Natural variation of OsGATA16 contributes to differential immunity against Magnaporthe oryzae in rice
Abstract
Rice blast, caused by the fungal pathogen Magnaporthe oryzae, constitutes a critical threat to global rice production. Leveraging functional genes from germplasm resources to breed resistant varieties remains the most effective and sustainable strategy for blast control. Here, we identify a GATA transcription factor, OsGATA16, as a candidate regulator of blast resistance by genome-wide association study (GWAS) using a diverse rice germplasm panel. Functional analysis shows that OsGATA16 overexpression significantly reduces blast resistance, whereas knockout lines exhibit enhanced resistance, establishing OsGATA16 as a negative regulator of rice immunity. Transcriptome, qRT-PCR, dual-luciferase, and DAP-seq assays reveal that OsGATA16 directly represses diterpenoid biosynthetic genes. UPLC-MS/MS reveals increased accumulation of pimarane-type diterpenoids in osgata16 mutants. Further analysis indicates that the key pimarane-type diterpenoid abietic acid promotes blast resistance but compromises cold tolerance. Given the known role of OsGATA16 in cold tolerance, haplotype analysis of 137 core-collection rice accessions uncovers a trade-off between blast resistance and cold tolerance. The japonica-dominant Hap1, featuring key residues Val292 and Gly333, shows stronger transcriptional repression activity than indica Hap2, with population genetics supporting divergent allele selection. Collectively, OsGATA16 negatively regulates blast resistance by repressing pimarane-type diterpenoid biosynthesis, serving as a valuable target for breeding dual stress-resilient rice.
Fields of Study & Subjects
Plant-Microbe Interactions and Immunity
Fungal and yeast genetics research
Polysaccharides and Plant Cell Walls
Publication details
- Journal / source
- Journal of genetics and genomics/Journal of Genetics and Genomics
- Publisher
- Elsevier BV
- Volume
- 53
- Issue
- 6
- Pages
- 1045–1057
- Publication date
- 17 April 2026
- Language
- EN