Page Scott L, Hawley R Scott
Stowers Institute for Medical Research, Kansas City, Missouri 64110, USA.
Genetics. 2005 Aug;170(4):1797-807. doi: 10.1534/genetics.105.041194. Epub 2005 Jun 18.
The semisterile meiotic mutant mei-352 alters the distribution of meiotic exchanges without greatly affecting their total frequency. We show that the mei-352 mutation is an allele of the klp3A gene, which encodes a kinesin-like protein of the Kinesin-4 family. The semisterility observed in mei-352 females results from a known defect of klp3A oocytes in mediating pronuclear fusion. Interestingly, other klp3A alleles also exhibit defects in meiotic recombination similar to those of mei-352. Finally, we show that the Klp3A protein localizes within the oocyte nucleus during meiotic prophase, the time at which exchange distribution is established, and extensively colocalizes with DNA. The parallel of the klp3A phenotype with a meiotic defect observed for kar3 mutants in yeast suggests a role for kinesins in early meiosis and might reflect a previously suggested role for this class of kinesins in chromosome condensation.
半不育减数分裂突变体mei-352改变了减数分裂交换的分布,而对其总频率影响不大。我们发现mei-352突变是klp3A基因的一个等位基因,该基因编码一种驱动蛋白4家族的类驱动蛋白。在mei-352雌性中观察到的半不育是由klp3A卵母细胞在介导原核融合时的已知缺陷导致的。有趣的是,其他klp3A等位基因在减数分裂重组中也表现出与mei-352类似的缺陷。最后,我们表明Klp3A蛋白在减数分裂前期定位于卵母细胞核内,这是建立交换分布的时期,并且与DNA广泛共定位。klp3A表型与酵母中kar3突变体观察到的减数分裂缺陷相似,这表明驱动蛋白在减数分裂早期发挥作用,可能反映了此前认为这类驱动蛋白在染色体凝聚中的作用。