Background: Maize rough dwarf disease (MRDD) is a devastating viral disease that results in considerable yield losses worldwide. Three major strains of virus cause MRDD, including maize rough dwarf virus in Europe, Mal de Río Cuarto virus in South America, and rice black-streaked dwarf virus in East Asia. These viral pathogens belong to the genus fijivirus in the family Reoviridae. Resistance against MRDD is a complex trait that involves a number of quantitative trait loci (QTL). The primary approach used to minimize yield losses from these viruses is to breed and deploy resistant maize hybrids. Results: Of the 50 heterogeneous inbred families (HIFs), 24 showed consistent responses to MRDD across different years and locations, in which 9 were resistant and 15 were susceptible. We performed trait-marker association analysis on the 24 HIFs and found six chromosomal regions which were putatively associated with MRDD resistance. We then conducted QTL analysis and detected a major resistance QTL, qMrdd1, on chromosome 8. By applying recombinant-derived progeny testing to self-pollinated backcrossed families, we fine-mapped the qMrdd1 locus into a 1.2-Mb region flanked by markers M103-4 and M105-3. The qMrdd1 locus acted in a recessive manner to reduce the disease-severity index (DSI) by 24.2–39.3%. The genetic effect of qMrdd1 was validated using another F₆ recombinant inbred line (RIL) population in which MRDD resistance was segregating and two genotypes at the qMrdd1 locus differed significantly in DSI values. Conclusions: The qMrdd1 locus is a major resistance QTL, acting in a recessive manner to increase maize resistance to MRDD. We mapped qMrdd1 to a 1.2-Mb region, which will enable the introgression of qMrdd1-based resistance into elite maize hybrids and reduce MRDD-related crop losses.

Sclerotinia sclerotiorum is a notorious soilborne fungal pathogen that causes white mold in a wide range of host plants, leading to globally significant yield loss in many crops. Hydrophobins (HPs) are small, secreted proteins unique to filamentous fungi, with diverse roles in fungal biology. However, their functions in S. sclerotiorum remain poorly understood. Here, we systematically investigated the roles of three HP genes, SsHP1, SsHP2, and SsHP3, through reverse genetic analyses. By analyzing their deletion mutant phenotypes, we demonstrate that class I HP (SsHP1) is specifically required for proper sclerotia development, whereas class II HPs (SsHP2 and SsHP3) are essential for compound appressoria functionality. All three HPs contribute to fungal surface hydrophobicity, cell wall integrity, and stress tolerance. Using mycelial fusion, we generated double mutants lacking both class II HPs, which exhibited more severe defects in appressoria development, virulence, cell wall integrity, and stress adaptation, indicating their partially redundant roles. SsHP2 is required for both host penetration and post-penetration virulence, whereas SsHP3 mainly affects host penetration, revealing their overlapping yet distinct contributions to pathogenic development. Although all HP mutants formed normal apothecia and asci, they released significantly fewer ascospores, suggesting that HPs are dispensable for sexual morphogenesis but crucial for the biophysical process of ascospore dispersal. Furthermore, carbohydrate analyses uncovered that these HPs affect cell wall composition, more broadly influencing stress adaptation and virulence. Taken together, our study reveals both conserved and divergent roles of HPs across fungi and highlight their multifaceted contributions to S. sclerotiorum biology, offering new perspectives for disease management.