Death control

Abstract

During meiosis, homologous chromosomes must recombine to establish the physical connections required for their proper segregation. Recombination is initiated by resection of double-strand break (DSB) ends to generate single-stranded DNA tails that associate with the Rad51 and Dmc1 recombinases. The resultant nucleoprotein filaments catalyze double-stranded DNA invasion and strand exchange that links homologous pairs to form joint molecules (JMs). Although Rad51 and meiosis-specific Dmc1 co-localize to nuclear foci, and both can promote strand exchange in vitro, it is not clear that they have equivalent roles in meiotic recombination. Now, Bishop and colleagues have created a Rad51 mutation that uncouples filament assembly from JM formation to dissect the functional contributions of each recombinase during meiosis in yeast. They show that specifically abolishing the JM-forming activity of Rad51 has no effect on recombination between homologs during meiosis, whereas the analogous mutation in Dmc1 produces severe recombination defects. However, Rad51 JM activity is essential for mitotic DNA repair. Although JM formation by Dmc1 is sufficient to direct normal interhomolog recombination during meiosis, this activity is regulated by Rad51. The authors show that Rad51 functions with the known Dmc1 cofactor complex Mei5–Sae3 to stimulate formation of recombination intermediates in vitro and that Rad51 JM activity is dispensable for this stimulation. Thus, Rad51 functions indirectly in meiotic recombination by stimulating Dmc1 activity and functions directly in mitotic recombination by catalyzing strand exchange. (Science 337, 1222–1225, 2012) BM branching regulation

DOI: 10.1038/nsmb.2408

Cite this paper

@article{Montoya2012DeathC, title={Death control}, author={Michelle Montoya}, journal={Nature Structural &Molecular Biology}, year={2012}, volume={19}, pages={982-982} }