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Osmotic shrinkage of cells of Synechocystis sp. PCC 6803 by water efflux via aquaporins regulates osmostress-inducible gene expression

机译:SyneChocystis sp细胞的渗透收缩。 PCC 6803通过水上水素来调节Osmostress-Invucible基因表达

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Osmotic stress causes water molecules to efflux from cells through the cytoplasmic membrane. This study reveals that targeted mutation of the aqpZ gene, encoding an aquaporin water channel protein, in the cyanobacterium Synechocystis sp. PCC 6803 prevents the osmotic shrinkage of cells, suggesting that it is the water channel rather than the lipid bilayer that is primarily responsible for water transition through the membrane of this organism. The observations suggest that the aquaporin-mediated shrinkage of the Synechocystis cells plays an important role in changes of gene expression in response to hyperosmotic stress.
机译:渗透胁迫导致水分子通过细胞质膜从细胞中排出。该研究表明,在蓝藻综合症SP中,编码Aquaporin水通道蛋白的AQPZ基因的靶向突变。 PCC 6803防止细胞的渗透收缩,表明它是水通道而不是脂质双层,主要负责通过该生物体的膜的水过渡。观察结果表明,综合症介导的细胞的收缩率在基因表达的变化中发挥着重要作用,响应于高骨肉胁迫。

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