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The Arabidopsis SRR1 gene mediates phyB signaling and is required for normal circadian clock function

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UNSPECIFIED. (2003) The Arabidopsis SRR1 gene mediates phyB signaling and is required for normal circadian clock function. GENES & DEVELOPMENT, 17 (2). pp. 256-268. ISSN 0890-9369

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Official URL: http://dx.doi.org/10.1101/gad.244103

Abstract

Plants possess several photoreceptors to sense the light environment. In Arabidopsis cryptochromes and phytochromes play roles in photomorphogenesis and in the light input pathways that synchronize the circadian clock with the external world. We have identified SRR1 (sensitivity to red light reduced), a gene that plays an important role in phytochrome B (phyB)-mediated light signaling. The recessive srr1 null allele and phyB mutants display a number of similar phenotypes indicating that SRR1 is required for normal phyB signaling. Genetic analysis suggests that SRR1 works both in the phyB pathway but also independently of phyB. srr1 mutants are affected in multiple outputs of the circadian clock in continuous light conditions, including leaf movement and expression of the clock components, CCA1 and TOC1. Clock-regulated gene expression is also impaired during day-night cycles and in constant darkness. The circadian phenotypes of srr1 mutants in all three conditions suggest that SRR1 activity is required for normal oscillator function. The SRR1 gene was identified and shown to code for a protein conserved in numerous eukaryotes including mammals and flies, implicating a conserved role for this protein in both the animal and plant kingdoms.

Item Type: Journal Article
Subjects: Q Science > QH Natural history > QH301 Biology
Q Science > QH Natural history > QH426 Genetics
Journal or Publication Title: GENES & DEVELOPMENT
Publisher: COLD SPRING HARBOR LAB PRESS
ISSN: 0890-9369
Date: 15 January 2003
Volume: 17
Number: 2
Number of Pages: 13
Page Range: pp. 256-268
Identification Number: 10.1101/gad.244103
Publication Status: Published
URI: http://wrap.warwick.ac.uk/id/eprint/10136

Data sourced from Thomson Reuters' Web of Knowledge

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