Cohen J, Beisson J
Genetics. 1980 Aug;95(4):797-818. doi: 10.1093/genetics/95.4.797.
In Paramecium tetraurelia, a number of mutations have been shown to affect simultaneously cortical organization (attachment of trichocysts to the cortex) and nuclear divisions (Ruiz et al. 1976). In order to analyze the genetic and physiological basis of this correlation, and we have isolated new mutations affecting the properties of the trichocysts and studied their genetic relationships with other previously known mutations. Of 24 to 28 loci controlling the biogenesis and properties of the trichocysts, mutations only in the 16 to 20 loci tht control trichocysts attachment to the cortex result in nuclear defects. Cytological observations show that all these mutants display the same set of nucler abnormalities: in particular, rounded shape of the resting macronucleus mispositioning and defective elongation of the dividing macronucleus and unequal repartition of the marco- and micronuclei. This common syndrome is independent of both the mutagenic origin and the mutated locus. Furthermore, by microinjection, it is possible to localize the site of action of the mutations in either the trichocyst compartment or the nontrichocyst compartment. It was found by this technique that the nuclear syndrome is also independent of the site of action of the mutation. All the genetic and physiological data support the conclusion that the nuclear defects are the consequence of the lack of trichocyst attachement to the cortex: in wild-type cells, trichocyst attachment would induce a membranar or perimembranar state necessary for correct nuclear positioning during cell division. In the absence of trichocyst attachment, the cortical control of nuclear division would be abolished. The possible involvement of cytoskeletal links between surface and nuclei is discussed.
在四膜虫中,已发现许多突变会同时影响皮层组织(刺丝泡与皮层的附着)和核分裂(Ruiz等人,1976年)。为了分析这种相关性的遗传和生理基础,我们分离出了影响刺丝泡特性的新突变,并研究了它们与其他先前已知突变的遗传关系。在控制刺丝泡生物发生和特性的24至28个基因座中,只有控制刺丝泡与皮层附着的16至20个基因座发生突变才会导致核缺陷。细胞学观察表明,所有这些突变体都表现出相同的一组核异常:特别是,静止大核呈圆形,分裂大核定位错误且伸长有缺陷,大核和小核分配不均。这种常见的综合征与诱变起源和突变基因座均无关。此外,通过显微注射,可以将突变的作用位点定位在刺丝泡区室或非刺丝泡区室中。通过这项技术发现,核综合征也与突变的作用位点无关。所有的遗传和生理数据都支持这样的结论,即核缺陷是刺丝泡缺乏与皮层附着的结果:在野生型细胞中,刺丝泡的附着会诱导一种膜状或膜周状态,这是细胞分裂期间正确核定位所必需的。在没有刺丝泡附着的情况下,核分裂的皮层控制将被取消。文中还讨论了表面与细胞核之间细胞骨架连接的可能作用。