Academy of Agricultural Sciences, Biotechnology Research Center, Southwest University, Chongqing, P. R. China.
Pest Manag Sci. 2023 Jul;79(7):2611-2624. doi: 10.1002/ps.7446. Epub 2023 Mar 18.
Homolog of the yeast Fus3/Kss1 mitogen-activated protein kinase (MAPK) pathway and its target transcription factor, Ste12-like, are involved in penetration of host cuticle/pathogenicity in many ascomycete pathogens. However, details of their interaction during fungal infection, as well as their controlled other virulence-associated traits, are unclear.
Ste12-like (BbSte12) and Fus3/Kss1 MAPK homolog (Bbmpk1) interacted in nucleus, and phosphorylation of BbSte12 by Bbmpk1 was essential for penetration of insect cuticle in an insect fungal pathogen, Beauveria bassiana. However, some distinct biocontrol-traits were found to be mediated by Ste12 and Bbmpk1. In contrast to ΔBbmpk1 colony that grew more rapid than wild-type strain, inactivation of BbSte12 resulted in the opposite phenotype, which was consistent with their different proliferation rates in insect hemocoel after direct injection of conidia bypass the cuticle. Reduced conidial yield with decreased hydrophobicity was examined in both mutants, however they displayed distinct conidiogenesis, accompanying with differently altered cell cycle, distinct hyphal branching and septum formation. Moreover, ΔBbmpk1 showed increased tolerance to oxidative agent, whereas the opposite phenotype was seen for ΔBbSte12 strain. RNA sequencing analysis revealed that Bbmpk1 controlled 356 genes depending on BbSte12 during cuticle penetration, but 1077 and 584 genes were independently controlled by Bbmpk1 and BbSte12.
BbSte12 and Bbmpk1 separately participate in additional pathways for control of conidiation, growth and hyphal differentiation, as well as oxidative stress response besides regulating cuticle penetration via phosphorylation cascade. © 2023 Society of Chemical Industry.
酵母 Fus3/Kss1 丝裂原激活蛋白激酶(MAPK)途径及其靶转录因子 Ste12 样蛋白参与许多子囊菌病原体穿透宿主表皮/致病性。然而,它们在真菌感染过程中的相互作用细节,以及它们控制的其他与毒力相关的特征尚不清楚。
Ste12 样蛋白(BbSte12)和 Fus3/Kss1 MAPK 同源物(Bbmpk1)在细胞核中相互作用,并且 Bbmpk1 对 BbSte12 的磷酸化对于昆虫病原白僵菌穿透昆虫表皮是必不可少的。然而,发现一些不同的生防性状是由 Ste12 和 Bbmpk1 介导的。与生长速度快于野生型菌株的ΔBbmpk1 菌落相反,BbSte12 的失活导致相反的表型,这与它们在直接注射孢子绕过表皮后在昆虫血腔中的不同增殖率一致。在这两种突变体中都检查了产孢量减少和疏水性降低,但是它们表现出不同的分生孢子发生,伴随着不同的细胞周期改变、不同的菌丝分支和隔膜形成。此外,ΔBbmpk1 对氧化应激剂的耐受性增加,而ΔBbSte12 菌株则表现出相反的表型。RNA 测序分析显示,Bbmpk1 在穿透表皮过程中依赖于 BbSte12 控制 356 个基因,但 1077 个和 584 个基因分别由 Bbmpk1 和 BbSte12 独立控制。
除了通过磷酸化级联调节表皮穿透外,BbSte12 和 Bbmpk1 还分别参与了控制分生孢子形成、生长和菌丝分化以及氧化应激反应的其他途径。 © 2023 化学工业协会。