Samantha

Summary of Velicer’s “Comprehensive mutation identification in an evolved bacterial cooperator and its cheating ancestor”

samantha — Thu, 17 Apr 2008 08:00:08 +0000

Hey guys I think you may have gone over this paper in class while I was sick but Vaughn told me to summarize it so here i go:

-They took GJVI which was a clone of the standard lab strain DK1622 = The ANCESTOR

-They evolged 12 lineages for 1000 generations in nutrient-rich medium. There was no positive selection on any social traits (social motility or social development) only on competitiveness in asocial growth conditions
~Replicate lineages improved maximum growth rates by about 37%
~There was a partial to complete loss of the capasity for social motility and development

-After 1000 generations several evolved clones that were able to cheat on the ancestor in a mixed population were isolated
~There was defective sporulation in clonal culture
~But they are more efficient than the ancestor in a mixed population (when rare)
1. One of the cheating clones is the OC (obligate cheater)
2. OC is completely defective at social development during starvation and needs other socially proficient to sporulate
3. OC is marked with Kanamycin resistance

-OC w/ Kan resistance was mixed with a marked Rif resistanct variant of GJVI

-They did 6 sequential cycles of alternating starvation and growth
~After 4 cycles, OC re-evolved the ability of multicellular development which resulted into the PX genotype

-They sequenced PX in 2 ways
~Pico-Titer-Plate
~Capillary-based

-Compared against DK1622
~27 real discrepencies found

-Then they compared PX to three other strains:
~GJVI (identical clone of DK1622)
~GVB207.3 (unmarked immediate parent of OC isolated from 1000 generations evolved from GJVI)
~OC (evolutionary ancestor of PX)
1. 26 of the 27 discrepencies we also present in GVB207.3 and OC
2. 1 discrepency was unique to PX (phenotypic transition from OC—> PX

Problematic Prisoners

samantha — Tue, 15 Apr 2008 10:52:41 +0000

My criticism for the “Escape From Prisoner’s Dilemma in RNA Phage 6″ is the 6% fitness cost they tacked on that the h marker created. Its all well and good that they actually figured out it was a 6% change, but they dont show the data for us to visualize. I feel like they should have a table comparing the fitness measurements without the effect of the 6% cost to the adjusted measurments.

Saving the Grand Canyon; In a way replaying life’e tape…

samantha — Thu, 03 Apr 2008 16:55:42 +0000

Hey guys,

I briefly mentioned something about the flooding of the Grand Canyon in class tuesday and i figured I could post a link if anyone was interested in looking at it. They are trying to rebuild the canyon by flooding the Colorado river. The sediment that was once distributed by the flow of the water has been stopped by the Dam so they hope to distribute build up sediment by flooding for three days. This seems like its also a good thing to read about towards the end of the class when we talk about developing communities because with new sand bars comes new ecological habitats, or at least returning ecological habitats. The change in the canyon by the dam accelerated the extinction of 4 fish species, and caused another to get dangerously close to extinction…it will be interested to see what new diversity this act to save the canyon brings.

the link button is not working but here is the web address: http://www.cbsnews.com/stories/2008/03/05/tech/main3908934.shtml

Fisher-Muller Proof…

samantha — Thu, 27 Mar 2008 06:14:48 +0000

To be completely honest this paper was a little dense for me to really get in there and comprehend. Im not sure if it was the pounding headache when i read it or that it was just difficult. I thought figure 2 was a bit confusing at first and i think I missed a big point by not grasping that. But one thing I did like about this paper is the author summary. Despite not understanding alot of the nitty gritty details that summary allowe me to get something out of the paper at least. Im gonna give it another whack at it…

Seeing the light: Brucella

samantha — Thu, 06 Mar 2008 05:18:34 +0000

I thought Inga Sidor’s presentation on Brucell was really interesting. There’s something about a bug that can cause disease that is scary yet exciting to explore. So, I googled Brucella to try and find something beyond the phylogenic debate and the disease it causes and I found something pretty cool.

Its been discovered that Brucella as well as other bacteria have a light-sensing capability that was unknown. Apparently they use this light-sensing capability to regulate their virulence in a way. Researchers spliced the genes in what they call the LOV domain, which are responsible, into E. coli. They grew them the dark with radioactive markers and subjected them to a strobe light. When the light hit them, a temporary bond was formed in the domain acting like a hinge. When the light hit, the hinge opened exposing the rest of the protein. When it was dark again the bonds break and the hinge closes again.

“When Brucella comes under attack from a host’s immune system, light received by the LOV domain activates the bacterium’s counter-defenses, allowing it to reproduce rapidly and making it highly virulent. In the dark, without these defenses activated, Brucella’s division rate drops by 90 percent. When the team grew experimental Brucella in the light but with the LOV domain disabled, they found an identical drop in division rate.”

It is unknown how the bacteria uses this mechanism to regulate virulence but researchers think that the light-sensing is used to detect when they are outside the host. When the light hits them they rapidly reproduce making big numbers to increase their chances of survival and transfer into a new host.

