MOE Key Laboratory of Biosystems Homeostasis & Protection, Institute of Microbiology, College of Life Science, Zhejiang University, Hangzhou, China.
MOE Key Laboratory of Biosystems Homeostasis & Protection, Institute of Microbiology, College of Life Science, Zhejiang University, Hangzhou, China.
Fungal Genet Biol. 2019 Oct;131:103244. doi: 10.1016/j.fgb.2019.103244. Epub 2019 Jun 19.
Metarhizium robertsii is a versatile fungus with multifactorial lifestyles, and it is an emerging fungal model for investigating the mechanisms of multiple lifestyle transitions that involve trans-kingdom host jumping. Penetration of the insect cuticle is the necessary step for the transition from saprophytic or symbiotic to pathogenic lifestyle. Previously, we found the transcription factor AFTF1 plays an important role in cuticle penetration, which is precisely regulated by Fus3-MAPK, Slt2-MAPK, and the membrane protein Mr-OPY2. Here, we identified a transcription factor (MrSt12) that directly regulated the transcription of Aftf1 by physically interacting with the cis-acting element (ATGAAACA) in the promoter of Aftf1. The deletion mutant of MrSt12 failed to form the infection structure appressorium and was thus nonpathogenic. We further found that the regulation of Aftf1 by MrSt12 was directly controlled by the Fus3-MAPK. In conclusion, we found a new signaling cascade containing Fus3-MAPK, MrSt12, and AFTF1, which regulates cuticle penetration by M. robertsii.
罗伯茨绿僵菌是一种多功能真菌,具有多因素生活方式,它是一种新兴的真菌模式生物,可用于研究涉及跨王国宿主跳跃的多种生活方式转变的机制。穿透昆虫的表皮是从腐生或共生到致病生活方式转变的必要步骤。以前,我们发现转录因子 AFTF1 在穿透昆虫表皮中起着重要作用,该过程受到 Fus3-MAPK、Slt2-MAPK 和膜蛋白 Mr-OPY2 的精确调控。在这里,我们鉴定了一个转录因子(MrSt12),它通过与 Aftf1 启动子中的顺式作用元件(ATGAAACA)物理相互作用,直接调控 Aftf1 的转录。MrSt12 的缺失突变体无法形成侵染结构附着胞,因此不具有致病性。我们进一步发现,MrSt12 对 Aftf1 的调控受 Fus3-MAPK 的直接控制。总之,我们发现了一个包含 Fus3-MAPK、MrSt12 和 AFTF1 的新信号级联,它调控罗伯茨绿僵菌穿透昆虫表皮。