Lake Cathleen M, Nielsen Rachel J, Guo Fengli, Unruh Jay R, Slaughter Brian D, Hawley R Scott
Stowers Institute for Medical Research, Kansas City, United States.
Department of Molecular and Integrative Physiology, Kansas University Medical Center, Kansas City, United States.
Elife. 2015 Oct 9;4:e08287. doi: 10.7554/eLife.08287.
Meiotic recombination begins with the induction of programmed double-strand breaks (DSBs). In most organisms only a fraction of DSBs become crossovers. Here we report a novel meiotic gene, vilya, which encodes a protein with homology to Zip3-like proteins shown to determine DSB fate in other organisms. Vilya is required for meiotic DSB formation, perhaps as a consequence of its interaction with the DSB accessory protein Mei-P22, and localizes to those DSB sites that will mature into crossovers. In early pachytene Vilya localizes along the central region of the synaptonemal complex and to discrete foci. The accumulation of Vilya at foci is dependent on DSB formation. Immuno-electron microscopy demonstrates that Vilya is a component of recombination nodules, which mark the sites of crossover formation. Thus Vilya links the mechanism of DSB formation to either the selection of those DSBs that will become crossovers or to the actual process of crossing over.
减数分裂重组始于程序性双链断裂(DSB)的诱导。在大多数生物中,只有一小部分DSB会形成交叉。在此,我们报告了一个新的减数分裂基因vilya,它编码一种与Zip3样蛋白具有同源性的蛋白质,在其他生物中,该蛋白被证明可决定DSB的命运。Vilya是减数分裂DSB形成所必需的,这可能是其与DSB辅助蛋白Mei-P22相互作用的结果,并且定位于那些将成熟为交叉的DSB位点。在粗线期早期,Vilya沿着联会复合体的中央区域定位并定位于离散的焦点。Vilya在焦点处的积累依赖于DSB的形成。免疫电子显微镜显示Vilya是重组结节的一个组成部分,重组结节标记了交叉形成的位点。因此,Vilya将DSB形成机制与那些将成为交叉的DSB的选择或实际的交叉过程联系起来。