As part of an effort to isolate new Arabidopsis mutants specifically defect
ive in responsiveness to red light, we identified srl1 (short hypocotyl in
red light) by screening an EMS-mutagenized M-2 population derived from a ph
ytochrome B (phyB)-overexpressor line (ABO). The srl1 mutant shows enhanced
responsiveness to continuous red but not far-red light, in both wild-type
and ABO backgrounds, consistent with involvement in the phyB-signaling path
way but not that of phyA. The hypersensitive phenotype of srl1 is not due t
o overexpression of endogenous phyA or phyB, and the locus maps to the cent
er of chromosome 2, distinct from any other known photomorphogenic mutants.
srl1 seedlings display enhancement of several phyB-mediated responses, inc
luding shorter hypocotyls, more expanded cotyledons, shorter petioles and m
odestly higher levels of CAB gene expression under red light than the wild
type. Double mutant analyses show that the hypersensitive phenotype of srl1
is completely phyB-dependent. The data suggest, therefore, that SRL1 may e
ncode a negatively acting component specific to the phyB-signaling pathway.