Journal
NATURE GENETICS
Volume 45, Issue 3, Pages 269-278Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ng.2541
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Funding
- CNRS
- Association pour la Recherche sur le Cancer
- Agence Nationale de la Recherche [ANR-09-BLAN-0269-01]
- US National Institutes of Health (NIH) [R01GM084955]
- Agence Nationale de la Recherche (ANR) [ANR-09-BLAN-0269] Funding Source: Agence Nationale de la Recherche (ANR)
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Crossing-over ensures accurate chromosome segregation during meiosis, and every pair of chromosomes obtains at least one crossover, even though the majority of recombination sites yield non-crossovers. A putative regulator of crossing-over is RNF212, which is associated with variation in crossover rates in humans. We show that mouse RNF212 is essential for crossing-over, functioning to couple chromosome synapsis to the formation of crossover-specific recombination complexes. Selective localization of RNF212 to a subset of recombination sites is shown to be a key early step in the crossover designation process. RNF212 acts at these sites to stabilize meiosis-specific recombination factors, including the MutS gamma complex (MSH4-MSH5). We infer that selective stabilization of key recombination proteins is a fundamental feature of meiotic crossover control. Haploinsufficiency indicates that RNF212 is a limiting factor for crossover control and raises the possibility that human alleles may alter the amount or stability of RNF212 and be risk factors for aneuploid conditions.
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