Cold tolerance of postharvest fungal pathogens is regulated by the conserved high osmolarity glycerol (HOG) pathway

Abstract

The cold-tolerant pathogenic fungi, typically represented by the grey mold fungus Botrytis cinerea, can pose a serious threat to the quality and safety of postharvest fruits in the cold chain period. However, the mechanism of cold tolerance in fungal pathogens is rarely known and control measures are lacking. In this study, gene expression, genetic mutation, biochemistry, and cellular studies were carried out, revealing that low temperature could rapidly and continuously induce expression levels of the genes related to glycerolipid metabolism and HOG-MAPK pathway in B. cinerea. Western blot analysis showed that low temperature treatment could enhance the phosphorylation level of BcSAK1, the core component of the HOG-MAPK pathway of B. cinerea, and increase the proportion of BcSAK1 localization in nuclei. Deletion of BcSAK1 significantly inhibited fungal growth at low temperature. Addition of HOG-MAPK inhibitor could also inhibit nuclear localization of BcSAK1, and suppress the spore germination and mycelial growth of grey mold at low temperature. These results indicate that low temperature treatment can regulate the cold tolerance of B. cinerea by activating the HOG-MAPK signaling pathway. Analysis of Hog1 homologous gene deletion mutants in Fusarium asiaticum and Alternaria alternata showed that Hog1 is also essential for the cold tolerance of these two pathogenic fungi. In conclusion, this study suggests that the HOG-MAPK pathway plays a highly conserved role in regulating the cold tolerance of postharvest pathogens. Future study that aims to reveal the downstream key targets and regulatory networks of HOG-MAPK in response to cold temperature will lay foundations for the control of cold tolerant diseases of postharvest fruits.