Our Science – Lichten Website
Michael Lichten, Ph.D.
|Picture 1. Our group, fall 2013|
|From left to right: Robert Shroff, Hardeep Kaur, Darpan Medhi, Jianhong Chen, Michael Lichten|
|Picture 2. Meiotic double-strand breaks detected genome-wide|
|Distribution of meiotic double-strand breaks in the first three chromosomes of
the yeast genome, mapped by microarray analysis of break-associated ssDNA.
Blue: Signal from a dmc1 mutant, which forms breaks normally but does not
Red: Signal from a spo11 dmc1 mutant, which does not form meiotic DSBs.
From Buhler et al., PLoS Biology 5:e324.
|Picture 3. Genome-wide distribution of H2A phosphorylation|
|Distribution of DSB-associated ssDNA (blue) and of phosphorylated histone H2A
(gammaH2A, yellow), which is formed by DSB-activated checkpoint kinases.
The top panels show chromosome-wide patterns; subregions are magnified
below, showing alternating domains of DSBs and phosphorylated H2A.
|Picture 4. Model for Sgs1 regulation of meiotic recombination|
|In this model, Sgs1 helicase disassembles all branched DNA structures,
including early strand invasion intermediates. Recombination intermediates
escape Sgs1 disassembly by forming unbranched noncrossovers (SDSA, synthesis-
dependent strand annealing) or by being captured by protein complexes
associated with meiotic chromosomes (ZMM proteins); these intermediates form
double Holliday junction intermediates, and are resolved by a meiosis-specific
resolvase (Mlh1-Mlh3-Exo1). Infrequent recombination events that escape Sgs1
form unregulated joint molecules, which are resolved by structure-selective
nucleases (Mus81-Mms4, Yen1, Slx1-Slx4) that are also active during the
mitotic cell cycle. In the absence of Sgs1, this minor central pathway becomes
the default mode for meiotic recombination, and the SDSA noncrossover and
ZMM-dependent crossover pathways are depopulated.
This page was last updated on 12/6/2013.