Gene mapping, genome-wide transcriptome analysis, and wgcna reveals the molecular mechanism for triggering programmed cell death in rice mutant PIR1

Abstract

Programmed cell death (PCD) is involved in plant growth and development and in resistance to biotic and abiotic stress. To understand the molecular mechanism that triggers PCD, phenotypic and physiological analysis was conducted using the first three leaves of mutant rice PCD-induced-resistance 1(pir1) and its wild-type ZJ22. The 2nd and 3rd leaves of pir1 had a lesion mimic phenotype, which was shown to be an expression of PCD induced by H2O2-accumulation. The PIR1 gene was mapped in a 498 kb-interval between the molecular markers RM3321 and RM3616 on chromosome 5, and further analysis suggested that the PCD phenotype of pir1 is controlled by a novel gene for rice PCD. By comparing the mutant with wild type rice, 1679, 6019, and 4500 differentially expressed genes (DEGs) were identified in the three leaf positions, respectively. KEGG analysis revealed that DEGs were most highly enriched in phenylpropanoid biosynthesis, alpha-linolenic acid metabolism, and brassinosteroid biosynthesis. In addition, conjoint analysis of transcriptome data by weighted gene co-expression network analysis (WGCNA) showed that the turquoise module of the 18 identified modules may be related to PCD. There are close interactions or indirect cross-regulations between the differential genes that are significantly enriched in the phenylpropanoid biosynthesis pathway and the hormone biosynthesis pathway in this module, which indicates that these genes may respond to and trigger PCD.