禾谷镰刀菌GIL1基因和FGK3基因调控隔膜形态发生、DON毒素产生的作用机制

Fusarium head blight caused by Fusarium graminearum not only leads to extensive reduction of crop, but also bring health hazard to humans and livestock by mycotoxin it secrets. However, due to lack of effective resistance gene and clear pathogenic mechanism, wheat scab is continuously causing serious damage. Therefore, screening for and characterizing pathogenicity-related genes, analyzing the pathogenic mechanism, seeking new strategies for prevention and cure the disease are of momentous significance. Previous studies showed that deletion mutants of FGK3 or GIL1 gene were defective in pathogenicity, DON production and septa morphogenesis. This project will detailedly study the role of GIL1 and FGK3 genes in septa morphogenesis and DON production, on the basis of previous studies. The septal defects of the mutants, the interaction and co-localization between Gil1 or Fgk3 and septins, the defects of toxisome, as well as the expression of toxin-related genes will be studied. The results will demonstrated the regulatory role of GIL1 and FGK3 genes in septa morphogenesis and DON production. The relationship between septa morphology and pathogenicity will also be preliminarily studied, which will help to lay a foundation for understanding the pathogenic mechanism of Fusarium graminearum.

禾谷镰刀菌引起的赤霉病不仅导致大规模粮食减产，并且使人畜健康面临真菌毒素的危害。 但是，由于缺乏有效的抗病基因及抗病机制不明确，赤霉病对小麦、玉米等农作物不断产生严重的危害。因此，筛选和鉴定致病基因、加快解析致病机理、寻找新的防治策略具有重要的现实意义。本课题组的前期研究发现，GIL1和FGK3基因的缺失使禾谷镰刀菌的致病性及DON毒素产量显著下降，隔膜形态产生异常。本项目拟在前期的研究基础上，开展对GIL1基因和FGK3基因在隔膜形态发生及DON毒素产生过程中作用机制的研究，从突变体的隔膜缺陷、Gil1和Fgk3蛋白与隔膜蛋白的相互作用关系、产毒小体缺陷、产毒相关基因表达等几方面进行分析。研究结果将揭示GIL1基因和FGK3基因在隔膜形态发生以及DON毒素产生过程中的协同调控机制，初步揭示隔膜形态与致病性的关系，为全面明确禾谷镰刀菌致病机理提供理论依据。

禾谷镰刀菌是引起小麦和玉米赤霉病的主要病原，常造成严重的产量损失，染病籽粒中还含有病原菌产生的多种毒素，对人和牲畜的健康造成严重威胁。本项目对GIL1基因和FGK3基因在禾谷镰刀菌致病过程中的功能进行研究。结果表明gil1突变体在细胞形态、子囊发育等方面存在缺陷。fgk3gil1双敲突变体在菌体生长发育、有性生殖及对小麦的致病力等方面存在缺陷。此外，我们在对gsk3突变体的自发突变体进行基因组测序过程中，发现有4个角变子在几丁质合成酶基因CHS5上发生了提前终止突变。进一步的研究表明gsk3chs5双敲突变体只能部分恢复由FGK3缺失所造成的生长缺陷，而在有性生殖和致病性方面依然存在严重缺陷，CHS5基因在gsk3缺失突变体中的表达量较野生型上调约3倍，说明GSK3基因的存在抑制了几丁质合成酶基因CHS5的表达。本项目阐明了致病基因GSK3、GIL1和CHS5在禾谷镰刀菌生长发育及致病过程中的功能，研究结果为解析禾谷镰刀菌致病的分子机理提供重要的理论依据，为发掘更有效的病害控制策略、降低病原菌的危害奠定了应用基础。