidence and prevalence. When treatments were originally started strains of pre-MDR strains emerged quickly, so incidence and prevalence of pre-MDR strains increased, and this subsequently led to possible amplification of resistance and MDRtb epidemics in certain areas. The question is: Why certain areas and not others? This question is explained by Blower and Chou. Interestingly, areas with bad treatment programs do not necessarily have a really high incidence of MDRtb, it has stayed pretty steady at a 5%-14% (Blower and Chou 2004). This to me seems like an argument that MDRtb is not as easily transmissible, because its rates overall have stayed pretty low, but there was no significant evidence for this. The WHO predictions state that a >5% prevalence OR incidence in MDRtb equals a hot zone. Blower and Chou found the mathematical relationship between MDR prevalence and incidence. MDR prevalence can be three times greater then MDR incidence. They used the results to evaluate the hot zones on prevalence or incidence. If it is by incidence then only 20% of those areas would be considered hot zones and 51% if criterion is prevalence (Blower and Chou 2004). I see this as an argument for the fitness of MDRtb to be very high and transmissible ability to be lower, because there are less new cases, and more cases that have just become more resistant.



When looking at the four strains the hot zones had a much lower R0 for pansensitive strains (median=.82), which suggests that the wild type strain should be slowly eradicated. The R0 for the pansensitive strains in non-hot zones were all above 1 (median=1.39) Looking at the rate of detection of cases and treatment rates in hot zones versus non-hot zones it is 55% to 25% (Blower and Chou 2004). This shows that places where they have control programs were successful at fighting pansensitive strains but ironically it created more MDRtb strains, making it more likely to become a hot zone.



The importance of this research is that they have figured out that the difference between incidence and prevalence rates is significant enough to change the view of an area as being a hot zone or not. Their research looks at many factors that go into the evolution of these hot zones. Out of the many factors they actually saw that case detection and treatment rates were the most important factors. They came to this conclusion because if case detection and treatment rates were low, and the amplification was high, it still did not generate a hot zone. Vise versa, if the case detection and treatment rates were high and the amplification rates were low; it was likely to become a hot zone. The point is that these areas with high case detection and treatment rates should not increase these rates unless high cure rates are achieved first. Blower and Chou have created a model that has multiple dimensions and can help the WHO in the future to prevent hot zones from popping up in high risk regions. The WHO already had a model for this but it was nowhere complex enough to correctly calculate prevalence and incidence of MDRtb, and how their mathematical relationship.


Reference:



Sally M Blower, Tom Chou (2004). Modeling the emergence of the 'hot zones': tuberculosis and the amplification dynamics of drug resistance Nature Medicine, 10 (10), 1111-1116 DOI: 10.1038/nm1102




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On Hormonal and environmental control of neuroplasticity

Andrew Mora review's Christy Strand's seminar on neuroplasticity.



Nueroplasticity is an interesting concept that deals with changes in the brain due to experiences. In order to study neuroplasticity better, Dr. Christy Strand used hormonal and environmental cues to see how they would affect the brain. The specific region of the brain that Strand was interested in was called HVC (high vocal center in birds) and the size of this region of the brain was recorded before and after experiments. According to Strand, this region in birds is important in motoring song output, and is also involved in song learning. She asserted that testosterone, an important steroid that affects the brain, did in fact increase HVC volume, but was uncertain as to how the region got bigger. Did individual neurons get bigger? Was the density decreased? Or were there simply more neurons from new cells?



In order to test for the size of the HVC, Strand used bromodeoxyuridine (BrdU) which is a cell birth marker. She used house finches because they are very common throughout the US and they are great song birds to test for the HVC region. Besides using testosterone treatment for the birds, she also wanted to know the role of the photoperiod in increasing HVC growth. Her results indicated that testosterone treatment does affect HVC growth, that photoperiod alone might affect HVC growth, and that testosterone treatment does not affect the number of new HVC neurons, despite an increase in total neuron number. Her reasoning for this might be because of a natural turnover; that is, there is no new neurons being created, but there is a decrease in cell death. Corticosterone (a stress hormone) had no affect on HVC growth.



In another related experiment, Strand used rufus-winged sparrows to test environmental cues on HVC. She used these birds because they have a unique characteristic of beginning their breeding season after the first monsoon in southern Arizona and northern Mexico. Breeding season is important for HVC size because the birds are singing frequently when they are looking for a mate. According to strand, the testes of these birds are big in March, but only used in July when the first rain falls. Her results found that during breeding of these sparrows, HVC neuron number does not increase, and testosterone levels were not different on sampling dates. She did find that singing behavior increases during the breeding season, but was still unsure whether or not HVC affects singing behavior or if the reverse was true.