When I read this article I was like…”wicked cool!” Its from Brightsource.com. Unfortunately I couldn’d find the original paper in Science but check out the article it’s pretty interesting.
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best blog…

samantha — Sun, 02 Mar 2008 06:40:30 +0000

I guess my best would be the most recent about adaptation chance and histroy…enjoy!

also, heres a pic for those of you that couldnt make the seminar…

http://www.unbc.ca/nlui/wildlife_diseases_bc/brucellosis_caribou.

Adaptation, Chance, and History

samantha — Thu, 28 Feb 2008 18:00:58 +0000

In the opening of this paper the authors say, “adaptation has sometimes been regarded as the sole influence on evolution”. Really? I think it is pretty unrealistic to think of adaptation as the SOLE influence on evolution. We need to look at all three influences, adaptation, chance and history. Even though the effect of one, two or two of these phenomena may be small, that small affect can still be important or at least present. I think this paper does a decent job illuminating the complicated relationships between the three influences and their complexity alone and together.

I had a couple of issues and or confusions with this paper:
-On page 87 Travisan et al say, “adaptation may depend on random mutations”. I understand that a random mutation can lead to a beneficial trait that could help fitness. I also understand that this mutation could have been present for a while before it became beneficial which would put it in the category of adaptation. BUT if all mutations are random what happens when you get a mutation that immediately and directly affects fitness? Will that be attributed to chance? Or adaptation? Would that affect the data, kind of inflating the adaptation or chance support? Im not sure If i’m asking this clearly but i guess i just dont get that if all mutations happen by chance, are the distinctions between the affects of the two sound?

-The second issue i had with the paper is the error bars on figures 2b, 3b, 4b, and 5b. Is it acceptable to have error bars that large? I dont know too much about how they determined them or what EXACTLY the depict but I do know that they are called ERROR bars for a reason…having to do with a little thing people call error. Does the magnitude of the error bars discredit their findings at all or are they not very significant? It just bothered me to see them.

- The last issue i had was on the page 89. They state. “The effects of chance and history are estimated by ANOVA, but are confounded because genotypes were not replicated at the start of the period at 20C, we therefore estimate their combined effects in this experiment.” That to me sounds like they should have done a third experiment to try and prove their estimated outcome. Its called a hypothesis, and it should be tested.

Microbial species..O brother!

samantha — Tue, 12 Feb 2008 07:45:25 +0000

It seems quite obvious that the same system for classifying higher organisms simply doesn’t cut it when looking at the microbial world. How do we distinguish between populations that are so genetically similar? Where do we draw the line? I can’t really answer those questions but the Cohan and Perry paper did convince me that their approach was a good place to start.

I would start off with whole genome sequencing. Expensive? Ya, probably but i feel that some bacteria are too similar to compare with just MLST or 16srRNA sequencing. Seeing the whole sequence and seeing exactly what percentage of the genome is different is a good place to start. Obviously, there needs to be some cut off percentage that would determine a unit (or ecotype, or species whatever you want to call it), but I don’t know how one would determine what that percentage would be. This sequencing will give the first division of groups. Then you could look at the ecological factors, then physiology (expression levels, metabolic properties, biochemical traits). They might be able to survive in the same niche but by utilizing different resources or different amounts of the same resources.

Im sure there are lots of other factors that would be useful in making the species/ecotype distinction. Im not really sure I even know what I’m talking about. But when thinking about the problem I feel that using whole genome sequencing is important. And, as abe, laura and dave said, recombination rates are important as well seeing as among larger forms of live interbreeding is a defining factor of species.

Everything Everywhere, or Does the Environment Select?

samantha — Thu, 31 Jan 2008 07:38:09 +0000

“Everything is everywhere; the environment selects”. I’ve heard this statement a few times over the years and I have always thought it was a phrase comprised of two contradicting statements. If everything is everywhere it wouldn’t matter what the environment is, everything would be everywhere. Abe posted something the other day that totally made sense to me. Apparently Baas-Becking’s words weren’t quite translated accurately because they left out the BUT, a very strong and almost feared word in the English language. People are always afraid to hear good things followed by a BUT. The “but” indicates that the second part of the phrase, “the environment selects” trumps the preceding fragment. In this case, I was plesantly surprised. “Everything is everywhere, BUT the environment selects.” This makes more sense to me.

As far as the Whitaker paper goes…their experiment showed that physical/geological boundries have an affect on population differentiation. Many species of bacteria are everywhere, but in my opinion extremophiles are an exception. Their need for extreme growth conditions makes dispersal a difficult task so it makes sence the geographic distance correlates to genetic distance.

Who knows? Everything may have been everywhere at one point until the environment selected.

Why am I here?

samantha — Thu, 24 Jan 2008 08:29:46 +0000

I am in this class to fill a gap in my education. I have taken countless microbiology classes, chemistry classes, and biology classes, but I have yet to take any class that takes a serious look at ecology. Seeing as I am a microbiology major, I figured a class that deals with ecology and microorganisms was the way to go.