RT Journal Article
SR Electronic
T1 Meiotic crossover patterning in the absence of ATR: Loss of interference and assurance but not the centromere effect
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 143651
DO 10.1101/143651
A1 Morgan M. Brady
A1 Susan McMahan
A1 Jeff Sekelsky
YR 2017
UL http://biorxiv.org/content/early/2017/06/12/143651.abstract
AB Meiotic crossovers must be properly patterned to ensure accurate disjunction of homologous chromosomes during meiosis I. Disruption of the spatial distribution of crossovers can lead to nondisjunction, aneuploidy, gamete dysfunction, miscarriage, or birth defects. One of the earliest identified genes involved proper crossover patterning is mei-41, which encodes the Drosophila ortholog of the checkpoint kinase ATR. Although analysis of hypomorphic mutants suggested the existence of crossover patterning defects, it has not been possible to assess these in null mutants because these mutants exhibit maternal-effect embryonic lethality. To overcome this lethality, we expressed wild-type Mei-41 only after the completion of meiotic recombination, allowing embryos to survive. We find that crossovers are decreased more severely in null mutants, to about one third of wild-type levels. Crossover interference, a patterning phenomenon that ensures that crossovers are widely spaced along a chromosome, is eliminated in these mutants. Similarly, crossover assurance, which describes the distribution of crossovers among chromosomes, is lost. Despite the loss of interference and assurance, a third important patterning phenomenon – the centromere effect – remains intact. We propose a model in which the centromere effect is established prior to and independently of interference and assurance.