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首页> 外文期刊>Genes to cells : >Inner nuclear membrane protein Lem2 augments heterochromatin formation in response to nutritional conditions
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Inner nuclear membrane protein Lem2 augments heterochromatin formation in response to nutritional conditions

机译：内膜蛋白Lem2响应营养状况而增加异染色质的形成

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Inner nuclear membrane proteins interact with chromosomes in the nucleus and are important for chromosome activity. Lem2 and Man1 are conserved members of the LEM-domain nuclear membrane protein family. Mutations of LEM-domain proteins are associated with laminopathy, but their cellular functions remain unclear. Here, we report that Lem2 maintains genome stability in the fission yeast Schizosaccharomyces pombe. S.pombe cells disrupted for the lem2(+) gene (lem2) showed slow growth and increased rate of the minichromosome loss. These phenotypes were prominent in the rich culture medium, but not in the minimum medium. Centromeric heterochromatin formation was augmented upon transfer to the rich medium in wild-type cells. This augmentation of heterochromatin formation was impaired in lem2 cells. Notably, lem2 cells occasionally exhibited spontaneous duplication of genome sequences flanked by the long-terminal repeats of retrotransposons. The resulting duplication of the lnp1(+) gene, which encodes an endoplasmic reticulum membrane protein, suppressed lem2 phenotypes, whereas the lem2 lnp1 double mutant showed a severe growth defect. A combination of mutations in Lem2 and Bqt4, which encodes a nuclear membrane protein that anchors telomeres to the nuclear membrane, caused synthetic lethality. These genetic interactions imply that Lem2 cooperates with the nuclear membrane protein network to regulate genome stability.
机译：内核膜蛋白与细胞核中的染色体相互作用，对染色体活性很重要。 Lem2和Man1是LEM域核膜蛋白家族的保守成员。 LEM结构域蛋白的突变与椎板病相关，但其细胞功能仍不清楚。在这里，我们报告说，Lem2维持裂殖酵母粟酒裂殖酵母中的基因组稳定性。破坏lem2（+）基因（lem2）的S.pombe细胞显示出缓慢的生长和微染色体丢失率的增加。这些表型在丰富的培养基中很明显，但在最低培养基中却没有。着丝粒异染色质的形成在转移至野生型细胞中的丰富培养基后得以增强。 lem2细胞中异染色质形成的这种增加受到损害。值得注意的是，lem2细胞偶尔会在逆转录转座子的长末端重复序列旁出现基因组序列的自发复制。结果，Inp1（+）基因的编码内质网膜蛋白的重复，抑制了lem2表型，而lem2 lnp1双重突变体显示出严重的生长缺陷。 Lem2和Bqt4中的突变组合编码一种将端粒固定在核膜上的核膜蛋白，导致合成杀伤力。这些遗传相互作用暗示Lem2与核膜蛋白网络协同调节基因组稳定性。

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