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The small glycine‐rich RNA binding protein At GRP7 promotes floral transition in Arabidopsis thaliana
Author(s) -
Streitner Corinna,
Danisman Selahattin,
Wehrle Franziska,
Schöning Jan C.,
Alfano James R.,
Staiger Dorothee
Publication year - 2008
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.2008.03591.x
Subject(s) - arabidopsis thaliana , rna binding protein , glycine , arabidopsis , transition (genetics) , microbiology and biotechnology , rna , biology , chemistry , biochemistry , gene , amino acid , mutant
Summary The RNA binding protein At GRP7 is part of a circadian slave oscillator in Arabidopsis thaliana that negatively autoregulates its own mRNA, and affects the levels of other transcripts. Here, we identify a novel role for AtGRP7 as a flowering‐time gene. An atgrp7‐1 T‐DNA mutant flowers later than wild‐type plants under both long and short days, and independent RNA interference lines with reduced levels of At GRP7, and the closely related At GRP8 protein, are also late flowering, particularly in short photoperiods. Consistent with the retention of a photoperiodic response, the transcript encoding the key photoperiodic regulator CONSTANS oscillates with a similar pattern in atgrp7‐1 and wild‐type plants. In both the RNAi lines and in the atgrp7‐1 mutant transcript levels for the floral repressor FLC are elevated. Conversely, in transgenic plants ectopically overexpressing At GRP7, the transition to flowering is accelerated mainly in short days, with a concomitant reduction in FLC abundance. The late‐flowering phenotype of the RNAi lines is suppressed by introducing the flc‐3 loss‐of‐function mutation, suggesting that At GRP7 promotes floral transition, at least partly by downregulating FLC . Furthermore, vernalization overrides the late‐flowering phenotype. Retention of both the photoperiodic response and vernalization response are features of autonomous pathway mutants, suggesting that At GRP7 is a novel member of the autonomous pathway.