The MAPK kinase BcMkk1 suppresses oxalic acid biosynthesis via impeding phosphorylation of BcRim15 by BcSch9 in Botrytis cinerea

Abstract

The mitogen-activated protein kinase (MAPK) cassette of the cell wall integrity (CWI) pathway is primarily responsible for orchestrating changes of cell wall. However, functions of this cassette in other cellular processes are not well understood. Here, we found that the Botrytis cinerea mutant of MAPK kinase (BcMkk1) displays more serious defects in mycelial growth, conidiation, responses to cell wall and oxidative stresses, but possesses less reduced virulence than the mutants of its upstream (BcBck1) and downstream (BcBmp3) kinases. Interestingly, BcMkk1, but not BcBck1 and BcBmp3, negatively regulates production of oxalic acid (OA) and activity of extracellular hydrolases (EHs) that are proposed to be virulence factors of B. cinerea. Moreover, we obtained evidence that BcMkk1 negatively controls OA production via impeding phosphorylation of the Per-Arnt-Sim (PAS) kinase BcRim15 by the Ser/Thr kinase BcSch9. In addition, the fungal Pro40 homolog BcPro40 was found to interact simultaneously with three MAPKs, implying that BcPro40 is a scaffold protein of the CWI pathway in B. cinerea. Taken together, results of this study reveal that BcMkk1 negatively modulates virulence via suppressing OA biosynthesis in B. cinerea, which provides novel insight into conserved and species-specific functions of the MAPK kinase in fungi.

Comparative quantitative proteomics of osmotic signal transduction mutants in Botrytis cinerea explain mutant phenotypes and highlight interaction with cAMP and Ca2+ signalling pathways

“…Among the SM pathways detected, one can mention those of the toxins botrydial and botcinic acid, both involved in B. cinerea virulence [55,56], but also oxalic acid. Although not essential to B. cinerea virulence, this organic acid contributes to lesion expansion through acidification essential for lytic enzymes [66,70,71]. The strong reduction (100x) of oxaloacetate hydrolase (OAH) in the ∆sak1 mutant may contribute to its reduced aggressiveness.…”

A Single Nucleotide Mutation in Adenylate Cyclase Affects Vegetative Growth, Sclerotial Formation and Virulence of Botrytis cinerea

“…Besides growth defects associated with the bac point mutation, we explored the relationship of the S1407 site in BAC to cell wall integrity, a parameter that is closely related to fungal development and virulence [15]. The sensitivity of point mutants to cell wall-damaging agents and degrading enzymes was determined ( Figure 6).…”

“…The MAPK signaling pathway transmits signals through the sequential activation of three interacting protein kinases. In B. cinerea, it has been reported that three MAPKs, Bmp1, Bmp3, and Bcsak1, are involved in growth and pathogenicity [13][14][15][16]. Furthermore, the filamentous fungi have evolved light signaling pathways which regulate growth, development and metabolism and allow them to adapt to changes in the environment.…”

Comparative proteomics of osmotic signal transduction mutants inBotrytis cinereaexplain loss of pathogenicity phenotypes and highlight interaction with cAMP and Ca2+signalling pathways

“…Among the SM pathways detected, one can mention those of the toxins botrydial and botcinic acid, both involved in B. cinerea virulence (Dalmais et al, 2011;Rossi et al, 2011), but also oxalic acid. Although not essential to B. cinerea virulence, this organic acid contributes to lesion expansion through acidification essential for lytic enzymes (Kunz et al, 2006;Müller et al, 2018;Yin et al, 2018). The strong reduction (100x) of oxaloacetate hydrolase (OAH) in the ∆sak1 mutant may certainly contribute to its reduced aggressiveness.…”

“…The finding that OAH production is under Sak1 control is interesting as well. A recent publication revealed that OAH expression and the production of oxalate is controlled by the MAPKK of the CWI pathway via the protein kinase Sch9 without involvement of the MAPK Bmp3 (Yin et al, 2018). It would now be interesting to analyse the respective roles of Sch9 and Sak1 in addition to their connection with respect to the regulation of OAH production.…”