The Velvet Proteins VosA and VelB Play Different Roles in Conidiation, Trap Formation, and Pathogenicity in the Nematode-Trapping Fungus Arthrobotrys oligospora

Abstract

The velvet family proteins VosA and VelB are involved in growth regulation and differentiation in the model fungus Aspergillus nidulans and other filamentous fungi. In this study, the orthologs of VosA and VelB, AoVosA, and AoVelB, respectively, were characterized in the nematode-trapping fungus Arthrobotrys oligospora , which captures nematodes by producing trapping devices (traps). Deletion of the AovelB gene resulted in growth defects in different media, and the aerial hyphae from the Δ AovelB mutant lines were fewer in number and their colonies were less dense than those from the wild-type (WT) strain. The Δ AovelB mutants each displayed serious sporulation defects, and the transcripts of several sporulation-related genes (e.g., abaA , flbC , rodA , and vosA ) were significantly down-regulated compared to those from the WT strain. Furthermore, the Δ AovelB mutant strains became more sensitive to chemical reagents, including sodium dodecyl sulfate and H 2 O 2 . Importantly, the Δ AovelB mutants were unable to produce nematode-capturing traps. Similarly, extracellular proteolytic activity was also lower in the Δ AovelB mutants than in the WT strain. In contrast, the Δ AovosA mutants displayed no obvious differences from the WT strain in these phenotypic traits, whereas conidial germination was lower in the Δ AovosA mutants, which became more sensitive to heat shock stress. Our results demonstrate that the velvet protein AoVelB is essential for conidiation, trap formation, and pathogenicity in A. oligospora , while AoVosA plays a role in the regulation of conidial germination and heat shock stress.

Natural diversity in the predatory behavior facilitates the establishment of a robust model strain for nematode-trapping fungi

“…For example, a recent work has generated a strain lacking the signaling scaffold protein Soft and shown that cell-cell fusion is required for ring closure in Duddingtonia flagrans (40). In A. oligospora, ATCC24927-background trapping-deficient mutations have been isolated: adhesin protein Mad1 (41), autophagy protein Atg8 (42), mitogen-activated protein kinase Slt2 (43), pH sensor PalH (44), NADPH oxidase NoxA (45), low-affinity calcium uptake system proteins (46), Rab GTPase Rab7A (38), actin-associated protein Crn1 (47), Woronin body component Hex1 (48), malate synthase Mls (49), glycogen phosphorylase Gph1 (50), transcription factors VelB (51) and StuA (52), and microRNAprocessing protein Qde2 (53), to which we add the G-protein β-subunit Gpb1. However, a mechanistic view of how these and other molecular players are interconnected during the interaction of A. oligospora with their prey is totally lacking.…”

Natural diversity in the predatory behavior facilitates the establishment of a new robust model strain for nematode-trapping fungi

“…For example, a recent work has generated a strain lacking the signaling scaffold protein Soft and shown that cell-cell fusion is required for ring closure in Duddingtonia flagrans (41). In A. oligospora , ATCC24927-background trapping-deficient mutants have been isolated: adhesin protein Mad1 (42), autophagy protein Atg8 (43), mitogen-activated protein kinase Slt2 (44), pH sensor PalH (45), NADPH oxidase NoxA (46), low-affinity calcium uptake system proteins Fig1 and Fig2 (47), Rab GTPase Rab7A (48), actin-associated protein Crn1 (49), Woronin body component Hex1 (50), malate synthase Mls (51), glycogen phosphorylase Gph1 (52), transcription factors VelB (53) and StuA (54), and microRNA processing protein Qde2 (55), to which we add the G-protein β subunit Gpb1. However, a mechanistic view of how these and other molecular players are interconnected during the interaction of A. oligospora with their prey is totally lacking.…”

The Autophagy-Related Gene Aolatg4 Regulates Hyphal Growth, Sporulation, Autophagosome Formation, and Pathogenicity in Arthrobotrys oligospora

“…These genes play a crucial role in conidiation in filamentous fungi. For example, abaA, brlA, and wetA are the key genes encoding central regulators of conidiation in species of Aspergillus (Park and Yu, 2012), F. graminearum (Son et al, 2013), and B. bassiana (Zhang et al, 2019).…”

“…The rodA gene is required for the rodlet layer formation and hydrophobicity in conidia of A. fumigatus (Park and Yu, 2016); and gene velB is required for conidiation in A. oligospora; ΔAovelB mutants displayed serious sporulation defects (Zhang et al, 2019). Interestingly, the conidiation defect in the ΔAolatg4 mutants could be restored by glucose, suggested that it was directly related to autophagy defect.…”

“…For example, abaA , brlA , and wetA are the key genes encoding central regulators of conidiation in species of Aspergillus ( Park and Yu, 2012 ), F. graminearum ( Son et al, 2013 ), and B. bassiana ( Zhang et al, 2019 ). The rodA gene is required for the rodlet layer formation and hydrophobicity in conidia of A. fumigatus ( Park and Yu, 2016 ); and gene velB is required for conidiation in A. oligospora ; Δ AovelB mutants displayed serious sporulation defects ( Zhang et al, 2019 ). Interestingly, the conidiation defect in the Δ Aolatg4 mutants could be restored by glucose, suggested that it was directly related to autophagy defect.…”