Fus3/Kss1‐MAP kinase and Ste12‐like control distinct biocontrol‐traits besides regulation of insect cuticle penetration via phosphorylation cascade in a filamentous fungal pathogen

Abstract

BACKGROUND: 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.RESULTS: 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.CONCLUSION: 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.

A network of transcription factors in complex with a regulating cell cycle cyclin orchestrates fungal oxidative stress responses

“…Despite this increase, however, one consequence of Msg5 upregulation in the ΔBbOsrR2 strain may be dampening of the Fus3/Kss1 MAP kinase signaling which would result in decreased virulence and reduced conidial production, phenotypes seen for the ΔBbOsrR2 strain. Disruption of the Fus3/Kss1 MAP kinase gene, Bbmpk1, in B. bassiana also results in decreased virulence, but unlike the ΔBbOsrR2 mutant, increased growth is also seen [54,55]. Expression of Cdc28, involved in cell cycle progression, acting as downstream factor of the Fus3/Kss1 MAP and Hog1 MAP kinase pathways [47,56,57], was also significantly upregulated in the ΔBbOsrR2 strain, potentially helping account for the conidiation and germination defects seen.…”

A transcription factor-mediated regulatory network controls fungal pathogen colonization of insect body cavities

“…The Fus3-MAP kinase-mediated cascades have been shown to control the morphological transition of fungal pathogens, such as the infection structure (appressorium) formation or function, development of infective hyphae, dimorphism, and sporulation, despite the difference in fungal species ( 10 , 40 ). The pathway also mediates adaptation to oxidative stress derived from insect immune response-generated reactive oxygen species in some fungal species ( 41 ). The Hog1-MAP kinase pathway controls osmotic, oxidative, and thermal stress responses, as well as sporulation, viability, and fungal virulence ( 33 ), and has been implicated in mediating adaptation to low oxygen niches in fungal-infected insect hemocoel ( 28 ).…”

A fungal pathogen secretes a cell wall‐associated β‐N‐acetylhexosaminidase that is co‐expressed with chitinases to contribute to infection of insects

“…62 Msn2 controls cell wall integrity-included multi-stress responses, growth, conidiation and virulence, and negatively regulates protease, lipase and oosporein production. 63,64 Ste12 regulates growth, conidiation and cuticle penetration, 65 and a C repressor CreA plays a much broader role in fungal development, cell homeostasis, cuticle penetration and virulence in the fungal pathogen. 44 These results suggested that those chitinase genes and BbHex1 might be commonly or cooperatively regulated by these transcription factors, contributing cell wall (chitin) biosynthesis, cuticle penetration and virulence, as well as evasion of immune response.…”