Carbendazim-resistance associated β2-tubulin substitutions increase deoxynivalenol biosynthesis by reducing the interaction between β2-tubulin and IDH3 in Fusarium graminearum
Zehua Zhou, Yabing Duan, Mingguo Zhou
Journal:ENVIRONMENTAL MICROBIOLOGY
IF:5.15
DOI:10.1111/1462-2920.14874
PMID:31760682
Published:2019-11-24
research field:分子生物学真菌学植物病理学
Abstract
Summary Microtubule is a well-known structural protein participating in cell division, motility and vesicle traffic. In this study, we found that β 2 -tubulin, one of the microtubule components, plays an important role in regulating secondary metabolite deoxynivalenol (DON) biosynthesis in Fusarium graminearum by interacting with isocitrate dehydrogenase subunit 3 (IDH3). We found IDH3 negatively regulate DON biosynthesis by reducing acetyl-CoA accumulation in F. graminearum and DON biosynthesis was stimulated by exogenous acetyl-CoA. In addition, the expression of IDH3 significantly decreased in the carbendazim-resistant mutant nt167 (Fgβ 2 F167Y ). Furthermore, we found that carbendazim-resistance associated β 2 -tubulin substitutions reducing the interaction intensity between β 2 -tubulin and IDH3. Interestingly, we demonstrated that β 2 -tubulin inhibitor carbendazim can disrupt the interaction between β 2 -tubulin and IDH3. The decreased interaction intensity between β 2 -tubulin and IDH3 resulted in the decreased expression of IDH3, which can cause the accumulation of acetyl-CoA, precursor of DON biosynthesis in F. graminearum . Thus, we revealed that carbendazim-resistance associated β 2 -tubulin substitutions or carbendazim treatment increases DON biosynthesis by reducing the interaction between β 2 -tubulin and IDH3 in F. graminearum . Taken together, the novel findings give the new perspectives of β 2 -tubulin in regulating secondary metabolism in phytopathogenic fungi.
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