线粒体天门冬氨酸氨基转移酶(maa1)失活导致球囊酵母发生谷氨酸需要的 glu1 突变。

microPublication biology Pub Date : 2024-10-21 eCollection Date: 2024-01-01 DOI:10.17912/micropub.biology.001338
Kenji Kitamura
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引用次数: 0

摘要

研究发现了两个基因组基因,它们能挽救谷氨酸需要型球囊酵母菌glu1突变体的铵同化缺陷。编码线粒体天冬氨酸氨基转移酶的 maa1 是 glu1 突变的致病基因,因为 maa1 和 glu1 在染色体上有不可分割的联系,而且 glu1 突变株在 maa1 编码区内有一个无义突变,这是其缺陷表型的原因。线粒体 2-氧代戊二酸载体 yhm2 也被分离为一个弱的多拷贝抑制基因。这些发现重申了线粒体在利用氨基酸进行细胞氮代谢方面的重要性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Mitochondrial aspartate aminotransferase ( maa1 ) inactivation causes glutamate-requiring glu1 mutation in Schizosaccharomyces pombe.

Two genomic genes, which rescue ammonium assimilation defect in the glutamate-requiring Schizosaccharomyces pombe glu1 mutant, were identified. The maa1 , encoding a mitochondrial aspartate aminotransferase, is the causative gene of glu1 mutation because an inseparable linkage between maa1 and glu1 on the chromosome, and also the glu1 mutant strain has a nonsense mutation within the maa1 coding region, which is responsible for its defective phenotype. The yhm2 , 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.

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