Both ATM and ATR promote the efficient and accurate processing of programmed meiotic double-strand breaks
Abstract
The ATM and ATR protein kinases play central roles in the cellular response to double-strand breaks (DSBs) by regulating DNA repair, cell-cycle arrest and apoptosis. During meiosis, SPO11-dependent DSBs are generated, initiating recombination between homologous chromosomes. Previous studies in mice and plants have shown that defects in ATM result in the appearance of abnormally fragmented chromosomes. However, the role of ATR in promoting normal meiosis has not yet been elucidated. Employing null Arabidopsis mutants of ATR and ATM, we demonstrate here that although atr mutants display no obvious defects in any phase of meiotic progression, the combination of defects in atr and atm exacerbates the fragmentation observed in the atm single mutant, prevents complete synapsis of chromosomes, and results in extensive and persistent interactions between non-homologous DNAs. The observed non-homologous interactions require the induction of programmed breaks: the combination of either the atm single or the atr atm double mutant with a spo11 defect eliminates the ectopic interactions observed in the double mutant, as well as significantly reducing the fragmentation seen in atm or in atr atm. Our results suggest that ATM is required for t...Continue Reading
References
The Atr and Atm protein kinases associate with different sites along meiotically pairing chromosomes
Citations
Homologous Recombination Defective Arabidopsis Mutants Exhibit Enhanced Sensitivity to Abscisic Acid
HIGH CROSSOVER RATE1 encodes PROTEIN PHOSPHATASE X1 and restricts meiotic crossovers in Arabidopsis.
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