The University of Osaka · Biochemistry, Genetics and Molecular Biology
Professor Akira Shinohara's research lab focuses on the molecular mechanisms underlying DNA double-strand break repair and meiotic recombination in eukaryotes. The lab investigates the distinct and cooperative roles of recombinase proteins such as Rad51 and Dmc1 in homologous recombination, with a particular emphasis on their regulation, structural dynamics, and functional interplay during meiosis. Key research directions include the regulation of sister chromatid cohesion, the role of cohesin and condensin complexes in chromosome dynamics, and the mechanisms of ssDNA annealing mediated by proteins like Rad52 and RPA. The lab integrates structural biology, biochemistry, and cell biology to elucidate fundamental processes in genome stability and inheritance.
Figures are computed from collected data and may differ slightly.
Rad52 forms a ring-like structure and binds to ssDNA. Its structure and DNA binding properties are different from those of Rad51. The interaction of Rad52 with RPA plays an important role in the enhancement of annealing of complementary ssDNAs. We therefore propose that Rad52 mediates the RAD51-independent recombination through an ssDNA annealing, assisted by RPA.
RecA protein is involved in homology search and strand exchange processes during recombination. Mitotic cells in eukaryotes express one RecA, Rad51, which is essential for the repair of double-strand breaks (DSBs). Additionally, meiotic cells induce the second RecA, Dmc1. Both Rad51 and Dmc1 are necessary to generate a crossover between homologous chromosomes, which ensures the segregation of the chromosomes at meiotic division I. It is largely unknown how the two RecAs cooperate during meiotic
Sister chromatid cohesion on chromosome arms is essential for the segregation of homologous chromosomes during meiosis I while it is dispensable for sister chromatid separation during mitosis. It was assumed that, unlike the situation in mitosis, chromosome arms retain cohesion prior to onset of anaphase-I. Paradoxically, reduced immunostaining signals of meiosis-specific cohesin, including the kleisin Rec8, were observed on chromosomes during late prophase-I of budding yeast. This decrease is s
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