Colletotrichum gloeosporioides is a hemibiotrophic ascomycetous fungus that causes anthracnose in many plants worldwide. During infections, C. gloeosporioides produces an appressorium in response to various plant surface signals. However, the mechanism mediating host surface signal recognition remains unclear. In this study, C. gloeosporioides ΔCgMsb2 and ΔCgMsb2Sho1 mutants lacking hypothetical sensors of plant surface signals were examined. The mutations in ΔCgMsb2 and ΔCgMsb2Sho1 adversely affected conidial size and sporulation, while also inhibiting growth. Significant transcriptional changes were detected for nearly 19% and 26% of the genes in ΔCgMsb2 and ΔCgMsb2Sho1, respectively. The lack of these plasma membrane receptors altered the expression of specific genes, especially those encoding hydrolases, ABC transporters, and mitogen-activated protein kinases (MAPKs). The encoded MAPKs participate in the signal transduction of ERK and JNK signaling pathways, activate downstream signals, and contribute to metabolic regulation. Our data demonstrate that the C. gloeosporioides membrane proteins Msb2 and Sho1 affect gene regulation, thereby influencing conidial growth, metabolism, and development. These findings provide new insights into the regulation of C. gloeosporioides's development and infection of plant hosts.
Keywords: Colletotrichum gloeosporioides; membrane receptor; pathogenicity; signal recognition and transduction.