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在一个 突变体中,对 的抑制作用并不导致由 的 - 标记缺失所赋予的合成生长缺陷。 (你提供的原文中部分内容缺失,请补充完整以便更准确翻译)

Repression of does not contribute to the synthetic growth defect conferred by an -marked deletion of in a mutant.

作者信息

Zhang Fan, Sen Neelam Dabas, Hinnebusch Alan G

机构信息

Division of Molecular and Cellular Biology, Eunice K. Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892, USA.

School of Life Sciences, Jawaharlal Nehru University, New Delhi 110067, India.

出版信息

bioRxiv. 2024 Jan 31:2024.01.30.578007. doi: 10.1101/2024.01.30.578007.

Abstract

Powers et al. recently demonstrated that the cassette used to delete in yeast mutants leads to reduced expression in of the adjacent gene encoding the mitochondrial small subunit (SSU) ribosomal protein Mrp51. Here we provide evidence that elimination of Dbp1, not reduced expression, underlies the synthetic growth defect of a mutant on glucose-containing medium, where respiration is dispensable, consistent with our previous conclusion that Dbp1 and Ded1 perform overlapping functions in stimulating translation initiation on mRNAs burdened with long or structured 5'UTRs in cells cultured with glucose.

摘要

鲍尔斯等人最近证明,用于在酵母突变体中删除基因的盒式结构会导致相邻基因(编码线粒体小亚基(SSU)核糖体蛋白Mrp51)在酵母中的表达降低。在这里,我们提供证据表明,Dbp1的缺失而非表达降低,是某一突变体在含葡萄糖培养基上合成生长缺陷的基础,在这种培养基上呼吸作用并非必需,这与我们之前的结论一致,即在葡萄糖培养的细胞中,Dbp1和Ded1在刺激具有长或结构化5'非翻译区(UTR)的mRNA的翻译起始方面发挥重叠功能。

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