INVESTIGADORES
YANOVSKY Marcelo Javier
artículos
Título:
Regulation of phytochrome B signaling by phytochrome A
Autor/es:
CERDAN, PD; YANOVSKY, MJ; REYMUNDO, C; NAGATANI, A; STANELONI, RJ; WHITELAM, GC; CASAL, JJ
Revista:
PLANT JOURNAL
Editorial:
WILEY-BLACKWELL PUBLISHING, INC
Referencias:
Año: 1999 vol. 18 p. 499 - 507
ISSN:
0960-7412
Resumen:
Phytochrome A (phyA) and phytochrome B (phyB) share
the control of many processes but little is known about
mutual signaling regulation. Here, we report on the
interactions between phyA and phyB in the control of the
activity of an Lhcb1*2 gene fused to a reporter, hypocotyl
growth and cotyledon unfolding in etiolated Arabidopsis
thaliana. The very-low ¯uence responses (VLFR) induced
by pulsed far-red light and the high-irradiance responses
(HIR) observed under continuous far-red light were
absent in the phyA and phyA phyB mutants, normal in
the phyB mutant, and reduced in the fhy1 mutant that is
defective in phyA signaling. VLFR were also impaired in
Columbia compared to Landsberg erecta. The low-¯uence
responses (LFR) induced by red-light pulses and reversed
by subsequent far-red light pulses were small in the wild
type, absent in phyB and phyA phyB mutants but strong
in the phyA and fhy1 mutants. This indicates a negative
effect of phyA and FHY1 on phyB-mediated responses.
However, a pre-treatment with continuous far-red light
enhanced the LFR induced by a subsequent red-light
pulse. This enhancement was absent in phyA, phyB, orLhcb1*2 gene fused to a reporter, hypocotyl
growth and cotyledon unfolding in etiolated Arabidopsis
thaliana. The very-low ¯uence responses (VLFR) induced
by pulsed far-red light and the high-irradiance responses
(HIR) observed under continuous far-red light were
absent in the phyA and phyA phyB mutants, normal in
the phyB mutant, and reduced in the fhy1 mutant that is
defective in phyA signaling. VLFR were also impaired in
Columbia compared to Landsberg erecta. The low-¯uence
responses (LFR) induced by red-light pulses and reversed
by subsequent far-red light pulses were small in the wild
type, absent in phyB and phyA phyB mutants but strong
in the phyA and fhy1 mutants. This indicates a negative
effect of phyA and FHY1 on phyB-mediated responses.
However, a pre-treatment with continuous far-red light
enhanced the LFR induced by a subsequent red-light
pulse. This enhancement was absent in phyA, phyB, orArabidopsis
thaliana. The very-low ¯uence responses (VLFR) induced
by pulsed far-red light and the high-irradiance responses
(HIR) observed under continuous far-red light were
absent in the phyA and phyA phyB mutants, normal in
the phyB mutant, and reduced in the fhy1 mutant that is
defective in phyA signaling. VLFR were also impaired in
Columbia compared to Landsberg erecta. The low-¯uence
responses (LFR) induced by red-light pulses and reversed
by subsequent far-red light pulses were small in the wild
type, absent in phyB and phyA phyB mutants but strong
in the phyA and fhy1 mutants. This indicates a negative
effect of phyA and FHY1 on phyB-mediated responses.
However, a pre-treatment with continuous far-red light
enhanced the LFR induced by a subsequent red-light
pulse. This enhancement was absent in phyA, phyB, orThe very-low ¯uence responses (VLFR) induced
by pulsed far-red light and the high-irradiance responses
(HIR) observed under continuous far-red light were
absent in the phyA and phyA phyB mutants, normal in
the phyB mutant, and reduced in the fhy1 mutant that is
defective in phyA signaling. VLFR were also impaired in
Columbia compared to Landsberg erecta. The low-¯uence
responses (LFR) induced by red-light pulses and reversed
by subsequent far-red light pulses were small in the wild
type, absent in phyB and phyA phyB mutants but strong
in the phyA and fhy1 mutants. This indicates a negative
effect of phyA and FHY1 on phyB-mediated responses.
However, a pre-treatment with continuous far-red light
enhanced the LFR induced by a subsequent red-light
pulse. This enhancement was absent in phyA, phyB, orphyA and phyA phyB mutants, normal in
the phyB mutant, and reduced in the fhy1 mutant that is
defective in phyA signaling. VLFR were also impaired in
Columbia compared to Landsberg erecta. The low-¯uence
responses (LFR) induced by red-light pulses and reversed
by subsequent far-red light pulses were small in the wild
type, absent in phyB and phyA phyB mutants but strong
in the phyA and fhy1 mutants. This indicates a negative
effect of phyA and FHY1 on phyB-mediated responses.
However, a pre-treatment with continuous far-red light
enhanced the LFR induced by a subsequent red-light
pulse. This enhancement was absent in phyA, phyB, orphyB mutant, and reduced in the fhy1 mutant that is
defective in phyA signaling. VLFR were also impaired in
Columbia compared to Landsberg erecta. The low-¯uence
responses (LFR) induced by red-light pulses and reversed
by subsequent far-red light pulses were small in the wild
type, absent in phyB and phyA phyB mutants but strong
in the phyA and fhy1 mutants. This indicates a negative
effect of phyA and FHY1 on phyB-mediated responses.
However, a pre-treatment with continuous far-red light
enhanced the LFR induced by a subsequent red-light
pulse. This enhancement was absent in phyA, phyB, orerecta. The low-¯uence
responses (LFR) induced by red-light pulses and reversed
by subsequent far-red light pulses were small in the wild
type, absent in phyB and phyA phyB mutants but strong
in the phyA and fhy1 mutants. This indicates a negative
effect of phyA and FHY1 on phyB-mediated responses.
However, a pre-treatment with continuous far-red light
enhanced the LFR induced by a subsequent red-light
pulse. This enhancement was absent in phyA, phyB, orphyB and phyA phyB mutants but strong
in the phyA and fhy1 mutants. This indicates a negative
effect of phyA and FHY1 on phyB-mediated responses.
However, a pre-treatment with continuous far-red light
enhanced the LFR induced by a subsequent red-light
pulse. This enhancement was absent in phyA, phyB, orphyA and fhy1 mutants. This indicates a negative
effect of phyA and FHY1 on phyB-mediated responses.
However, a pre-treatment with continuous far-red light
enhanced the LFR induced by a subsequent red-light
pulse. This enhancement was absent in phyA, phyB, orphyA, phyB, or
phyA phyB and partial in fhy1. The levels of phyB were
not affected by the phyA or fhy1 mutations or by far-red
light pre-treatments. We conclude that phyA acting in the
VLFR mode (i.e. under light pulses) is antagonistic to
phyB signaling whereas phyA acting in the HIR mode (i.e.
under continuous far-red light) operates synergistically
with phyB signaling, and that both types of interaction
require FHY1.and partial in fhy1. The levels of phyB were
not affected by the phyA or fhy1 mutations or by far-red
light pre-treatments. We conclude that phyA acting in the
VLFR mode (i.e. under light pulses) is antagonistic to
phyB signaling whereas phyA acting in the HIR mode (i.e.
under continuous far-red light) operates synergistically
with phyB signaling, and that both types of interaction
require FHY1.phyA or fhy1 mutations or by far-red
light pre-treatments. We conclude that phyA acting in the
VLFR mode (i.e. under light pulses) is antagonistic to
phyB signaling whereas phyA acting in the HIR mode (i.e.
under continuous far-red light) operates synergistically
with phyB signaling, and that both types of interaction
require FHY1.