Dan

Today’s not fun

dan — Thu, 01 May 2008 12:19:35 +0000

So today, for those who read my blog (and because I can’t seem to find Vaughn’s email), I’m going to announce that I won’t be in class. I woke up this morning with a case of nausea that hasn’t gone away yet, so I would like to take it easy for the rest of the day. I think the communities of bacteria in my stomach are fighting amongst themselves… giving me a bad case of gas as collateral damage. I hope class goes well, and I’ll be checking the site for new news. I did post my paper on the evolution of virulence, so at least I gave you guys some reading material. =p

Virulence and Plants

dan — Thu, 01 May 2008 03:10:45 +0000

I enjoy a good discourse on plants. Always riveting. I found an evolution of virulence paper today and it dealt with a simple system. The central issue danced around the theory that for every virulence gene present in a pathogen, a counter-virulence gene was present in the host, and trade-offs occur on both sides until selection becomes neutral on one side so the other can catch up. Linum marginale, the host plant, and Melampsora lini, the fungal parasite, were observed in their interactions and were found to have inverse relationships. Broadly virulent strains of the fungus were observed when there was a high susceptibility of L. marginale, while specifically virulent strains were observed in resistant L. marginale. Here’s the link: http://www.sciencemag.org/cgi/reprint/299/5613/1735.pdf

Rescuing Social Motility

dan — Fri, 11 Apr 2008 19:18:42 +0000

In this paper, Velicer et al focus on testing whether or not maintaining genes for social motility is costly in an unstructured environment. In a nutshell, they evolved 12 M. xanthus cell lines in a liquid broth for 1000 generations, determined which lines had lost social motility function, and attempted to rescue the social motility functionality with one of two plasmids. Each of these plasmids contained a different portion of the “pil” region. This region was identified as the locus responsible for varying kinds of motility. One plasmid, pSWU257, contained an upstream portion of the pil region, while the other, pDW79, contained the downstream portion. Several lines were saved by both plasmids, in particular R2a. Sequencing of R2a’s genome revealed that three genes, pilH, pilD, and pilI were likely the largest players in the motility rescue. R2a, along with S2, were tested for cheating as well. It was discovered that S2 was a developmental cheater as both the S2 ancestor and its rescued counterpart. This suggests that other loci, not just the pil region, were responsible for the cheating ability. R2a, by contrast, actually aided the ancestor’s sporulation ability. Ultimately, evolutionary loss of S motility in M. xanthus was able to disrupt its sporulation ability, despite being rescued by the pil genes.

So much to write, so little time.

dan — Thu, 03 Apr 2008 12:53:39 +0000

The semester is starting to bear down on me these past few days. So much to write and so little time… life is sooo great. At any rate, regarding the papers this week, the concept of sex in virus is a farfetched one indeed. The idea is made a tad more swallowable when discussing the phi viruses in these studies that utilize segmented genomes in their capsid packages. When coinfection occurs, swappage of the various segments of the viruses can mix and match and form new particles when lysis occurs. The “prisoner’s dilemma”, a theory that describes cheating, payoffs and punishments, is explored in two of the papers this week by Turner and Chao. The viruses are compared at high MOI and low MOI to determine their relative fitness as compared to their ancestor virus particle. At high MOI, the viruses can cheat on one another which brings down the total fitness of the population. The surprising result was that even though the fitness is decreasing as cheating viruses become more numerous, the cheating viruses themselves are favored in the population due to their selfish nature - or, in other words, that is to say that they are more fit than a non-defector being cheated. One would think that a cheating organism competing against another similar cheating organism would yield no fitness or death of that organism because they may lack important functions required by the good standing members of the original populations. But surprisingly they do not. I am not too certain what to make of this, which is why I’m looking forward to the discussion later today about the Prisoner’s Dilemma and the applications in this viral study.

Immigration is a touchy subject for some…

dan — Thu, 27 Mar 2008 15:59:18 +0000

… when speaking on the current border issues in the United States. But concerning these lovely smooth, wrinkly and fuzzy morphs of pseudomonas fluorescens, they are the subject of an intriguing experiment by Paul Rainey et al which describes the effects of temporal relationships of introducing “rare” organisms to populations of “common” organisms. I thought it was quite interesting to see how the time of introduction of SM to populations of WS always ended in the formation of the two genotypes no matter when you introduce the invader. In the reverse situation, when WS was introduced to SM populations, depending on the time, several WS sub-genotypes would form and would effect the impact SM would have on the total population. I definitely think that the first organism that colonizes a niche before other similar organisms will definitely have an edge in keeping the niche.

