Plant Physiol, July 2001, Vol. 126, pp. 1291-1298
Light-Induced Growth Promotion by SPA1 Counteracts
Phytochrome-Mediated Growth Inhibition during
De-Etiolation1
Brian M.
Parks,*
Ute
Hoecker, and
Edgar P.
Spalding
Department of Botany, University of Wisconsin, 430 Lincoln Drive,
Madison, Wisconsin 53706 (B.M.P., E.P.S.); and Institut für
Entwicklungs-und Molekularbiologie der Pflanzen, Universitaet
Duesseldorf, D-40225 Duesseldorf, Germany (U.H.)
Previous evidence has suggested that SPA1 is a signal transduction
component that appears to require phytochrome A for function in
seedling photomorphogenesis. Using digital image analysis, we examined
the time course of growth inhibition induced by red light in
spa1 mutants to test the interpretation that SPA1
functions early in a phyA-specific signaling pathway. By comparing
wild-type and mutant responses, we found that SPA1 caused an increase
in hypocotyl growth rate after approximately 2 h of continuous red light, whereas the onset of phyA-mediated inhibition was detected within several minutes. Thus, SPA1-dependent growth promotion began
after phyA started to inhibit growth. The action of SPA1 persisted for
approximately 2 d of red light, a period well beyond the time when
the phyA photoreceptor and its influence on growth have both decayed to
undetectable levels. Also, SPA1 promoted growth for many hours in the
complete absence of a light stimulus when red-light-grown seedlings
were shifted to darkness. We propose that SPA1 functions in a
light-induced mechanism that promotes growth and thereby counteracts
growth inhibition mediated by phyA and phyB. Our finding that
spa1 seedlings do not display growth promotion in
response to end-of-day pulses of far-red light, even in a phyA-null
background, supports this interpretation. Combined, these results lead
us to the view that the rate of hypocotyl elongation in light is
determined by at least two independent, opposing processes; an
inhibition of growth by the phytochromes and a promotion of growth by
light-activated SPA1.
1
This work was supported by the U.S.
Department of Agriculture (grant no. 99-01833 to B.M.P. and E.P.S.)
and by the Deutsche Forschungsgemeinschaft (grant to U.H.).
*
Corresponding author; e-mail bmparks{at}facstaff.wisc.edu; fax
608-262-7509.
© 2001 American Society of Plant Physiologists