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Environmental stresses influence the growth of plants and the productivity of crops. Salinity is one of the most important abiotic stresses for agricultural crops. Programmed cell death (PCD) is induced by a variety of biotic and abiotic stresses in plants, including high salinity treatment. OsPDCD5, an ortholog of the mammalian-programmed cell death 5 gene, is up-regulated under low temperature and salt treatments in rice ( Oryza sativa). In this study, transgenic rice that constitutively expressed antisense- OsPDCD5 increased salt stress tolerance in unique ways by inhibiting PCD pathways and regulating specific groups of stress-related genes. Real-time quantitative PCR analysis showed that PCD pathways were inhibited under both normal conditions and salt stress in transgenic rice. Using transcript microarray analysis, 38 stress-related genes regulated in transgenic rice were identified, which appeared to render the transgenic rice adapted for salt stress conditions. Our results suggested that PCD pathways were inhibited and salt stress signaling pathways were regulated in transgenic rice even under normal growth conditions without stress. PCD was further inhibited and these stress-related genes were further regulated to increase tolerance to high salinity under salt stress conditions, thereby leading to build-up of stress protection mechanisms in transgenic rice. [ABSTRACT FROM AUTHOR]

OsPDCD5 is the rice ( Oryza sativa L.) homolog of PDCD5, a gene involved in programmed cell death (PCD) regulation and highly conserved over time. PDCD5 overexpression in tumor cells enhances apoptosis triggered by growth factor or serum deprivation. In our previous research, constitutive OsPDCD5 overexpression induces early death in transgenic plants. In this study, an inducible OsPDCD5 expression strategy was employed to systematically study the role of OsPDCD5 in rice. With this system, OsPDCD5 was found to be capable of independently inducing cell death in three-leaf stage and older seedlings. These altered plants exhibited lesion mimic phenotype, abnormal leaf morphology, DNA fragmentation, hydrogen peroxide production, and mitochondrial distortion. In nature, RNA hybridization in situ has shown that OsPDCD5 expression was predominantly localized to the tapetal layer where PCD occurred. Transcript microarray analyses here revealed that many PCD-related genes were involved. These data, taken together, indicated that OsPDCD5-induced cell death is a kind of PCD. Nevertheless, OsPDCD5 failed to induce any visible morphological phenotypes in two-leaf stage and younger seedlings. Transcript microarray analyses and quantitative real-time polymerase chain reaction showed that the Bax inhibitor-1 (BI-1) mRNA concentration and the activity of an ubiquitin gene were specifically changed. Endogenous OsPDCD5 upregulation, induced by ectopic OsPDCD5 expression in three-leaf stage seedlings, was also absent in two-leaf stage seedlings, suggesting strongly that young seedlings could inhibit PCD at some level. [ABSTRACT FROM AUTHOR]