Two Regulators of G-protein signaling (RGS) proteins FlbA1 and FlbA2 differentially regulate fumonisin B1 biosynthesis in Fusarium verticillioides

Abstract

Fumonisins are a group of mycotoxins produced by maize pathogen Fusarium verticillioides that pose health concerns to humans and animals. Yet we still lack a clear understanding of the mechanism of fumonisins regulation during pathogenesis. The heterotrimeric G protein complex, which consists of Gα, Gβ, and Gγ subunits, plays an important role in transducing signals under environmental stress. Furthermore, regulators of G-protein signaling (RGS) proteins act as negative regulators in heterotrimeric G protein signaling. Earlier studies demonstrated that Gα and Gβγ subunits are positive regulators of fumonisin B1 (FB1) biosynthesis and that two RGS genes, FvFlbA1 and FvFlbA2, were highly upregulated in Gβγ deletion mutant ΔFvgbb1. Saccharomyces cerevisiae and Aspergillus nidulans contain a single copy of FlbA, but F. verticillioides has two putative FvFlbA paralogs, FvFlbA1 and FvFlbA2. Importantly, FvFlbA2 has a negative role in FB1 regulation. In this study, we further characterized functional roles of FvFlbA1 and FvFlbA2. While ΔFvflbA1 deletion mutant exhibited no significant defects, ΔFvflbA2 and ΔFvflbA2/A1 mutants showed thinner aerial hyphal growth while promoting FB1 production. FvFlbA2 is required for proper expression of key conidia regulation genes, including putative FvBRLA, FvWETA, and FvABAA, while suppressing FUM21, FUM1, and FUM8 expression. Split luciferase assays suggest that FvFlbA paralogs interact with key heterotrimeric G protein components to impact F. verticillioides FB1 production and asexual development.

Conductance Artery Wall Layers and Their Respective Roles in the Clearance Functions

“…However, it has been suggested that regulators of G protein (RGS)/Gα i interactions promote trafficking and clearance of aged neutrophils. 155 Similarly, following exposure to phosphatidylserine and oxidative stress, aging glycated erythrocytes are engulfed by EC, thereby fostering atherothrombotic events. 156 More recently, models of extreme trajectories of vascular aging have been described, ranging from early vascular aging with premature cell senescence, to later, supernormal vascular aging characterized by delayed cell senescence.…”