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.
Highlights
Programmed cell death (PCD) is a ubiquitous process in the development of organisms, a genetic mechanism for killing cells that is both active and orderly [1]
Our research found that the gene expression levels of SAMS, ACC synthase (ACS), and ACC oxidase (ACO), the key enzymes of ET biosynthesis, increased significantly in pir1 (Figure S8), which might cause the increase in ET content
Our results show that the lesion mimic phenotype in rice mutant pir1 was caused by PCD, induced by H2 O2 accumulation
Summary
Programmed cell death (PCD) is a ubiquitous process in the development of organisms, a genetic mechanism for killing cells that is both active and orderly [1]. PCD is essential for plants to maintain their cell growth and development because PCD mechanisms are often used in the expression of tissue and organ functions, and for efficient nutrition and reproduction [3]. PCD, and the synthesized brassinosteroids induce PCD and the formation of secondary walls [4,5]. Senescence in plant leaves or petals involves much PCD, and the triggering of PCD can lead to premature senescence [6]. Rice plants with reduced OsMADs29 expression showed an abnormal persistence of nucellar tissue and the atrophy of seeds. In Arabidopsis, the peripherally located lateral root cap (LRC) cells first divide and differentiate and elongate until the LRC reaches the transition zone at the end of the meristem when the cells undergo PCD to control the location of the root cap and the size of the root cap organ [9]
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