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Arrestins are a family of scaffold proteins that play a crucial role in regulating numerous cellular processes, such as GPCR signaling. The  Arthrobotrys oligospora  arrestin family contains 12 members, which have highly conserved N-terminal and C-terminal domains. In the presence of ammonia,  A. oligospora  can change its lifestyle from saprotrophic to carnivorous. During this transition, the expression pattern of arrestin-coding ( AoArc ) genes was markedly upregulated. Therefore, we disrupted seven  AoArc  genes from  A. oligospora  to identify their functions. Although individual arrestin mutant strains display similar pathogenesis, phenotypes, and stress resistance, the fundamental data on the roles of  AoArc  genes in  A. oligospora  are obtained in this study. Membrane endocytosis in  AoArc  mutants was significantly reduced. Meanwhile, the capacity of trap device formation against nematodes and ammonia was impaired due to  AoArc  deletions. We also found that  AoArc  genes could regulate conidial phenotypes, cell nuclear distribution, pH response, and stress resistance. Results of qRT-PCR assays revealed that sporulation-regulated genes were affected after the deletion of  AoArc  genes. In particular, among the 12 arrestins,  AoArc2  mediates pH signaling in the fungus  A. oligospora . Notably, combined with the classical paradigm of arrestin–GPCR signal transduction, we suggest that arrestin-regulated trap formation in  A. oligospora  may be directly linked to the receptor endocytosis pathway.

Arrestin-Coding Genes Regulate Endocytosis, Sporulation, Pathogenicity, and Stress Resistance in Arthrobotrys oligospora