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Salt tolerance (STO), a stress‐related protein, has a major role in light signalling
Author(s) -
Indorf Martin,
Cordero Julio,
Neuhaus Gunther,
RodríguezFranco Marta
Publication year - 2007
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/j.1365-313x.2007.03162.x
Subject(s) - photomorphogenesis , arabidopsis , biology , etiolation , microbiology and biotechnology , mutant , phytochrome , transcription factor , rna interference , transcription (linguistics) , gene , repressor lexa , genetics , botany , repressor , biochemistry , rna , red light , linguistics , philosophy , enzyme
Summary The salt tolerance protein (STO) of Arabidopsis was identified as a protein conferring salt tolerance to yeast cells. In order to uncover its function, we isolated an STO T‐DNA insertion line and generated RNAi and overexpressor Arabidopsis plants. Here we present data on the hypocotyl growth of these lines indicating that STO acts as a negative regulator in phytochrome and blue‐light signalling. Transcription analysis of STO uncovered a light and circadian dependent regulation of gene expression, and analysis of light‐regulated genes revealed that STO is involved in the regulation of CHS expression during de‐etiolation. In addition, we could show that CONSTITUTIVE PHOTOMORPHOGENESIS 1 (COP1) represses the transcription of STO and contributes to the destabilization of the protein in etiolated seedlings. Microscopic analysis revealed that the STO:eGFP fusion protein is located in the nucleus, accumulates in a light‐dependent manner, and, in transient transformation assays in onion epidermal cells, co‐localizes with COP1 in nuclear and cytoplasmic aggregations. However, the analysis of gain‐ and loss‐of‐function STO mutants in the cop1‐4 background points towards a COP1‐independent role during photomorphogenesis.