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Reference - PMID:39502420 - Mitochondrial aspartate aminotransferase ( maa1 ) inactivation causes glutamate-requiring glu1 mutation in Schizosaccharomyces pombe .

Reference summary

PubMed ID
PMID:39502420
Title
Mitochondrial aspartate aminotransferase ( maa1 ) inactivation causes glutamate-requiring glu1 mutation in Schizosaccharomyces pombe .
Authors
Kitamura K
Citation
MicroPubl Biol 2024;2024
Publication year
2024
Abstract
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.

Annotation

GO molecular function

GO:0015139 - alpha-ketoglutarate transmembrane transporter activity

Genes:

GO:0004069 - L-aspartate:2-oxoglutarate transaminase activity

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Multi-locus phenotype

FYPO:0000249 - decreased cell population growth on ammonia nitrogen source

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Genotypes:

FYPO:0000242 - normal growth on ammonia nitrogen source

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Genotypes:

Single locus phenotype

FYPO:0000249 - decreased cell population growth on ammonia nitrogen source

Genes:

Genotypes:

FYPO:0002271 - growth auxotrophic for glutamine

Genes:

Genotypes:

FYPO:0001357 - normal vegetative cell population growth

Genes:

Genotypes: