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首页> 外文期刊>Genes to cells : >Regulation of LRG1 expression by RNA-binding protein Puf5 in the budding yeast cell wall integrity pathway
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Regulation of LRG1 expression by RNA-binding protein Puf5 in the budding yeast cell wall integrity pathway

机译：RNA结合蛋白PUF5在萌芽酵母细胞壁完整性途径中调节LRG1表达

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The PUF RNA-binding protein Puf5 is involved in regulation of the cell wall integrity (CWI) pathway in yeast. Puf5 negatively regulates expression of LRG1 mRNA, encoding for a GTPase-activating protein for Rho1 small GTPase. Here, we further analyzed the effect of Puf5 on LRG1 expression, together with Ccr4 and Pop2 deadenylases, Dhh1 decapping activator, and other PUF proteins. We found that the growth defect of puf5 increment mutant was enhanced by ccr4 increment mutation, which was partially suppressed by LRG1 deletion. Consistently, Lrg1 protein level was much more up-regulated in ccr4 Delta puf5 Delta double mutant than in each single mutant. Interestingly, LRG1 poly(A) tail length was longer in ccr4 increment mutant but not in puf5 increment mutant. Thus, Puf5 regulates LRG1 expression independently from Ccr4, although Puf5 recruits the Ccr4-Not deadenylase complex for mRNA destabilization. Unexpectedly, puf6 Delta mutation suppressed the growth defect caused by ccr4 Delta puf5 increment mutation. Loss of Rpl43a and Rpl43b ribosomal proteins, the previously identified Puf6 interactors, also suppressed the growth defect of ccr4 Delta puf5 Delta mutant. Our results suggest that Puf5 functions in the CWI pathway by regulating LRG1 expression in a deadenylase-independent manner, and that Puf6 is involved in the Ccr4- and Puf5-mediated regulation of cell growth through association with Rpl43.
机译：PUF RNA结合蛋白PUF5涉及酵母中细胞壁完整性（CWI）途径的调节。 PUF5负调节LRG1 mRNA的表达，对RHO1小GTP酶进行GTP酶活化蛋白的表达。在这里，我们进一步分析了PUF5对LRG1表达的影响，以及CCR4和POP2硬烯基酶，DHH1卷积活化剂和其他PUF蛋白。我们发现，通过CCR4增量突变增强了PUF5增量突变体的生长缺陷，其通过LRG1缺失部分抑制。始终如一地，LRG1蛋白质水平在CCR4 Delta Puf5 delta双突变体中更加调节，而不是每种突变体。有趣的是，LRG1 Poly（a）尾长在CCR4增量突变体中更长，但不在PUF5增量突变体中。因此，PUF5通过CCR4独立调节LRG1表达，尽管PUF5为mRNA稳定化募集CCR4-not Deadenyl酶复合物。意外地，PUF6δ突变抑制了CCR4 Delta Puf5增量突变引起的生长缺陷。 RPL43A和RPL43B核糖体蛋白的丧失，先前鉴定的PUF6交流剂，也抑制了CCR4 delta puf5 delta突变体的生长缺陷。我们的研究结果表明，通过以依赖性苯基化酶的方式调节LRG1表达，通过与RPL43结合涉及CCR4和PUF5介导的细胞生长调节，通过调节LRG1表达，在CWI途径中起作用。

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