When transcriptome meets metabolome

fast cellular responses of yeast to sudden relief of glucose limitation.

Journal Article (2006)
Author(s)

MTAP Kresnowati (TU Delft - OLD BT/Cell Systems Engineering)

WA van Winden (TU Delft - OLD BT/Cell Systems Engineering)

M.J.H. Almering (TU Delft - BT/Industriele Microbiologie)

Angela Ten Pierick (TU Delft - OLD BT/Cell Systems Engineering)

C Ras (TU Delft - OLD BT/Cell Systems Engineering)

TA Knijnenburg (TU Delft - Multimedia Computing)

P.A.S. Daran-Lapujade (TU Delft - BT/Industriele Microbiologie)

J.T. Pronk (TU Delft - BT/Industriele Microbiologie)

J.J. Heijnen (TU Delft - OLD BT/Cell Systems Engineering)

J.G. Daran (TU Delft - BT/Industriele Microbiologie)

Research Group
OLD BT/Cell Systems Engineering
DOI related publication
https://doi.org/10.1038/msb4100083
More Info
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Publication Year
2006
Research Group
OLD BT/Cell Systems Engineering
Issue number
49
Volume number
2
Pages (from-to)
1-16

Abstract

Within the first 5 min after a sudden relief from glucose limitation, Saccharomyces cerevisiae exhibited fast changes of intracellular metabolite levels and a major transcriptional reprogramming. Integration of transcriptome and metabolome data revealed tight relationships between the changes at these two levels. Transcriptome as well as metabolite changes reflected a major investment in two processes: adaptation from fully respiratory to respiro‐fermentative metabolism and preparation for growth acceleration. At the metabolite level, a severe drop of the AXP pools directly after glucose addition was not accompanied by any of the other three NXP. To counterbalance this loss, purine biosynthesis and salvage pathways were transcriptionally upregulated in a concerted manner, reflecting a sudden increase of the purine demand. The short‐term dynamics of the transcriptome revealed a remarkably fast decrease in the average half‐life of downregulated genes. This acceleration of mRNA decay can be interpreted both as an additional nucleotide salvage pathway and an additional level of glucose‐induced regulation of gene expression.

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