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线粒体天冬氨酸氨基转移酶( )失活导致 中需要谷氨酸的 突变。 (注:原文括号处信息缺失,翻译时保留原样)

Mitochondrial aspartate aminotransferase ( ) inactivation causes glutamate-requiring mutation in .

作者信息

Kitamura Kenji

机构信息

Department of Gene Science, Natural Science Center for Basic Research and Development, Hiroshima University, Higashi-Hiroshima, Hiroshima, Japan.

Genome Biotechnology, Graduate School of Integrated Sciences for Life, Hiroshima University, Higashi-Hiroshima, Hiroshima, Japan.

出版信息

MicroPubl Biol. 2024 Oct 21;2024. doi: 10.17912/micropub.biology.001338. eCollection 2024.

Abstract

Two genomic genes, which rescue ammonium assimilation defect in the glutamate-requiring mutant, were identified. The , encoding a mitochondrial aspartate aminotransferase, is the causative gene of mutation because an inseparable linkage between and on the chromosome, and also the mutant strain has a nonsense mutation within the coding region, which is responsible for its defective phenotype. The , a mitochondrial 2-oxoglutarate carrier, was also isolated as a weak multicopy suppressor gene. These findings reiterate the importance of the mitochondria in utilizing the amino acids for cellular nitrogen metabolism.

摘要

鉴定出了两个能挽救谷氨酸需求型突变体中铵同化缺陷的基因组基因。编码线粒体天冬氨酸氨基转移酶的基因是突变的致病基因,因为它与染色体上的基因存在不可分割的连锁关系,而且突变菌株在该基因的编码区域内存在无义突变,这导致了其缺陷表型。线粒体2-氧代戊二酸载体基因也作为一个弱多拷贝抑制基因被分离出来。这些发现重申了线粒体在利用氨基酸进行细胞氮代谢中的重要性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8102/11536045/a363b93dbf04/25789430-2024-micropub.biology.001338.jpg

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