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ARS Home » Pacific West Area » Albany, California » Plant Gene Expression Center » Research » Publications at this Location » Publication #135949
Title: SPA1: A NEW GENETIC LOCUS INVOLVED IN PHYTOCHROME A- SPECIFIC SIGNAL TRANSDUCTION

Author
item HOECKER, UTE - USDA/UCB PGEC
item XU, YONG - USDA/UCB PGEC
item QUAIL, PETER - USDA/UCB PGEC

Submitted to: The Plant Cell
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/1/1998
Publication Date: N/A
Citation: Hoecker, U., Xu, Y., Quail, P.H. 1998. SPA1: A New Genetic Locus Involved in Phytochrome A-Specific Signal Transduction. The Plant Cell 10:19-34.

Interpretive Summary: A new recessive mutant, designated spa1 (for suppressor of phyA105), was isolated and mapped to the bottom of chromosome 2. The data suggest that spa1 mutations specifically amplify phyA signaling and therefore that the SPA1 locus encodes a component that acts negatively early in the phyA-specific signaling pathway.

Technical Abstract: To identify mutants potentially defective in signaling intermediates specific to phytochrome A (phyA), we screened for extragenic mutations that suppress the morphological phenotype exhibited by a weak phyA mutant phyA105 of Arabidopsis. A new recessive mutant, designated spa1 (for suppressor of phyA105), was isolated and mapped to the bottom of chromosome 2. spa1 phyA105 double mutants exhibit restoration of several responses to limiting fluence rates of continuous farred light that are absent in the parental phyA105 mutant, such as deetiolation, anthocyanin accumulation, and a farred lightinduced inability of seedlings to green upon subsequent transfer to continuous white light. spa1 mutations do not cause a phenotype in darkness, indicating that the suppression phenotype is light dependent. Enhanced photoresponsiveness was observed in spa1 seedlings in a wildtype PHYA background as well as in the mutant phyA105 background but not in a mutant phyA null background. These results indicate that phyA is necessary in a nonallelespecific fashion for the expression of the spa1 mutant phenotype and that phyB to phyE are not sufficient for this effect. Taken together, the data suggest that spa1 mutations specifically amplify phyA signaling and therefore that the SPA1 locus encodes a component that acts negatively early in the phyA-specific signaling pathway.