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丝裂原活化蛋白激酶基因CfMKK1调控果生炭疽菌的生长发育和致病力
引用本文:肖宇,李河. 丝裂原活化蛋白激酶基因CfMKK1调控果生炭疽菌的生长发育和致病力[J]. 微生物学报, 2021, 61(1): 141-151
作者姓名:肖宇  李河
作者单位:南方人工林病虫害防控国家林草局重点实验室, 森林有害生物防控湖南省重点实验室, 经济林培育与保护教育部重点实验室, 中南林业科技大学, 湖南 长沙 410004
基金项目:湖南省自然科学基金(2019JJ40531);国家自然科学基金(31570641)
摘    要:【目的】由果生炭疽菌引起的炭疽病是油茶的主要病害,造成油茶产量下降。本文研究果生炭疽菌中丝裂原活化蛋白激酶CfMkk1的生物学功能,旨在为解析油茶炭疽病菌的致病机理提供依据。【方法】根据同源重组原理构建CfMKK1基因敲除载体片段,采用PEG介导法将载体导入原生质体中筛选获得突变体菌株DCfmkk1;PCR扩增果生炭疽菌含有启动子的CfMKK1基因回补片段,构建回补载体pYF11::CfMKK1;采用PEG介导法把回补载体转化至突变体的原生质体中,荧光筛选回补菌株ΔCfmkk1-C。测定野生型菌株、突变体菌株DCfmkk1及基因回补菌株ΔCfmkk1-C在营养生长、附着胞形成、胁迫应答和致病力等生物学表型。【结果】与野生型和回补菌株相比,CfMKK1基因敲除突变体ΔCfmkk1菌丝生长速率明显减缓;在含刚果红的PDA培养基上菌丝生长受到明显抑制,无法穿透玻璃纸,丧失了侵染寄主的能力;而且无法形成附着胞。【结论】研究结果表明CfMKK1基因参与调控油茶果生炭疽菌的生长发育、附着胞形成、致病力以及响应外界胁迫过程。

关 键 词:油茶  果生炭疽菌  丝裂原活化蛋白激酶  CfMkk1  致病力
收稿时间:2020-03-07
修稿时间:2020-04-28

MAPKK-encoding gene CfMKK1 in Colletotrichum fructicola is required for its growth and pathogenicity
Yu Xiao,He Li. MAPKK-encoding gene CfMKK1 in Colletotrichum fructicola is required for its growth and pathogenicity[J]. Acta microbiologica Sinica, 2021, 61(1): 141-151
Authors:Yu Xiao  He Li
Affiliation:Key Laboratory of National Forestry and Grassland Administration for Control of Diseases and Pests of South Plantation, Hunan Provincial Key Laboratory for Control of Forest Diseases and Pests, Key Laboratory for Non-Wood Forest Cultivation and Conservation of Ministry of Education, Central South University of Forestry and Technology, Changsha 410004, Hunan Province, China
Abstract:[Objective]Colletotrichum fructicola is an important pathogen that results in yield loss of Camellia oleifera.We studied the functions of the mitogen-activated protein kinase gene CfMKK1 in C.fructicola for analyzing the pathogenic mechanism of oil-tea tree anthracnose.[Methods]The homologous recombination method was used to construct the CfMKK1 gene-deleted fragment,which was transformed into the protoplasts generated by using PEG-mediated method to obtain the mutant strainΔCfmkk1.The PCR-amplified CfMKK1 gene-containing complement of the promoter of C.fructicola was taken to construct a complementary vector pYF11::CfMKK1,then the complementary vector was transformed into the mutant protoplasts by using PEG-mediated method to screen the complementary strainΔCfmkk1-C.The biological phenotypes of the wild-type strain CFLH16,the mutant strainΔCfmkk1,and the complementary strainΔCfmkk1-C were measured in vegetative growth,appressorium formation,stress response and pathogenicity.[Results]The mycelial growth rate ofΔCfmkk1 was significant slowed down compared to the wild-type strain CFLH16 and the complementary strainΔCfmkk1-C,more sensitive to Congo red,lost the ability to infect hosts and was unable to form appressoria.[Conclusion]CfMkk1 is involved in regulating the growth,response to external stress and appressorium formation of C.fructicola,affecting the pathogenicity.
Keywords:Camellia oleifera  Colletotrichum fructicola  mitogen-activated protein kinases  CfMkk1  pathogenicity
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