Septins are involved in nuclear division, morphogenesis and pathogenicity in Fusarium graminearum

Septins are involved in nuclear division, morphogenesis and pathogenicity in Fusarium graminearum
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DOI:
10.1016/j.fgb.2016.07.005
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发表时间:
2016-09-01
影响因子:
3
通讯作者:
Wang, Zonghua
Wang, Zonghua
中科院分区:
生物学3区
文献类型:
--
作者:
Chen, Ahai;Xie, Qiurong;Wang, Zonghua

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septin是调节细胞极性、细胞分裂和细胞形态发生的gtp结合蛋白。小麦赤霉病(Fusarium head blight, FHB)是由小麦赤霉病(Fusarium graminearum)引起的世界范围内最具破坏性的病害之一。在这项研究中,我们对F. graminearum的核心蛋白酶Cdc3、Cdc10、Cdc11和Cdc12进行了功能表征。FgCdc3、FgCdc11、FgCdc12突变体的缺失,而FgCdc10突变体的缺失,在生长、分生和毒力方面均有显著降低。显微分析显示它们都参与隔形成和核分裂。此外,septin基因的破坏导致子囊孢子和分生孢子的形态缺陷。有趣的是,Delta Fgcdc3、Delta Fgcdc11和Delta Fgcdc12突变体产生的分生孢子与它们的亲本野生型菌株PH-1和产生正常分生孢子的Delta Fgcdc10突变体相比,具有相互连接的分生孢子表现出变形。通过酵母双杂交实验,我们确定了FgCdc3、FgCdc10、FgCdc11和FgCdc12之间的相互作用。综上所述,我们的研究结果表明,septin在禾粒镰刀菌的核分裂、形态发生和致病性中起重要作用。(C) 2016 Elsevier Inc.版权所有。
Septins are GTP-binding proteins that regulate cell polarity, cytokinesis and cell morphogenesis. Fusarium head blight (FHB), caused by Fusarium graminearum, is one of the most devastating diseases worldwide. In this study, we have functionally characterized the core septins, Cdc3, Cdc10, Cdc11 and Cdc12 in F. graminearum. The loss of FgCdc3, FgCdc11, FgCdc12, but not FgCdc10, mutants showed significant reduction in growth, conidiation and virulence. Microscopic analyses revealed that all of them were involved in septum formation and nuclear division. Moreover, disruption of septin genes resulted in morphological defects in ascospores and conidia. Interestingly, conidia produced by Delta Fgcdc3, Delta Fgcdc11 and Delta Fgcdc12 mutants exhibited deformation with interconnecting conidia in contrast to their parent wild-type strain PH-1 and the Delta Fgcdc10 mutant that produced normal conidia. Using yeast two-hybrid assays, we determined the interactions among FgCdc3, FgCdc10, FgCdc11 and FgCdc12. Taken together, our results indicate that septins play important roles in the nuclear division, morphogenesis and pathogenicity in F. graminearum. (C) 2016 Elsevier Inc. All rights reserved.