Back from Taos, New Mexico

Hi everyone,

I just thought I'd write a quick note to say that the meeting I at was at in Taos went well. It was a smaller conference with about 150 people in attendance. My talk was well received and I got alot of nice comments afterwards. My abstract can be found at the bottom of this post in case you are interested. I'm definitely glad my seminar was on the first day because I was pretty nervous beforehand and couldn't really concentrate on the other seminars until mine was over.

I never made it to the ski hill, but from what I understand it was a very bad year in terms of skiing conditions. We did get to do alot of hiking around the gorges. The wild rivers recreation area where the Rio Grand and the Red River meet was really spectacular. This picture doesn't really do it justice.



That's all for now....


Abstract

Uncoupling of the T4 Phage Replisome upon Encountering an Abasic Lesion in the Leading Strand DNA Template.

Scott W. Nelson and Stephen J. Benkovic, Department of Chemistry, The Pennsylvania State University, University Park, PA, USA, 16802

Efficient replication of DNA by the cell requires the ability to bypass DNA lesions that arise under normal growth conditions. In order to investigate the effects of a lesion on the T4 phage replisome, a large circular substrate containing a site specific abasic lesion in the leading strand template was constructed. In the presence of all eight T4 replication proteins, this substrate supports leading and lagging strand DNA synthesis, indicating that complete replisome formation occurs prior to arriving at the site of DNA damage. Once the lesion is reached, the leading and lagging strand polymerases uncouple, such that the primosome and lagging strand polymerase continue to unwind duplex DNA and synthesize Okazaki fragments, respectively, while the leading strand polymerase remains stalled. Preliminary evidence suggests that this uncoupling creates a DNA structure that is a substrate for the T4 recombination proteins UvsX and UvsY. Currently, we are investigating the possibility of an intramolecular template switch that may allow the replisome to bypass the lesion in an error free fashion.

This work was supported by NIH Grant GM13306 (S.J.B.). S.W.N is a Fellow of the Jane Coffin Childs Memorial Fund for Medical Research.