Evidence map›Paper›PMID 40956442›Full record

ArticleApplied microbiology and biotechnology2025

Multi-omics reveals glucose repression of citric acid catabolism in Pichia kudriavzevii.

Yichao Cheng, Xinyi Wang, Di Wu, Yao Lu, Yi Qin, Yanlin Liu, Yanying Liang, Yuyang Song

Abstract read
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Article in Applied microbiology and biotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

8 authors.

Yichao ChengCollege of Enology, Northwest A&F University, Yangling, 712100, Shaanxi, China.
Xinyi WangCollege of Enology, Northwest A&F University, Yangling, 712100, Shaanxi, China.
Di WuCollege of Enology, Northwest A&F University, Yangling, 712100, Shaanxi, China.
Yao LuCollege of Enology, Northwest A&F University, Yangling, 712100, Shaanxi, China.
Yi QinCollege of Enology, Northwest A&F University, Yangling, 712100, Shaanxi, China.
Yanlin LiuCollege of Enology, Northwest A&F University, Yangling, 712100, Shaanxi, China.
Yanying LiangCollege of Enology, Northwest A&F University, Yangling, 712100, Shaanxi, China.
Yuyang SongCollege of Enology, Northwest A&F University, Yangling, 712100, Shaanxi, China. yuyangsong@nwsuaf.edu.cn.

Funding

Earmarked Fund for CARS CARS-29-jg-3Key R&D project in Shaanxi Province 2023-ZDLNY-31, 2024GH-ZDXM-32National Natural Science Key Foundation of China U21A20269Ningxia Hui Autonomous Region Key R&D Project 2023BCF01025, 2024BBF02005
6 · The paper itself

Abstract

Pichia kudriavzevii is a widely used yeast in the wine industry that can degrade citric acid. However, this process can be hindered by the presence of glucose through a phenomenon called carbon catabolite repression (CCR). Herein, this study determined the underlying mechanism by examining the effects of glucose on P. kudriavzevii. Our findings indicated that glucose inhibited the reduction of citric acid and maintained elevated levels of fatty acids and glycerophospholipids. However, the inhibition of citric acid degradation under glucose addition was related to the retarded accumulation of metabolites involved in the biosynthesis of antibiotics, propanoate metabolism, microbial metabolism in diverse environments, C5-branched dibasic acid metabolism, and metabolic pathways in diverse environments. Additionally, the integrated data revealed that citrate catabolism of P. kudriavzevii was remarkably repressed in response to glucose by regulating glycerophospholipid metabolism, carbon metabolism and the biosynthesis pathways of secondary metabolites. Further investigations indicated that the increase of fatty acids (e.g., alpha-linolenic and arachidic) and glycerophospholipids (e.g., dihydroxyacetone phosphate and glycerophosphocholine) under glucose addition was related to the up-regulated GPD1, PISD, HIS1 and RPIA gene expressions in glycerophospholipid metabolism and the down-regulated FBP1, MDH, IDH3, ICL1, ACL and JEN1 gene expressions in carbon metabolism and the biosynthesis pathways of secondary metabolites. Meantime, glucose regulated the expression of transcription factors (e.g., MIG1 and GCN4) associated with three pathways, which were crucial genes of CCR regulatory networks. Overall, we uncovered the metabolic regulatory network through which CCR inhibits citric acid utilization in P. kudriavzevii. KEY POINTS: • Metabolic changes of P. kudriavzevii cells responding to carbon sources were observed • Potential genes regulating citric acid degradation contributing to CCR were screened • The inhibition of citric acid degradation is due to changes in the regulatory network.

Indexed as

Catabolite RepressionCitric AcidGlucosePichiaCarbonFatty AcidsGene Expression Regulation, FungalGlycerophospholipidsMetabolic Networks and PathwaysMultiomicsCarbonCitric AcidFatty AcidsGlucoseGlycerophospholipidsCarbon catabolism repression (CCR)Citrate acidMetabolomicsPichia kudriavzeviiTranscriptomics

Identifiers

PMID40956442
PMCPMC12441098

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.