Calcium-Associated Cellular Integrity and MAPK/cAMP Signaling Are Associated with Low-Temperature Acclimation in Schizophyllum commune 20R-7-F01

Abstract

Temperature is a critical environmental factor affecting fungal growth, morphogenesis, and reproduction. Schizophyllum commune, a model basidiomycete fungus, exhibits remarkable developmental plasticity under environmental fluctuations; however, the mechanisms underlying its adaptation to low-temperature conditions remain poorly understood. In this study, we show that low-temperature stress inhibited mycelial growth, delayed fruiting body development and basidiospore germination, and promoted chitin accumulation and chitin synthase genes (CHS) expression in S. commune 20R-7-F01. Low-temperature exposure triggered transient oxidative stress, followed by restoration of antioxidant capacity during acclimation. Mechanistically, mitogen-activated protein kinase (MAPK) inhibition impaired mycelial growth, whereas 3′-5′-cyclic adenosine monophosphate (cAMP) content increased under low-temperature stress, suggesting the involvement of cAMP signaling in the low-temperature response. Moreover, low-temperature exposure was associated with increased mycelial calcium (Ca2+) content, and Ca2+ chelation was accompanied by impaired cell membrane integrity and altered cell wall ultrastructure. Collectively, our findings suggest that the adaptation of S. commune 20R-7-F01 to low temperature is associated with Ca2+ content, cell integrity, antioxidant defense, MAPK, and cAMP. These results provide new insights into the molecular basis of fungal low-temperature acclimation.