An alpha tubulin mutation suppresses nuclear migration mutations in Aspergillus nidulans.
An alpha tubulin mutation suppresses nuclear migration mutations in Aspergillus nidulans.
复制标题
α微管蛋白突变抑制构巢曲霉的核迁移突变。
DOI：
10.1093/genetics/141.4.1287
复制
发表时间：
1995
期刊：
影响因子：
3.3
通讯作者：
Morris,NR
中科院分区：
文献类型：
--
作者：
Willins,DA;Xiang,X;Morris,NR
微管和细胞质动力蛋白是细胞核沿着丝状真菌菌丝移动所必需的，后者是微管依赖的运动。编码动力蛋白重链的nudA基因和编码类似G蛋白的β亚单位蛋白的nudF基因的热敏(hs-)突变阻止了Nidulans的核迁移。NudC和nudG基因的HS突变也阻止了核迁移。我们已经分离出了基因外抑制突变，这些突变可以逆转由这些突变引起的hs表型。在这里，我们显示了一个nudF抑制子也抑制了nudA、nudC和nudG中的hs-突变以及nuda和nudF中的缺失。这种抑制突变是在tubaα微管蛋白基因中，其特征表明它破坏了微管的稳定。这种突变改变了微管的染色，并使人对寒冷和苯菌灵敏感，这两种处理会破坏微管的稳定。低浓度苯菌灵治疗也抑制hs-nuda、nudC、nudF和nudG突变以及nudA和nudF缺失。抑制hs-nuda突变和nuda缺失特别有趣，因为这些菌株缺乏活性动力蛋白重链。综上所述，这些结果表明，即使在缺乏细胞质动力蛋白运动功能的情况下，微管失稳也允许细胞核迁移。
Microtubules and cytoplasmic dynein, a microtubule-dependent motor, are required for nuclei to move along the hyphae of filamentous fungi. Nuclear migration in Aspergillus nidulans is blocked by heat-sensitive (hs-) mutations in the nudA gene, which encodes dynein heavy chain, and the nudF gene, which encodes a G protein beta-subunit-like protein. Hs- mutations in the nudC and nudG genes also prevent nuclear migration. We have isolated extragenic suppressor mutations that reverse the hs- phenotypes caused by these mutations. Here we show that one nudF suppressor also suppresses hs- mutations in nudA, nudC, and nudG and deletions in nudA and nudF. This suppressor mutation is in the tubA alpha tubulin gene, and its characteristics suggest that it destabilizes microtubules. The mutation alters microtubule staining and confers sensitivity to cold and benomyl, two treatments that destabilize microtubules. Treatment with low concentrations of benomyl also suppresses the hs- nudA, nudC, nudF, and nudG mutations and the nudA and nudF deletions. Suppression of the hs- nudA mutation and the nudA deletion is especially interesting because these strains lack active dynein heavy chain. Together, these results suggest that microtubule destabilization allows nuclei to migrate even in the absence of cytoplasmic dynein motor function.