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The C2H2 transcription factor VdMsn2 controls hyphal growth, microsclerotia formation, and virulence of Verticillium dahliae

Verticillium dahliae is a notorious pathogen that causes vascular wilt disease in numerous plant species worldwide. The fungus produces melanized microsclerotia, which helps it survive adverse environmental conditions that it may encounter within its hosts and in the soil. Previously, we determined...

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Bibliographic Details
Published in:Fungal biology 2017-12, Vol.121 (12), p.1001-1010
Main Authors: Tian, Longyan, Yu, Jun, Wang, Yonglin, Tian, Chengming
Format: Article
Language:English
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Summary:Verticillium dahliae is a notorious pathogen that causes vascular wilt disease in numerous plant species worldwide. The fungus produces melanized microsclerotia, which helps it survive adverse environmental conditions that it may encounter within its hosts and in the soil. Previously, we determined that the high osmolarity glycerol (HOG) pathway is involved in the environmental stress response of V. dahliae. In this study, we investigated the function of VdMsn2, a homologue of the yeast C2H2 transcription factor Msn2, which is predicted to function as a downstream player in the HOG pathway. Disruption of VdMsn2 has a discernible effect on hyphal growth and septation, but not on diverse stresses including hyperosmotic stresses and cell wall inhibitory agents. Furthermore, we show that VdMsn2 deletion mutants produce significantly more microsclerotia than the wild-type and exhibit attenuated virulence to smoke trees because of poor penetration. Taken together, our findings suggest that VdMsn2 controls hyphal growth, microsclerotia formation, and virulence but does not significantly contribute to stress responses in V. dahliae. •Loss of VdMsn2 leads to a reduction in hyphal growth with extensive septation.•VdMsn2 negatively controls microsclerotia formation.•VdMsn2 plays no obvious role in the responses of osmotic stress and cell wall inhibitors.•Disruption of VdMsn2 exhibites attenuated virulence.
ISSN:1878-6146
1878-6162
DOI:10.1016/j.funbio.2017.08.005