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首页> 外文期刊>Protoplasma: An International Journal of Cell Biology >OSMOREGULATORY MUTANTS THAT AFFECT THE FUNCTION OF THE CONTRACTILE VACUOLE IN CHLAMYDOMONAS REINHARDTII
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OSMOREGULATORY MUTANTS THAT AFFECT THE FUNCTION OF THE CONTRACTILE VACUOLE IN CHLAMYDOMONAS REINHARDTII

机译：影响衣原体中收缩压功能的渗透调节性突变

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Four independent osmoregulatory mutants, osm1, osm3, osm4, and osm7, were isolated on the basis of their requirement for growth medium of high osmotic strength. In normal low-osmotic-strength medium, in contrast to wild-type cells, the mutants grow poorly or not at all; in distilled water mutant cells are immobilized and eventually swell and burst. The mutants were examined by ordinary brightfield and phase-contrast microscopy, videomicroscopy, and electron microscopy. The four mutants showed different defects in the contractile vacuole (CV) cycle. Timing of various stages of the CV cycle showed that osm1 was affected primarily in the early stage of the cycle when the CV begins to grow, osm3 primarily in midcycle when vacuoles fuse to form the CV proper, osm7 at a late stage of the cycle at docking and fusion of the CV with the plasma membrane, and osm4 during contraction of the CV. At the electron microscopic level, in dilute medium, mutant cells by comparison with wild-type cells had large autophagosomes, swollen mitochondria, and dilated ER cisternae. Although electron microscopy showed general abnormalities of the contractile vacuoles consistent with the videomicroscopic observations of living cells, no obvious vacuole membrane abnormalities were seen which would explain the mutational defects. The mutations help define the separate processes that contribute to the coordinated CV cycle in Chlamydomonas, and open the way to eventual isolation of some of the genes responsible for CV function. [References: 24]
机译：根据对高渗透强度生长培养基的要求，分离了四个独立的渗透调节突变体osm1，osm3，osm4和osm7。与野生型细胞相比，在正常的低渗透强度培养基中，突变体生长不良或根本没有生长;在蒸馏水中，突变细胞被固定并最终膨胀并破裂。通过普通的明场和相差显微镜，视频显微镜和电子显微镜检查突变体。这四个突变体在收缩液泡（CV）循环中显示出不同的缺陷。 CV循环各个阶段的时间表明osm1主要在循环的早期阶段开始，当CV开始增长时，osm3主要在循环中期，当液泡融合形成适当的CV时，osm7在循环的后期发生。 CV收缩期间CV与质膜和osm4的对接和融合。在电子显微镜下，在稀释培养基中，与野生型细胞相比，突变细胞具有较大的自噬体，线粒体肿胀和扩张的ER池。尽管电子显微镜显示出与活细胞的视频显微镜观察一致的收缩液泡的一般异常，但是没有观察到明显的液泡膜异常，这可以解释突变缺陷。突变有助于定义有助于衣藻体内协同CV循环的独立过程，并为最终分离出一些负责CV功能的基因开辟了道路。 [参考：24]

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