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Tid1/Rdh54 promotes dissociation of Dmc1 from nonrecombinogenic sites on meiotic chromatin

Teresa M Holzen1, Parisha P Shah, Heidi A Olivares

  • 1Department of Radiation and Cellular Oncology, University of Chicago, Illinois 60637, USA.

Genes & Development
|September 19, 2006
PubMed

Insights

The DNA recombinase Dmc1 can bind chromatin without DNA breaks, but Tid1 prevents this. Tid1 and Rad54 are essential for Dmc1 assembly at DNA breaks, facilitating homologous recombination.

Area of Science:

  • Molecular Biology
  • Genetics
  • DNA Repair

Background:

  • Meiosis-specific recombinase Dmc1 is crucial for DNA strand exchange during homologous recombination.
  • Tid1/Rdh54, a DNA translocase, stimulates Dmc1-dependent recombination.
  • Tid1 and its paralog Rad54 possess biochemical activities potentially contributing to their biological roles.

Purpose of the Study:

  • To investigate the interaction of Dmc1 with chromatin.
  • To elucidate the role of Tid1 and Rad54 in Dmc1 chromatin association and recombination.
  • To propose a model for Tid1's function in regulating Dmc1 activity.

Main Methods:

  • Chromatin immunoprecipitation experiments were employed.
  • Analysis of Dmc1 association with chromatin in the presence and absence of DNA double-strand breaks (DSBs).
  • Assessment of Tid1 and Rad54 activities in Dmc1 assembly.

Main Results:

  • Dmc1 can associate with chromatin independently of DSBs.
  • Tid1 suppresses the association of Dmc1 with non-DSB chromatin sites.
  • A shared activity of Tid1 and Rad54 is necessary for proper Dmc1 assembly at DSB sites.

Conclusions:

  • Tid1's ATP hydrolysis-dependent DNA translocase activity promotes Dmc1 dissociation from non-recombinogenic chromatin.
  • Rad54 can substitute for Tid1's function in Dmc1 dissociation.
  • ATP hydrolysis-dependent disruption of nonproductive recombinase-DNA interactions may be a conserved mechanism in homologous recombination.

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