Our Science – Lichten Website
Michael Lichten, Ph.D.
|1. Sgs1 prevents axis association in crossover-defective mer3∆ mutants|
|Nuclei from pachytene-stage mer3∆ and mer3∆ sgs1∆C795 cells, surface spread and probed with anti-Red1 (green) and anti-Zip (red) to illuminate chromosome axes and the central element of synaptonemal complex, respectively. Mer3 is a meiosis-specific helicase required for normal meiotic crossing-over and for homolog association; Sgs1 is the budding yeast homolog of the mammalian BLM helicase, which has been suggested to have anti-crossover activity. Removal of the Sgs1 helicase domain by the sgs1∆C795 mutant, when combined with crossover and synapsis-defective mer3∆ mutants, restores homolog synapsis (illustrated here) and crossover recombination. Light micrograph taken by Beth Rockmill of Yale University; see Jessop et al., PLoS Genetics 2: e155 for further details.|
|2. Genome-wide mapping of meiotic double-strand breaks|
|Meiotic recombination is initiated by double-strand breaks. Previous DSB maps (yellow, Spo11-ChIP from sae2 mutants) suggested that about 1/2 of the yeast genome is recombination-cold (grey bars). Using a new method to map DSBs using break-associated single-strand DNA (blue, ssDNA from dmc1), we showed that only a small fraction of the yeast genome is recombination-cold (black bars). From Buhler et al, PLoS Biology 5:e342, 2007. 5 of the 16 yeast chromosomes are shown here.|
This page was last updated on 11/9/2010.