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Show moreMeiosis is an important mechanism that generates genetic variation for sexually reproducing organisms through recombination. In order for an organism to successfully propagate its genetic material from one generation to the next, its genome must be properly delivered as gametes. Meiotic crossing over of DNA ensures proper homolog segregation by repairing programmed double-stranded breaks. Meiotic defects caused by chromosome structural variants are detrimental to reproduction. During the interchromosomal effect, heterozygous inversions suppress crossing over between affected chromosomes while increasing crossing over between normal chromosome pairs. These defects in chromosomal dynamics trigger the pachytene checkpoint, leading to a delay in prophase progression. It has been suggested that this delay in prophase causes the interchromosomal effect on recombination. However, whether the interchromosomal effect on crossing over is caused directly by defects in chromosome dynamics or indirectly by the delay in prophase remains unclear. We are distinguishing between these two hypotheses by investigating the distributions and frequencies of crossovers in Drosophila mutants when prophase is extended by utilizing maelstrom mutants that trigger the pachytene checkpoint independently of chromosome defects. We are analyzing the changes in crossover distribution and frequencies in these mutants using recessive markers on unaffected chromosome. We are also collecting confocal imaging data of the mutants’ germarium to visualize the effects of maelstrom mutations on meiosis. Our data will provide insights into the mechanisms of the interchromosomal effect and reveal whether or not the interchromosomal effect is directly mediated by a delay in pachytene or, alternatively, mediated by disrupted crossover control mechanisms.
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