Carbendazim‐resistance associated β2‐tubulin substitutions increase deoxynivalenol biosynthesis by reducing the interaction between β2‐tubulin and IDH3 in Fusarium graminearum. (4th December 2019)

• Record Type: Journal Article
• Authors: Zhou, Zehua; Duan, Yabing; Zhou, Mingguo
• Is Part Of: Environmental microbiology. Volume 22:Number 2(2020)
• Page Start: 598
• Page End: 614
• Publication Date: 2019-12-04
• Subjects: Microbial ecology -- Periodicals; Environmental Microbiology -- Periodicals; 579.17
• DOI: 10.1111/1462-2920.14874
• Languages: English
• ISSNs: 1462-2912

Abstract

Summary: Microtubule is a well‐known structural protein participating in cell division, motility and vesicle traffic. In this study, we found that β2 ‐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 (Fgβ2 F167Y ). Furthermore, we found that carbendazim‐resistance associated β2 ‐tubulin substitutions reducing the interaction intensity between β2 ‐tubulin and IDH3. Interestingly, we demonstrated that β2 ‐tubulin inhibitor carbendazim can disrupt the interaction between β2 ‐tubulin and IDH3. The decreased interaction intensity between β2 ‐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 β2 ‐tubulin substitutions or carbendazim treatment increases DON biosynthesis by reducing the interaction between β2 ‐tubulin and IDH3 in F. graminearum . Taken together, the novel findings give the new perspectives of β2 ‐tubulin in regulating secondary metabolism in phytopathogenic fungi.