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Scientific article
English

Transcription initiation of the yeast IMD2 gene is abolished in response to nutrient limitation through a sequence in its coding region

Published inMolecular and cellular biology, vol. 23, no. 17, p. 6279-6290
Publication date2003
Abstract

The yeast IMD2 to IMD4 and GUA1 genes, involved in GMP synthesis, are highly expressed in exponentially growing cells but are shut off when cells cease to grow upon nutrient limitation. We show for the IMD2 gene that this effect is not specific to certain carbon sources or to growth rate. Strikingly, the cis elements responsible for this nutritional response are contained within a 23-nucleotide sequence in the coding region of the IMD2 gene. Despite its very unusual location, this regulatory sequence mediates the repression of transcription initiation. From our data, we conclude that GMP synthesis is downregulated upon nutrient limitation through an active mechanism. We show that this transcriptional shutoff abolishes any possibility of the induction of IMD2, even under drastic conditions of guanylic nucleotide limitation. Taken together, these results indicate that low levels of guanylic nucleotides could be required for proper entry into stationary phase.

Keywords
  • Carbon/metabolism
  • Cell Division/drug effects
  • Culture Media/metabolism
  • Gene Expression Regulation, Fungal
  • Guanine/metabolism
  • IMP Dehydrogenase/genetics/metabolism
  • Mutation
  • Mycophenolic Acid/pharmacology
  • Open Reading Frames
  • Regulatory Sequences, Nucleic Acid
  • Saccharomyces cerevisiae/genetics/growth & development/metabolism
  • Saccharomyces cerevisiae Proteins/drug effects/genetics/metabolism
  • Transcription, Genetic
Funding
  • Swiss National Science Foundation - 3100-059199.99
Citation (ISO format)
ESCOBAR-HENRIQUES, Mafalda, COLLART, Martine, DAIGNAN-FORNIER, Bertrand. Transcription initiation of the yeast IMD2 gene is abolished in response to nutrient limitation through a sequence in its coding region. In: Molecular and cellular biology, 2003, vol. 23, n° 17, p. 6279–6290. doi: 10.1128/mcb.23.17.6279-6290.2003
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Article (Published version)
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Identifiers
ISSN of the journal0270-7306
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