Sex chromosomes: Navigating meiosis without a homologous partner
|演題||Sex chromosomes: Navigating meiosis without a homologous partner|
|講演者||Dr. JoAnne Engebrecht（Professor, Molecular and Cellular Biology, College of Biological Sciences, UC Davis）|
Meiosis is a special type of cell division that produces haploid gametes for sexual reproduction. During meiosis, chromosome pairing, synapsis and crossover recombination rely on homology between paternal and maternal chromosomes to ensure proper segregation and formation of gametes with the correct ploidy. Crossover formation is dependent upon the initiation of induced double-strand breaks (DSBs) that are repaired by homologous recombination. Defects in chromosome pairing disrupt DSB repair and result in checkpoint activation, leading to either apoptosis or formation of aneuploid gametes, the leading cause of birth defects. In males of many species, sex chromosomes are largely hemizygous (i.e., lack a homologous partner), which presents a special challenge to repair DSBs in the absence of a homologous chromosome, and moreover, to evade checkpoint activation. To uncover conserved mechanisms underlying meiotic sex chromosome behavior we are investigating meiosis in Caenorhabditis elegans males, which have a single, completely hemizygous X chromosome. Genetic and cellular analyses have revealed that meiotic DSBs are induced concomitant with a brief period of X chromosome synapsis that that may allow X sister chromatids to masquerade as homologs.Consistent with this, neither meiotic sister chromatid cohesion nor the SMC-5/6 complex, implicated in inter-sister repair, are required for DSB repair on the X. Furthermore, early processing of X DSBs is dependent on the CtIP/Sae2 homolog COM-1, suggesting that as with paired autosomes, homologous recombination is the preferred pathway. In contrast, the X chromosome is refractory to feedback mechanisms that ensure crossover formation on autosomes. Additionally, unlike autosomes, DSB repair on the X can proceed in the absence of homologous recombination; genetic analyses suggest that an error-prone single-strand annealing pathway is engaged when homologous recombination is impaired. Our findings indicate that alteration in sister chromatid interactions and flexibility in DSB repair pathway choice accommodate hemizygousity on sex chromosomes.
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