The NDT80-like transcription factor CmNdt80a affects the conidial formation and germination, mycoparasitism, and cell wall integrity of Coniothyrium minitans.

Abstract

NDT80, a known transcriptional factor, regulates various targets, including regulation of meiosis, stress responses, filamentous growth, sexual development, biofilm formation, drug resistance, and virulence. But the numbers and roles of Ndt80-like genes in different fungi are highly variable. This study aims to address the numbers and functions of Ndt80-like genes in Coniothyrium minitans, a well-known biocontrol agent against Sclerotinia diseases. Here, two genes (CmNdt80a and CmNdt80b) encoding NDT80-like proteins were obtained by searching the genomic sequence of C. minitans. RT-PCR analysis showed that both CmNdt80 genes were constitutively expressed in C. minitans from the hyphal growth stage (48 hpi) to the pycnidial maturation stage (120 hpi). The roles of CmNdt80a and CmNdt80b in C. minitans were verified through gene knockout and complementation experiments. The results showed that the ΔCmNdt80a mutants exhibited a lighter colour and normal growth rate on potato dextrose agar plates. The ability of the ΔCmNdt80a mutants to produce conidia and parasitize the colony and sclerotia of Sclerotinia sclerotiorum was markedly diminished compared with the wild-type strain and complemented strain. Interestingly, the ΔCmNdt80a mutant showed less sensitivity to cell wall stressors and cell wall-degrading enzymes, and had thicker cell walls than the wild-type strain and complemented strain. However, no phenotypic consequences were discovered for the deletion of CmNdt80b. Two Ndt80-like genes, CmNdt80a and CmNdt80b, were present in C. minitans. CmNdt80a, but not CmNdt80b, plays a crucial role in conidiogenesis, mycoparasitism, and cell wall integrity. Understanding the mechanisms that regulate the conidiation and parasitism of C. minitans could help us to more efficiently utilize this biological control agent and advance our knowledge of fungal biology.