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SET1/KMT2-governed histone H3K4 methylation coordinates the lifecycle in vivo and in vitro of the fungal insect pathogen Beauveria bassiana
Environmental Microbiology ( IF 4.3 ) Pub Date : 2021-08-14 , DOI: 10.1111/1462-2920.15701
Kang Ren 1 , Ya-Ni Mou 1 , Sen-Miao Tong 2 , Sheng-Hua Ying 1 , Ming-Guang Feng 1
Affiliation  

Biological control potential of insect-pathogenic fungi against pests is an overall output of various cellular processes regulated by signalling and epigenetic networks. In Beauveria bassiana, mono/di/trimethylation of histone H3 Lys 4 (H3K4me1/me2/m3) was abolished by inactivation of the histone lysine methyltransferase SET1/KMT2, leading to marked virulence loss, reductions in conidial hydrophobicity and adherence to insect cuticle, impeded proliferation in vivo, severe defects in growth and conidiation, and increased sensitivities to cell wall perturbation, H2O2 and heat shock. Such compromised phenotypes correlated well with transcriptional abolishment or repression of carbon catabolite-repressing transcription factor Cre1, classes I and II hydrophobins Hyd1 and Hyd2 required for cell hydrophobicity, key developmental regulators, and stress-responsive enzymes/proteins. Particularly, expression of cre1, which upregulates hyd4 upon activation by KMT2-mediated H3K4me3 in Metarhizium robertsii, was nearly abolished in the Δset1 mutant, leading to abolished expression of hyd1 and hyd2 as homologues of hyd4. These data suggest that the SET1-Cre1-Hyd1/2 pathway function in B. bassiana like the KMT2-Cre1-Hyd4 pathway elucidated to mediate pathogenicity in M. robertsii. Our findings unveil not only a regulatory role for the SET1-cored pathway in fungal virulence but also its novel role in mediating asexual cycle in vitro and stress responses in B. bassiana.

中文翻译:

SET1/KMT2 控制的组蛋白 H3K4 甲基化协调真菌昆虫病原体白僵菌的体内和体外生命周期

昆虫病原真菌对害虫的生物控制潜力是由信号和表观遗传网络调节的各种细胞过程的总体输出。在球孢白僵菌中,组蛋白 H3 Lys 4 (H3K4me1/me2/m3) 的单/二/三甲基化通过组蛋白赖氨酸甲基转移酶 SET1/KMT2 的失活而被消除,导致显着的毒力丧失、分生孢子疏水性降低和对昆虫角质层的粘附,体内增殖受阻,生长和分生孢子严重缺陷,对细胞壁扰动的敏感性增加,H 2 O 2和热休克。这种受损的表型与碳分解代谢物抑制转录因子 Cre1、细胞疏水性所需的 I 类和 II 类疏水蛋白 Hyd1 和 Hyd2、关键发育调节剂和应激反应酶/蛋白质的转录消除或抑制密切相关。特别是,在罗伯氏绿僵菌中被 KMT2 介导的 H3K4me3 激活后上调hyd4cre1 的表达在 Δ set1突变体中几乎被消除,导致hyd1hyd2作为hyd4 的同源物的表达被消除。这些数据表明 SET1-Cre1-Hyd1/2 通路在B 中起作用。白僵菌像KMT2-CRE1-Hyd4途径阐明调解致病性中号robertsii。我们的研究结果揭示,不仅用于真菌毒力SET1-芯途径中的调节作用,而且其在调节无性周期的新角色在体外的和应激反应巴西亚娜
更新日期:2021-09-22
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