Interactions of MAP Kinases, Histidine Kinase and YAP1 in the Citrus Fungal Pathogen Alternaria Alternate

The tangerine pathotype of Alternaria alternata utilizes the AaFUS3, AaHOG1 and AaSLT2 MAP kinase-mediated signaling pathways, in conjunction with the two-component histidine kinase (AaHSK1) and the AaAP1 transcription regulator, for stress response, development and pathogenesis to citrus. This study reveals possible interactions among these pathways at transcriptional and post-translational levels. Systemic loss-of-function genetics in A. alternata revealed that both AaFUS3 and AaSLT2 are required for conidia formation. AaSLT2 mutant is hypersensitive to cell wall-degrading enzymes, yet AaHSK1 mutant is less sensitive and AaHOG1 mutant is highly resistant to them. Accumulation of the AaHOG1 gene transcript is up-regulated considerably in the AaSLT2 mutant and only slightly in the AaFUS3 mutant. AaSLT2 positively regulates AaFUS3 expression and vice versa. AaSLT2 also promotes AaAP1 expression, whereas AaAP1 inhibits AaSLT2 expression. Furthermore, phosphorylation of AaHOG1 or AaFUS3 protein is affected when other genes are inactivated, indicating a functional antagonism or synergism among these signal transduction pathways. Interestingly, signaling transduction pathways-mediated by AaAP1, AaHSK1, AaHOG1, AaSLT2, and AaFUS3 play a critical and non-redundant role for resistance to 2-chloro-5-hydroxypyridine or 2,3,5-triiodobenzoic acid, likely via regulation of common membrane transporters, in A. alternata.