Transcription factors spt3 and spt8 are associated with conidiation, mycelium growth, and pathogenicity in Fusarium graminearum
Transcription factors spt3 and spt8 are associated with conidiation, mycelium growth, and pathogenicity in Fusarium graminearum
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转录因子 spt3 和 spt8 与禾谷镰刀菌的分生孢子形成、菌丝体生长和致病性相关
DOI：
10.1111/1574-6968.12350
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发表时间：
2014-02-01
影响因子：
2.1
通讯作者：
Zhou, Mingguo
中科院分区：
文献类型：
--
作者：
Gao, Tao;Zheng, Zhitian;Zhou, Mingguo
禾谷镰刀菌（有性型：玉米赤霉）是小麦赤霉病（FHB）的优势病原菌，可造成重大经济损失。由于复合物中存在功能独立的亚基模块，Spt-Ada-Gcn5-乙酰转移酶 (SAGA) 转录共激活因子在转录调节中发挥多种作用。转录因子 spt3 和 spt8 是 SAGA 复合体的组成部分，它们在酵母和包括禾谷镰刀菌在内的丝状真菌中很重要。在本研究中，我们使用blastp 程序鉴定了Fgspt3 和Fgspt8，它们是来自禾谷镰刀菌的酿酒酵母spt3 和spt8 的同源物。本研究的目的是研究 Fgspt3 和 Fgspt8 在禾谷镰刀菌中的功能。缺失突变体的生长速度明显慢于野生型亲本，并且不产生分生孢子。孢子形成相关基因 FgFlbC 和 FgRen1 的表达在突变体中显着下调。这些突变体在受感染的小麦籽粒上没有表现出有性繁殖，并且对小麦的毒力降低了 90%。突变体中的色素形成也发生了很大改变。所有缺陷均通过突变体与野生型 Fgspt3 和 Fgspt8 基因的遗传互补得到恢复。总体而言，Fgspt3和Fgspt8是禾谷镰刀菌的必需基因。
Fusarium graminearum (teleomorph: Gibberella zeae), the dominant pathogen of Fusarium head blight (FHB) on wheat, can cause substantial economic losses. The Spt-Ada-Gcn5-acetyltransferase (SAGA) transcription coactivator plays multiple roles in regulating transcription because of the presence of functionally independent modules of subunits within the complex. The transcription factors spt3 and spt8 are components of the SAGA complex and they are important in yeasts and filamentous fungi including F.graminearum. In this study, we identified Fgspt3 and Fgspt8, homologs of Saccharomyces cerevisiae spt3 and spt8 from F.graminearum using the blastp program. The aim of the present study was to investigate the functions of Fgspt3 and Fgspt8 in F.graminearum. The deletion mutants grew significantly more slowly than the wild-type parent and did not produce conidia. Expression of the sporulation-related genes FgFlbC and FgRen1 were significantly down-regulated in the mutants. The mutants exhibited no sexual reproduction on infected wheat kernels and a 90% decrease in virulence on wheat. Pigment formation was also greatly altered in the mutants. All of the defects were restored by genetic complementation of the mutant with wild-type Fgspt3 and Fgspt8 genes. Overall, Fgspt3 and Fgspt8 are essential genes in F.graminearum.