I particularly enjoyed the area of future research being done by Dr. Strand. She discussed that she will be experimenting with hormonal factors affecting neurogenesis and neuroplasticity in adult snakes and lizards. She will look at the affects of captivity on neurogenesis and affects of sex on neurogenesis. Instead of the HVC region she will look at the size of the medial cortex in adult rattlesnakes. I like this integration because it attempts to compare research done on birds with similar research done on reptiles. Hopefully we will see this work published soon.


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The role mtDNA plays in the evolutionary differentiation of species

Bob Koons shares his reflections on a Biogeography class discussion from some weeks ago. I've been unable to upload many student submissions to this blog due to severe tendonitis which limited my computer use for some time, but I'm beginning to catch up and hope to have the remaining student submissions uploaded before the semester ends!



Neotropical diversification of montane populations have been studied mainly in the lowlands of geographical regions simply due to the fact that there is a much larger diversity of species inhabiting the lowlands compared to the highlands. Studies use multiple approaches of statistical methods to get their data to agree. Which test is the best one depends upon the question being asked?



Species can be traced back to their origins using mtDNA, which is directly passed down from the mother. A species that has genetic ties to an ancestor and all its descendant taxa is called monophyletic and a species that has an ancestral taxon and some, but not all, of its descendant taxa; an artificial taxon. (Lomolino et al 2006) Geography plays a role in how a species diversifies over time as was demonstrated by the Finch scenario. The finches migrated south from Mexico to the Northern Andes Mountains of South America. Some finches traversed the Andes and migrated south along the east side of the Andes. The geographic isolation separating the two groups allows for natural selection to run its course allowing for the distinct differences we see in the finches today.



So does this apply to humans also? Can human mtDNA show this geographical divergence differentiating our species? An article entitled, “Geographic origin of human mitochondrial DNA: Accommodating phylogenetic uncertainty and model comparison” by John Huelsenbeck and Nikita Imennov compare the two main theories of the origin of the humans, which are the “out of Africa” and the “regional continuity hypothesis. The “out of Africa” hypothesis relates that modern humans all came from a common ancestor in Africa. Humans spread from there to all parts of the globe, and subsequently wiping out other “homos” that were encountered. The “regional continuity hypothesis” says a single species of homo originated throughout the old world connected through gene flow, after any migration from Africa occurred. Statistics using mtDNA show that the out of Africa scenario is the most possible origin for modern humans. A Bayesian inference statistical analysis was used to accommodate phylogenetic uncertainty from all trees then comparing the probabilities. Bayesian statistics is defined as, “Of or pertaining to statistical methods that regard parameters of a population as random variables having known probability distributions.”In their article Huelsenbeck and Imennov 2002 state, “In this study, we point out how Bayesian inference can be used to accommodate phylogenetic uncertainty when comparing five different models for the origin of modern human mtDNA.” 200 sequences of mtDNA were analyzed, each sequence was 428 sites long, from the hypervariable region I (HVRI) of the mitochondrial region of modern humans and an out group sequence from Neanderthal mtDNA. They used 40 sequences from each geographical region of the globe in their analysis; Africa, Europe, Asia, Americas, and Australia were represented. As discussed in class, and in this paper, a statistical analysis can be modified in many ways. This study used a uniform prior on all possible trees, another way to analyze the data would be to perform a coalescence prior, or to chose another method reconstructing the ancestral geographic area of human mtDNA. Another way of statistical modifications could include a stochastic two-stage model or a coalescence process with different populations connected by variable levels of migration. Still other ways exist that can modify an analysis; the trees could be reconstructed using a molecular clock restraint and incorporated into a Bayesian or maximum likelihood framework. (Huelsenbeck and Imennov 2002) A DNA sequence from Neanderthals may give a clearer answer to the out of Africa hypothesis. MtDNA can be useful to determine human geographic origin after all. Whew! From this we can clearly see that data can and is modified in many different ways to suit a desired outcome.



References:

Huelsenbeck, J. and Imennov, N., 2002. Geographic origin of human mitochondrial DNA: Accommodating phylogenetic uncertainty and model comparison. In Systematic Biology Vol. 51, No 1 pp.155-165.

Lomolino, M.V et al. 2006. Biogeography. MA: Sinauer Associates.

