TorC1 and nitrogen catabolite repression control of integrated GABA shunt and retrograde pathway gene expression.
GABA shunt
GAD1
Gln3
TorC1
UGA1
retrograde pathway
Journal
Yeast (Chichester, England)
ISSN: 1097-0061
Titre abrégé: Yeast
Pays: England
ID NLM: 8607637
Informations de publication
Date de publication:
08 2023
08 2023
Historique:
revised:
10
03
2023
received:
27
12
2022
accepted:
14
03
2023
pmc-release:
01
08
2024
medline:
8
8
2023
pubmed:
25
3
2023
entrez:
24
3
2023
Statut:
ppublish
Résumé
Despite our detailed understanding of how the lower GABA shunt and retrograde genes are regulated, there is a paucity of validated information concerning control of GAD1, the glutamate decarboxylase gene which catalyzes the first reaction of the GABA shunt. Further, integration of glutamate degradation via the GABA shunt has not been investigated. Here, we show that while GAD1 shares a response to rapamycin-inhibition of the TorC1 kinase, it does so independently of the Gln3 and Gat1 NCR-sensitive transcriptional activators that mediate transcription of the lower GABA shunt genes. We also show that GABA shunt gene expression increases dramatically in response to nickel ions. The α-ketoglutarate needed for the GABA shunt to cycle, thereby producing reduced pyridine nucleotides, derives from the retrograde pathway as shown by a similar high increase in the retrograde reporter, CIT2 when nickel is present in the medium. These observations demonstrate high integration of the GABA shunt, retrograde, peroxisomal glyoxylate cycle, and β-oxidation pathways.
Identifiants
pubmed: 36960709
doi: 10.1002/yea.3849
pmc: PMC10518031
mid: NIHMS1892764
doi:
Substances chimiques
Mechanistic Target of Rapamycin Complex 1
EC 2.7.11.1
Saccharomyces cerevisiae Proteins
0
GATA Transcription Factors
0
Nickel
7OV03QG267
Nitrogen
N762921K75
gamma-Aminobutyric Acid
56-12-2
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
318-332Subventions
Organisme : NIGMS NIH HHS
ID : R01 GM035642
Pays : United States
Informations de copyright
© 2023 John Wiley & Sons Ltd.
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