Tsubouchi Tomomi, Zhao Hongyu, Roeder G Shirleen
Howard Hughes Medical Institute, Yale University, New Haven, Connecticut 06520, USA.
Dev Cell. 2006 Jun;10(6):809-19. doi: 10.1016/j.devcel.2006.04.003.
We have characterized Zip4 (a.k.a. Spo22), a meiosis-specific protein essential for chromosome synapsis in budding yeast. In the absence of Zip4, the synaptonemal complex protein Zip1 fails to polymerize along chromosomes. Zip2 and Zip3 are previously characterized components of the synapsis initiation complex. Zip4 forms a functional unit with Zip2 that is distinct from Zip3. Zip2 and Zip4 are mutually dependent for their chromosomal localization; in polycomplexes, the pattern of Zip2/Zip4 localization is distinct from that of Zip3. Crossing-over is decreased in the zip4 mutant (as in zip1, zip2, and zip3); the remaining crossovers are largely dependent on a parallel pathway utilizing Mms4. zip4 displays a novel phenotype: negative crossover interference, meaning that crossovers tend to cluster. This clustering depends on Zip1. Our results suggest an interaction between crossover pathways such that a protein (Zip1) acting in one pathway influences the distribution of crossovers promoted by a parallel (Mms4-dependent) pathway.
我们已经对Zip4（又名Spo22）进行了表征，它是一种在芽殖酵母中对染色体联会至关重要的减数分裂特异性蛋白。在没有Zip4的情况下，联会复合体蛋白Zip1无法沿染色体聚合。Zip2和Zip3是先前已表征的联会起始复合体的组成部分。Zip4与Zip2形成一个不同于Zip3的功能单元。Zip2和Zip4在染色体定位上相互依赖；在多复合体中，Zip2/Zip4的定位模式与Zip3不同。在zip4突变体中（如同在zip1、zip2和zip3突变体中一样），交叉互换减少；剩余的交叉互换很大程度上依赖于利用Mms4的平行途径。zip4表现出一种新的表型：负交叉互换干扰，即交叉互换倾向于聚集。这种聚集依赖于Zip1。我们的结果表明交叉互换途径之间存在相互作用，使得在一条途径中起作用的一种蛋白（Zip1）会影响由平行（依赖Mms4）途径促进的交叉互换的分布。