Dictionary.com, Bayesian Statistics. Retrieved October 5,2008.


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Monday, December 1, 2008

On the Origin of Species - revisited via the ghost of Asa Gray

As you are probably aware, especially if you are a student in my Evolution class, Charles' Darwin's seminal work "On the Origin of Species by Means of Natural Selection" has just passed a significant milestone: its 150th birthday in print! As you may also have noticed, a number of print and online publications and websites have been marking the occasion in various ways; some I have bookmarked for sharing here, but haven't gotten around to as yet!


At the beginning of the semester (as I do every semester), I had asked you students to approach the book through as fresh (even naive) a perspective as you could muster, setting aside any preconceptions and trying to put yourself in the mind of an educated person in 1859 getting your hands on the book for the first time, hot off the presses. That, of course, is easier said than done; especially when in class we are surveying the latest discoveries and insights from evolutionary biology. How can one erase 150 years of scientific progress on the question from one's memory? I'm presuming, of course, that at least some of that accumulated wealth of knowledge from these 150 years has trickled down into your consciousness through your various classes (and despite perhaps your best efforts!). Well, I hope most of you have made it at least most of the way through the wonderful (if tedious to some modern eyes) book. If so, you will appreciate this classic review, reprinted by The Atlantic Monthly where it was first published in 1860 upon the book's maiden voyage across the pond to the American market, and written by Asa Gray, the eminent botanist, contemporary and close correspondent of Darwin himself. Here's a wikipedia excerpt about the two men:

Corresponding with Charles Darwin, Gray was helpful in providing information for the development of Darwin's theory on The Origin of Species. Gray, considered by Darwin to be his friend and "best advocate", also attempted to convince Darwin in these letters that design was inherent in all forms of life, and to return to his faith. Notwithstanding, Gray was a staunch supporter of Darwin in America, and collected together a number of his own writings to produce an influential book, Darwiniana. These essays argued for a conciliation between Darwinian evolution and the tenets of orthodox Protestant Christianity, at a time when many on both sides perceived the two as mutually exclusive.

That should prime you to go read the review, which is pretty sharp and honest, starting on this cautious note:

Novelties are enticing to most people: to us they are simply annoying. We cling to a long-accepted theory, just as we cling to an old suit of clothes. A new theory, like a new pair of breeches, ("The Atlantic" still affects the older type of nether garment,) is sure to have hardfitting places; or even when no particular fault can be found with the article, it oppresses with a sense of general discomfort. New notions and new styles worry us, till we get well used to them, which is only by slow degrees.


Wherefore, in Galileo's time, we might have helped to proscribe, or to burn had he been stubborn enough to warrant cremation-even the great pioneer of inductive research; although, when we had fairly recovered our composure, and had leisurely excogitated the matter, we might have come to conclude that the new doctrine was better than the old one, after all, at least for those who had nothing to unlearn.


Such being our habitual state of mind, it may well be believed that the perusal of the new book "On the Origin of Species by Means of Natural Selection" left an uncomfortable impression, in spite of its plausible and winning ways. We were not wholly unprepared for it, as many of our contemporaries seem to have been. The scientific reading in which we indulge as a relaxation from severer studies had raised dim forebodings. Investigations about the succession of species in time, and their actual geographical distribution over the earth's surface, were leading up from all sides and in various ways to the question of their origin. Now and then we encountered a sentence, like Professor Owen's "axiom of the continuous operation of the ordained becoming of living things," which haunted us like an apparition. For, dim as our conception must needs he as to what such oracular and grandiloquent phrases might really mean, we felt confident that they presaged no good to old beliefs. Foreseeing, yet deprecating, the coming time of trouble, we still hoped, that, with some repairs and make-shifts, the old views might last out our days. Après nous le deluge. Still, not to lag behind the rest of the world, we read the book in which the new theory is promulgated. We took it up, like our neighbors, and, as was natural, in a somewhat captious frame of mind.

and towards the end, warily acknowledges the "uncanny look" as well as the "mischief" of the book:

So the Darwinian theory, once getting a foothold, marches boldly on, follows the supposed near ancestors of our present species farther and yet farther back into the dim past, and ends with an analogical inference which "makes the whole world kin." As we said at the beginning, this upshot discomposes us. Several features of the theory have an uncanny look. They may prove to be innocent: but their first aspect is suspicious, and high authorities pronounce the whole thing to be positively mischievous.

Doesn't that make this your must read essay of the week?


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