GTPase Rac Regulates Conidiation, AFB1 Production and Stress Response in Pathogenic Fungus Aspergillus flavus

Toxins (Basel). 2022 Aug 24;14(9):581. doi: 10.3390/toxins14090581.

Abstract

As a member of the Rho family, Rac plays important roles in many species, including proliferation, differentiation, apoptosis, DNA damage responses, metabolism, angiogenesis, and immunosuppression. In this study, by constructing Rac-deleted mutants in Aspergillus flavus, it was found that the deletion of Rac gene led to the decline of growth and development, conidia production, AFB1 toxin synthesis, and seed infection ability of A. flavus. The deletion of Rac gene also caused the disappearance of A. flavus sclerotium, indicating that Rac is required for sclerotium formation in A. flavus. The sensitivity of Rac-deficient strains responding to cell wall stress and osmotic pressure stress increased when compared to A.flavus WT. The Western blot result showed that mitogen-activated serine/threonine-protein kinase Slt2 and mitogen-activated protein kinase Hog1 proteins were no longer phosphorylated in Rac-deficient strains of A. flavus, showing that Rac may be used as a molecular switch to control the Slt2-MAPK cascade pathway and regulate the osmotic Hog-MAPK cascade pathway in A. flavus in response to external stress. Altogether, these results indicated that Rac was involved in regulating the growth and development, conidia formation and AFB1 synthesis, and response to cell wall stress and osmotic pressure stress in A. flavus.

Keywords: A. flavus; Rac; aflatoxins; conidiation; stress response.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aflatoxins*
  • Aspergillus flavus* / metabolism
  • Fungal Proteins / metabolism
  • Fungi / metabolism
  • GTP Phosphohydrolases / metabolism
  • Mitogen-Activated Protein Kinases / metabolism
  • Mitogens
  • Serine / metabolism
  • Threonine / metabolism

Substances

  • Aflatoxins
  • Fungal Proteins
  • Mitogens
  • Threonine
  • Serine
  • Mitogen-Activated Protein Kinases
  • GTP Phosphohydrolases

Grants and funding

This research was funded by [National Natural Science Foundation of China] grant number [No. 31600118].