Project description:Salt stress is one of the most severe environmental conditions which cause huge losses in crop production worldwide. We identified an essential regulator of salt stress RSA3 and used the Affymetrix whole-genome arrays to study the effect of rsa3-1 mutation on global gene expression under salt stress. A set of genes differentially expressed in rsa3-1 under salt stress are identified.
Project description:Salt stress is one of the most severe environmental conditions which cause huge losses in crop production worldwide. We identified a novel calcium-binding protein and used the Affymetrix whole-genome arrays to define downstream targets of this important protein. We used the microarrays to reveal the effect of rsa1-1 mutation on global gene expression in response to 120 mM Nacl for 0 or 24 h. A set of genes differentially expressed in rsa1-1 with or without salt stress are identified.
Project description:A better understanding of the mechanisms for plant in response to abiotic stresses is key for the improvement of plant to resistant to the stresses. Much has been known for the regulation of gene expression in response to salt stress at transcriptional level, however, little is known at posttranscriptional level for this response. Recently, we identified that SKIP is a component of spliceosome and is necessary for the regulation of alternative splicing and mRNA maturation of clock genes. In this study, we observed that skip-1 is hypersensitive to salt stress. SKIP is necessary for the alternative splicing and mRNA maturation of several salt tolerance genes, e.g. NHX1, CBL1, P5CS1, RCI2A, and PAT10. Genome-wide analysis reveals that SKIP mediates the alternative splicing of many genes under salt stress condition, most of the new alternative splicing events in skip-1 is intron retention, which leads to the premature termination codon in their mRNA. SKIP also controls the alternative splicing by modulating the recognition or cleavage of 5' and 3' splice donor and acceptor sites under salt stress condition. Therefore, this study addresses a fundamental question on how the mRNA splicing machinery contributes to salt response at a posttranscriptional level.
