Monday, July 30, 2007

What I did for the last year....

I've just returned from the GRC: Microbial Population Biology conference where I presented a poster on my work for the past year. In a few installments I'd like to reproduce this poster here.

My major question of interest was, "How does molecular stochasticity in the individual cell affect major life history traits?" To address this question, I used the enterobacteriophage lambda strain cI857 as a model. Under normal circumstances, cI857 integrates itself into E. coli's genome where it is passed horizontally to daughter cells. Most of the phage's genome is repressed at this point. However, after a temperature spike, the phage is induced into the lytic cycle. Here the "late" genes are expressed, including the lysis cassette and the genes that make phage babies.The lysis cassette contains four genes that produce five proteins. I'll focus just on two: holin and endolysin. The best available model suggests that holin integrates itself into the host's inner membrane. Over time, the holin concentration in the membrane rises, until it spontaneously condenses into a raft. Subsequently the holin undergoes a conformational change producing a hole in the inner membrane. This permits endolysin to attack and degrade the outer membrane, leading to host cell lysis and the release of phage babies into the surrounding medium. Thus holin, and its rate of production, is the main determinant of lysis time, or in life history theory, generation time. The rate of holin production depends on protein translation from low copy mRNA transcripts. Since a single mRNA transcript can produce multiple holin molecules, small changes in mRNA numbers can have large effects on holin production and, hence, the timing of lysis. My project looked at how differences in mRNA production and differences in holin structure led to variability in lysis timing. I'll discuss these in greater detail in a later post and show some of my data.

A cool animation sequence of the lytic cycle is available here.

Lead photo: Maria Schnos, Institute for Molecular Virology, University of Wisconsin, Madison
Genetic Map of the λ genome from CA Reinhart, W. Kentucky University.
Figure by me.

Tuesday, July 24, 2007

Vacation is over...

Back to business... I'm now at the Gordon Research Conference for Microbial Population Biology. It's a small, fun meeting held every other year at Proctor Academy in Andover, NH. This year the talks have been decidedly hit or miss. The phrase, "Never judge a talk by its title" comes to mind. Some highly anticipated (to me anyway) talks have fallen signficantly short of the mark, while others, less obviously interesting, have thoroughly surprised. My favorite talk to date has been a presentation by Gary Schoolnik on "Chitin-induced natural transformation and the evolution of Vibrio cholerae in aquatic habitats."

Previously I was aware of cholera as a disease cycling between aquatic reservoirs and human hosts, where cholera numbers were amplified in the gut and transmitted through fecal contamination of drinking water etc. Schoolnik described how far back the causal chain of cholera outbreaks can be extended from the human host. Once cholera leaves the gut, it enters the aquatic habitat where it colonizes the chitinous exoskeletons of small aquatic crustaceans called copepods. Copepod numbers are largely regulated by their primary foodsource, algae. More algae, more copepods, more cholera.

Schoolnik elucidated how global climate change, deforestation and agricultural intensification have impacted cholera outbreaks. Seasonally cholera is associated with monsoons in India. It is suspected that global climate change is increasing the severity of monsoons, which in conjunction with deforestation, is leading to increased runoff in the Ganges watershed. In this runoff are increasing levels of fertilizers because of agricultural intensification and increasing levels of human wastes due to surging human population numbers. The nutrient and waste laden runoff is causing greater algal blooms and higher copepod densities leading to increased incidence of cholera in the drinking water and larger cholera outbreaks. Luckily the situation is can be partially remedied by providing clean drinking water, which can be as simple as filtering river water thru a sari. The whole story epitomized for me the fragile web of interactions that we disturb at our own peril.

The photo is of a cholera-carrying copepod taken by Rita Colwell and Anwarul Huq.

Monday, July 2, 2007


Off to the lake, see you soon :)

Animal Behavior

Any ideas on what is going on here?

Or here?

I suspect we don't know nearly as much about large mammal behavior as we think we know.

First photo:

Kauai, Hawaii, USA
Lori Mazzuca
Kailua Kona, Hawaii, USA

Second photo: Daily Mail: Striking aerial image of an unusually large herd moving through Chad toward the Tinga.