The Old Man and his Fitness Category.

dan — Tue, 25 Mar 2008 22:37:54 +0000

The Cooper article was an enlightening read, divulging on how adaptations converge to one point - a known theory called the Ficher-Muller theory of adaptation. I particularly liked his proof concerning the fixation of the spoT gene within recombinant (rec+) and non-recombinant (rec-) populations. The argument in itself makes sense - if organisms are able to freely transfer genes through sex, beneficial genes should be able to flow throughout the population. Likewise, isolated organisms are purely dependent on mutation for any sort of change to occur, positive or negative, and the likelihood of a particular BENEFICIAL mutation outcompeting others is low, if nonexistant. This is well illustrated in figure two of the paper, where the spoT gene was detected a second time in a separate rec- line and failed to fix within 1000 generations. The rec+ bacteria fixed rapidly, as they were able to transfer genetic material and outcompete other potentially beneficial alleles. I also found the information provided in figure three to be rather puzzling. Should not a late-generation member of a population who’s good alleles have been fixed be more fit than when the allele first appeared? It seems intuitive to me - something older and more “experienced” (though this analogy is difficult to apply to bacteria…) should be more solid and better able to handle itself. And indeed, this is the case for the first samples. But samples 3 and 4 show that the bacteria taken were less fit than before, but still had an advantage. I venture that this happening shows there is a link between when the good allele is jumpstarted into the population and how fit the organism is. Meh. I suppose this takes an example from human development. As one gets older his or her machinery wears out, and it no longer matters that he or she had an incredible gift that helped him or her survive. That gift gets lost with age or disease. Am I making sense? We’ll see, I guess =]. I wasn’t surprised by the data in the non-recombinant populations, though; they faced difficulty in outcompeting purely due to their inability to transfer genetic material between themselves. If I missed something, let me know, kay guys?

Best. Blog. Ever. At least up until my next one.

dan — Mon, 03 Mar 2008 18:56:52 +0000

Of course I’m being facetious. Everyone is great. I was just trying to break up the monotony of everyone else’s subject lines =]. Anyway, I think my best blog entry was my most current one - the post I made on February 28th. My reasoning behind my choice is that it reflects an actual reason I have for thinking the way I do on evolution. Most of my other posts have been summaries of some sort. Well, time to study for Prokaryotic Genetics. Wish me luck in my endeavors! Woohoo.

Post continued.

dan — Thu, 28 Feb 2008 16:30:44 +0000

Now that my head’s cleared, and now that I’ve gotten over the shock from accidently sleeping through Public Health, I think I can pull together a few coherent thoughts. The graphs and charts used to illustrate the results of the experiments make sense after scrutinizing them during class, but I can’t get comfortable with using three different entities to explain diversity in the world. How I view the three characteristics Travisano et al had described reflects my admittedly narrow understanding of evolution. I believe that chance and history fuel adaptation. Adaptation is the prime mode of evolution, where natural selection destroys anything not fit enough to survive. The effects of chance mutations and drift may not be directed by the environment, but the mutations that favorably effect the organism where it resides is when adaptation and natural selection takes its action. The historical aspect to adaptation is, as we discussed, reflected by genes that are already present and were common within the ancestor of the organism and are fully expressed when the requirements for fitness change and the adaptations can make use of those genes. I guess what I’m trying to say is that there is nothing else besides adaptation. Whatever affects it, whether it be chance mutations of historically present genes, are simply part of the larger aspect of the idea.

Boy, bacteria sure are prime targets for them statistical tests.

dan — Thu, 28 Feb 2008 04:49:59 +0000

I was hoping biostats lingo was going to retreat back into the recesses of obligatory, useless knowledge. Guess I was wrong. Travisano et al make a good point on these factors governing evolution and fitness. The statistical significance figures used to test all their theories was clever and - for once - I’m going to say I’m glad I sat through biostats. I thought the comparison between ancestral bacterial colonies and “derived” colonies drove home the points they were attempting to make. The consumption of glucose and maltose as carbon sources and the affects of temperature were compared, adaptation was found to be the most statistically significant factor governing the bacteria’s fitness. This makes sense to me as they are environmental factors that must be overcome in order for the cell to survive. Cell size was a different matter, though. Adaptation does not play any large role in something so tiny to begin with, so the use of history and chance to describe the traits governing this cellular property makes sense. I’ll write more in the morning after some discussion of the article in class. My head hurts; not from the article.

On the subject of ecotypes

dan — Thu, 07 Feb 2008 15:28:03 +0000

I’ll be honest, this article was very heavy and I didn’t quite understand its concepts at first - and I dare say I am struggling a fair bit with them now. But what I’ve taken home from this reading is that the challenge microbiologists face in classifying their subjects is a daunting one. The theory of ecotypes presented in this paper seems to make sense: clumping similarly sequenced clusters which share some sort of niche or environment. Genetic divergence is accounted for by periodic selection, a process defined by a major event that favors a new sequence cluster that has some sort of adaptive mutation that outcompetes and essentially kicks out the previous inhabitants of the ecotype. All of this seems so unnecessary. Most of the important bacteria that have been catalogued already have a genus and a species based on similar chemical reactions with food substrates and the like. And most pathogenic microbes are already well classified by their mode of infection. Am I wrong when I say when we mention legionella pneumophila we know we are speaking about an intracellular pathogen? But this begs the need for groupings of several kinds of intracellular pathogens into similarly named groups. I just recently discovered in class that salmonella “species” are very related to escherichia “species”. If their genomes are so close together, their names certainly don’t reflect the similarity. I would ask anyone who can to clarify the ecotype model for me if there was anything I missed in my summary at the beginning of this entry.