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RNA-sequencing of Cercospora beticola DMI-sensitive and -resistant isolates after treatment with tetraconazole identifies common and contrasting pathway induction

Melvin D Bolton, Malaika K Ebert, Luigi Faino, Vivivana Rivera-Varas, Ronnie de Jonge UGent, Yves Van de Peer UGent, Bart PHJ Thomma and Gary A Secor (2016) FUNGAL GENETICS AND BIOLOGY. 92. p.1-13
abstract
Cercospora beticola causes Cercospora leaf spot of sugar beet. Cercospora leaf spot management measures often include application of the sterol demethylation inhibitor (DMI) class of fungicides. The reliance on DMIs and the consequent selection pressures imposed by their widespread use has led to the emergence of resistance in C. beticola populations. Insight into the molecular basis of tetraconazole resistance may lead to molecular tools to identify DMI-resistant strains for fungicide resistance management programs. Previous work has shown that expression of the gene encoding the DMI target enzyme (CYP51) is generally higher and inducible in DMI-resistant C beticola field strains. In this study, we extended the molecular basis of DMI resistance in this pathosystem by profiling the transcriptional response of two C. beticola strains contrasting for resistance to tetraconazole. A majority of the genes in the ergosterol biosynthesis pathway were induced to similar levels in both strains with the exception of CbCyp51, which was induced several-fold higher in the DMI-resistant strain. In contrast, a secondary metabolite gene cluster was induced in the resistance strain, but repressed in the sensitive strain. Genes encoding proteins with various cell membrane fortification processes were induced in the resistance strain. Site-directed and ectopic mutants of candidate DMI-resistance genes all resulted in significantly higher EC50 values than the wild type strain, suggesting that the cell wall and/or membrane modified as a result of the transformation process increased resistance to tetraconazole. Taken together, this study identifies important cell membrane components and provides insight into the molecular events underlying DMI resistance in C beticola.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
PENICILLIUM-DIGITATUM, CANDIDA-ALBICANS, SACCHAROMYCES-CEREVISIAE, MYCOSPHAERELLA-GRAMINICOLA, SUGAR-BEET, AZOLE FUNGICIDE SENSITIVITY, 14-ALPHA-DEMETHYLASE GENE CYP51, Tetraconazole, EC50, Transformation, Cell-membrane, RTA1, Sterol demethylation inhibitor, Ergosterol, PATHOGEN, YEAST, BIOSYNTHESIS
journal title
FUNGAL GENETICS AND BIOLOGY
Fungal Genet. Biol.
volume
92
pages
1 - 13
Web of Science type
Article
Web of Science id
000377844400002
JCR category
MYCOLOGY
JCR impact factor
3.072 (2016)
JCR rank
8/30 (2016)
JCR quartile
2 (2016)
ISSN
1087-1845
DOI
10.1016/j.fgb.2016.04.003
project
Bioinformatics: from nucleotids to networks (N2N)
language
English
UGent publication?
yes
classification
A1
additional info
the contribution of the second and the third author should be considered equal
copyright statement
I have transferred the copyright for this publication to the publisher
id
8036454
handle
http://hdl.handle.net/1854/LU-8036454
date created
2016-07-14 09:29:41
date last changed
2016-12-19 15:43:38
@article{8036454,
  abstract     = {Cercospora beticola causes Cercospora leaf spot of sugar beet. Cercospora leaf spot management measures often include application of the sterol demethylation inhibitor (DMI) class of fungicides. The reliance on DMIs and the consequent selection pressures imposed by their widespread use has led to the emergence of resistance in C. beticola populations. Insight into the molecular basis of tetraconazole resistance may lead to molecular tools to identify DMI-resistant strains for fungicide resistance management programs. Previous work has shown that expression of the gene encoding the DMI target enzyme (CYP51) is generally higher and inducible in DMI-resistant C beticola field strains. In this study, we extended the molecular basis of DMI resistance in this pathosystem by profiling the transcriptional response of two C. beticola strains contrasting for resistance to tetraconazole. A majority of the genes in the ergosterol biosynthesis pathway were induced to similar levels in both strains with the exception of CbCyp51, which was induced several-fold higher in the DMI-resistant strain. In contrast, a secondary metabolite gene cluster was induced in the resistance strain, but repressed in the sensitive strain. Genes encoding proteins with various cell membrane fortification processes were induced in the resistance strain. Site-directed and ectopic mutants of candidate DMI-resistance genes all resulted in significantly higher EC50 values than the wild type strain, suggesting that the cell wall and/or membrane modified as a result of the transformation process increased resistance to tetraconazole. Taken together, this study identifies important cell membrane components and provides insight into the molecular events underlying DMI resistance in C beticola.},
  author       = {Bolton, Melvin D and Ebert, Malaika K and Faino, Luigi and Rivera-Varas, Vivivana and de Jonge, Ronnie and Van de Peer, Yves and Thomma, Bart PHJ and Secor, Gary A},
  issn         = {1087-1845},
  journal      = {FUNGAL GENETICS AND BIOLOGY},
  keyword      = {PENICILLIUM-DIGITATUM,CANDIDA-ALBICANS,SACCHAROMYCES-CEREVISIAE,MYCOSPHAERELLA-GRAMINICOLA,SUGAR-BEET,AZOLE FUNGICIDE SENSITIVITY,14-ALPHA-DEMETHYLASE GENE CYP51,Tetraconazole,EC50,Transformation,Cell-membrane,RTA1,Sterol demethylation inhibitor,Ergosterol,PATHOGEN,YEAST,BIOSYNTHESIS},
  language     = {eng},
  pages        = {1--13},
  title        = {RNA-sequencing of Cercospora beticola DMI-sensitive and -resistant isolates after treatment with tetraconazole identifies common and contrasting pathway induction},
  url          = {http://dx.doi.org/10.1016/j.fgb.2016.04.003},
  volume       = {92},
  year         = {2016},
}

Chicago
Bolton, Melvin D, Malaika K Ebert, Luigi Faino, Vivivana Rivera-Varas, Ronnie de Jonge, Yves Van de Peer, Bart PHJ Thomma, and Gary A Secor. 2016. “RNA-sequencing of Cercospora Beticola DMI-sensitive and -resistant Isolates After Treatment with Tetraconazole Identifies Common and Contrasting Pathway Induction.” Fungal Genetics and Biology 92: 1–13.
APA
Bolton, M. D., Ebert, M. K., Faino, L., Rivera-Varas, V., de Jonge, R., Van de Peer, Y., Thomma, B. P., et al. (2016). RNA-sequencing of Cercospora beticola DMI-sensitive and -resistant isolates after treatment with tetraconazole identifies common and contrasting pathway induction. FUNGAL GENETICS AND BIOLOGY, 92, 1–13.
Vancouver
1.
Bolton MD, Ebert MK, Faino L, Rivera-Varas V, de Jonge R, Van de Peer Y, et al. RNA-sequencing of Cercospora beticola DMI-sensitive and -resistant isolates after treatment with tetraconazole identifies common and contrasting pathway induction. FUNGAL GENETICS AND BIOLOGY. 2016;92:1–13.
MLA
Bolton, Melvin D, Malaika K Ebert, Luigi Faino, et al. “RNA-sequencing of Cercospora Beticola DMI-sensitive and -resistant Isolates After Treatment with Tetraconazole Identifies Common and Contrasting Pathway Induction.” FUNGAL GENETICS AND BIOLOGY 92 (2016): 1–13. Print.