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Transcriptomic and phenotypic analysis of the effects of T-2 toxin on Saccharomyces cerevisiae: evidence of mitochondrial involvement

Jossé, Lyne, Li, Xingmin, Coker, Raymond D., Gourlay, Campbell W., Evans, Ivor H. (2011) Transcriptomic and phenotypic analysis of the effects of T-2 toxin on Saccharomyces cerevisiae: evidence of mitochondrial involvement. FEMS Yeast Research, 11 (1). pp. 133-150. ISSN 1567-1356. (doi:10.1111/j.1567-1364.2010.00699.x) (The full text of this publication is not currently available from this repository. You may be able to access a copy if URLs are provided) (KAR id:31356)

The full text of this publication is not currently available from this repository. You may be able to access a copy if URLs are provided.
Official URL:
http://dx.doi.org/10.1111/j.1567-1364.2010.00699.x

Abstract

At 5 ?g mL?1, T-2 toxin significantly upregulated the transcription of 281 genes and downregulated 86. Strongly upregulated genes included those involved in redox activity, mitochondrial functions, the response to oxidative stress, and cytoplasmic rRNA transcription and processing. Highly repressed genes have roles in mitochondrial biogenesis, and the expression and stability of cytoplasmic rRNAs. T-2 toxin inhibition of growth was greater in a medium requiring respiration, and was antagonized by antioxidants. T-2 toxin treatment induced reactive oxygen species, caused nucleolytic damage to DNA, probably mitochondrial, and externalization of phosphatidylserine. Deletion mutations causing respiratory deficiency substantially increased toxin tolerance, and deletion of some TOR (target of rapamycin) pathway genes altered T-2 toxin sensitivity. Deletion of FMS1, which plays an indirect role in cytoplasmic protein synthesis, markedly increased toxin tolerance. Overall, the findings suggest that T-2 toxin targets mitochondria, generating oxy-radicals and repressing mitochondrial biogenesis genes, thus inducing oxidative stress and redox enzyme genes, and triggering changes associated with apoptosis. The large transcriptional changes in genes needed for rRNA transcription and expression and the effects of deletion of FMS1 are also consistent with T-2 toxin damage to the cytoplasmic translational mechanism, although it is unclear how this relates to the mitochondrial effects.

Item Type: Article
DOI/Identification number: 10.1111/j.1567-1364.2010.00699.x
Uncontrolled keywords: T-2 toxin;Saccharomyces cerevisiae;transcriptomics;ROS;mitochondrion
Subjects: Q Science
Divisions: Divisions > Division of Natural Sciences > Biosciences
Depositing User: Lyne Josse
Date Deposited: 08 Oct 2012 11:18 UTC
Last Modified: 16 Nov 2021 10:09 UTC
Resource URI: https://kar.kent.ac.uk/id/eprint/31356 (The current URI for this page, for reference purposes)

University of Kent Author Information

Jossé, Lyne.

Creator's ORCID:
CReDIT Contributor Roles:

Gourlay, Campbell W..

Creator's ORCID: https://orcid.org/0000-0002-2373-6788
CReDIT Contributor Roles:
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