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In this study, we found that \u03b2\n                    <jats:sub>2<\/jats:sub>\n                    \u2010tubulin, one of the microtubule components, plays an important role in regulating secondary metabolite deoxynivalenol (DON) biosynthesis in\n                    <jats:styled-content style=\"fixed-case\">\n                      <jats:italic>Fusarium graminearum<\/jats:italic>\n                    <\/jats:styled-content>\n                    by interacting with isocitrate dehydrogenase subunit 3 (IDH3). We found IDH3 negatively regulate DON biosynthesis by reducing acetyl\u2010CoA accumulation in\n                    <jats:styled-content style=\"fixed-case\">\n                      <jats:italic>F. graminearum<\/jats:italic>\n                    <\/jats:styled-content>\n                    and DON biosynthesis was stimulated by exogenous acetyl\u2010CoA. In addition, the expression of IDH3 significantly decreased in the carbendazim\u2010resistant mutant nt167 (Fg\u03b2\n                    <jats:sub>2<\/jats:sub>\n                    <jats:sup>F167Y<\/jats:sup>\n                    ). Furthermore, we found that carbendazim\u2010resistance associated \u03b2\n                    <jats:sub>2<\/jats:sub>\n                    \u2010tubulin substitutions reducing the interaction intensity between \u03b2\n                    <jats:sub>2<\/jats:sub>\n                    \u2010tubulin and IDH3. Interestingly, we demonstrated that \u03b2\n                    <jats:sub>2<\/jats:sub>\n                    \u2010tubulin inhibitor carbendazim can disrupt the interaction between \u03b2\n                    <jats:sub>2<\/jats:sub>\n                    \u2010tubulin and IDH3. The decreased interaction intensity between \u03b2\n                    <jats:sub>2<\/jats:sub>\n                    \u2010tubulin and IDH3 resulted in the decreased expression of IDH3, which can cause the accumulation of acetyl\u2010CoA, precursor of DON biosynthesis in\n                    <jats:styled-content style=\"fixed-case\">\n                      <jats:italic>F. graminearum<\/jats:italic>\n                    <\/jats:styled-content>\n                    . Thus, we revealed that carbendazim\u2010resistance associated \u03b2\n                    <jats:sub>2<\/jats:sub>\n                    \u2010tubulin substitutions or carbendazim treatment increases DON biosynthesis by reducing the interaction between \u03b2\n                    <jats:sub>2<\/jats:sub>\n                    \u2010tubulin and IDH3 in\n                    <jats:styled-content style=\"fixed-case\">\n                      <jats:italic>F. graminearum<\/jats:italic>\n                    <\/jats:styled-content>\n                    . Taken together, the novel findings give the new perspectives of \u03b2\n                    <jats:sub>2<\/jats:sub>\n                    \u2010tubulin in regulating secondary metabolism in phytopathogenic fungi.\n                  <\/jats:p>","DOI":"10.1111\/1462-2920.14874","type":"journal-article","created":{"date-parts":[[2019,11,24]],"date-time":"2019-11-24T19:25:16Z","timestamp":1574623516000},"page":"598-614","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":61,"title":["Carbendazim\u2010resistance associated \u03b2\n                    <sub>2<\/sub>\n                    \u2010tubulin substitutions increase deoxynivalenol biosynthesis by reducing the interaction between \u03b2\n                    <sub>2<\/sub>\n                    \u2010tubulin and IDH3 in\n                    <scp>\n                      <i>Fusarium graminearum<\/i>\n                    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