Poster: Salinity

Abs # 163: Analysis of gene expression profile in vegetative tissue of Arabidopsis salt overly sensitive mutants, sos2-1 and sos3-1

Presenter:	Kamei, Ayako , kamei@rtc.riken.go.jp
Authors	Kamei, Ayako  (A)   Umezawa, Taishi  (A)   Seki, Motoaki  (B) (A)  Zhu, Jian-Kang  (C)   Shinozaki, Kazuo  (A) (B)
Affiliations:	(A): RIKEN, Laboratory of Plant Molecular Biology (B): RIKEN, Genomic Sciences Center (C): University of Arizona, Department of Plant Sceinces

Soil salinity is one of the severe abiotic stresses for plant growth and agriculture. Recently, several salt overly sensitive (sos) mutants have been isolated in Arabidopsis. SOS2 and SOS3 are the components of SOS signaling pathway, and encode protein kinase and a myristolated EF-hand calcium binding protein, respectively. To determine the target genes of SOS signaling pathway, we used cDNA microarray and detected genes that are differentially expressed between wild type and sos mutants (sos2-1 and sos3-1). The expression of DREB2A, RD29A and RD17 was high-salinity-stress-inducible in sos2-1 and sos3-1 mutants as well as in wild type. Also, the expression level of RD22BP1/AtMYC2 mRNA in sos mutants was similar to that of wild type. These results indicate that SOS signaling pathway is independent of DREB/CBF and MYC/MYB pathways. Several genes were expressed differentially in wild type and sos mutants. The expression level of At3g59930, At1g13990, and At3g46230 was reduced in sos2-1 and sos3-1. The expression of one transcription factor gene that belongs to WRKY family was lower in sos mutants after salt treatment for 1h. However, this gene was highly induced in sos2-1 mutant after 10h of salt treatment. In addition, a gene for At1g26380/FAD-linked oxidoreductase family protein showed similar expression pattern to this WRKY-type transcription factor. These results indicate that the gene expression of At3g59930, At1g13990, At1g26380, At3g46230, and a WRKY-type transcription factor is regulated by SOS signaling pathway under salt stress condition.