Alleva Benjamin, Balukoff Nathan, Peiper Amy, Smolikove Sarit
Department of Biology, University of Iowa, Iowa City, IA 52242.
Department of Biology, University of Iowa, Iowa City, IA 52242
J Cell Biol. 2017 Feb;216(2):393-408. doi: 10.1083/jcb.201606126. Epub 2017 Jan 11.
In meiotic prophase I, homologous chromosome pairing is promoted through chromosome movement mediated by nuclear envelope proteins, microtubules, and dynein. After proper homologue pairing has been established, the synaptonemal complex (SC) assembles along the paired homologues, stabilizing their interaction and allowing for crossing over to occur. Previous studies have shown that perturbing chromosome movement leads to pairing defects and SC polycomplex formation. We show that FKB-6 plays a role in SC assembly and is required for timely pairing and proper double-strand break repair kinetics. FKB-6 localizes outside the nucleus, and in its absence, the microtubule network is altered. FKB-6 is required for proper movement of dynein, increasing resting time between movements. Attenuating chromosomal movement in fkb-6 mutants partially restores the defects in synapsis, in agreement with FKB-6 acting by decreasing chromosomal movement. Therefore, we suggest that FKB-6 plays a role in regulating dynein movement by preventing excess chromosome movement, which is essential for proper SC assembly and homologous chromosome pairing.
在减数分裂前期I,同源染色体配对通过由核膜蛋白、微管和动力蛋白介导的染色体运动得以促进。在建立适当的同源物配对后,联会复合体(SC)沿着配对的同源物组装,稳定它们的相互作用并允许交叉互换发生。先前的研究表明,干扰染色体运动导致配对缺陷和SC多复合体形成。我们发现FKB-6在SC组装中起作用,并且是及时配对和适当的双链断裂修复动力学所必需的。FKB-6定位于细胞核外,在其缺失时,微管网络会发生改变。FKB-6是动力蛋白正常运动所必需的,它增加了运动之间的静止时间。在fkb-6突变体中减弱染色体运动部分恢复了联会缺陷,这与FKB-6通过减少染色体运动起作用一致。因此,我们认为FKB-6通过防止过度的染色体运动在调节动力蛋白运动中起作用,这对适当的SC组装和同源染色体配对至关重要。