Transcription factor StMAT1-2 regulates the pheromone receptor StSte2 to affect the growth, reproduction, and pathogenicity of Setosphaeria turcica
Northern corn leaf blight is a major disease in maize production in recent years, and its pathogen is Setosphaeria turcica, which belongs to the heterozygous mating-type fungi. Based on the mating-type locus genes (MAT) contained in the genome, namely StMAT1-1 and StMAT1-2, the S. turcica is divided into three mating type strains: A, a, and Aa. This study monitored the mating types of S. turcica in the primary corn-producing regions of China over a span of 13 consecutive years (from 2011 to 2023). It was observed that the a mating type was the dominant mating type in the field. In laboratory conditions, artificially inducing and constructing F1 generation populations also revealed that the a mating type strain exhibited high spore production, a rapid growth rate, strong pathogenicity, and better adaptability. The StMAT1-1 and StMAT1-2 are both essential for asexual reproduction, sexual reproduction, and the pathogenicity of the pathogen. However, the StMAT1-2 has a more significant impact. As transcription factors, the MAT genes influence metabolic activities, enzyme functions, and membrane components. Further evidence indicates that StMAT1-1 and StMAT1-2 directly regulate the expression of pheromone receptor genes. Specifically, StMAT1-1 regulates the expression of StSte3, while StMAT1-2 regulates the expression of StSte2. Knockdown of StSte2 and exogenous pheromone addition further demonstrated that the pheromone receptor was involved in the sexual reproduction of the pathogen and also affected the expression of genes downstream of the MAPK pheromone pathway. In conclusion, the research results have analyzed the reasons for the widespread existence of strain a mating type. It has elucidated that StMAT1-2 affects the MAPK signaling pathway by regulating the pheromone receptor StSte2, which results in the obstruction of pathogen development and reproduction, thereby reducing pathogenicity.