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Mol Plant. 2014 Sep;7(9):1415-1428. doi: 10.1093/mp/ssu078. Epub 2014 Jul 9.

Phytochrome A antagonizes PHYTOCHROME INTERACTING FACTOR 1 to prevent over-activation of photomorphogenesis.

Author information

1
IFEVA, Faculty of Agronomy, University of Buenos Aires, and Consejo Nacional de Investigaciones Científicas y Técnicas, Av. San Martín 4453, 1417-Buenos Aires, Argentina.
2
Fundación Instituto Leloir, IIBBA-CONICET, C1405BWE-Buenos Aires, Argentina.
3
Department of Molecular Biosciences and the Institute for Cellular and Molecular Biology, University of Texas, Austin, TX 78712, USA.
4
Plant Biology Laboratory, Howard Hughes Medical Institute, the Salk Institute for Biological Studies, La Jolla, CA 92037, USA.
5
IFEVA, Faculty of Agronomy, University of Buenos Aires, and Consejo Nacional de Investigaciones Científicas y Técnicas, Av. San Martín 4453, 1417-Buenos Aires, Argentina; Fundación Instituto Leloir, IIBBA-CONICET, C1405BWE-Buenos Aires, Argentina. Electronic address: casal@ifeva.edu.ar.

Abstract

Phytochrome A (phyA) is crucial to initiate the early steps of the transition between skoto- and photomorphogenesis upon light exposure and to complete this process under far-red light (typical of dense vegetation canopies). However, under prolonged red or white light, phyA mutants are hyper-photomorphogenic in many respects. To investigate this issue, we analyzed the late response of the transcriptome of the phyA mutant to red light. Compared to the wild-type (WT), hyper-responsive genes outnumbered the genes showing reduced response to red light in phyA. A network analysis revealed the co-expression of PHYTOCHROME INTERACTING FACTOR 1 (PIF1) with those genes showing hyper-promotion by red light in phyA. The enhanced responses of gene expression, cotyledon unfolding, hypocotyl growth, and greening observed in the phyA mutant compared to the WT were absent in the phyA pif1 double mutant compared to pif1, indicating that the hyper-photomorphogenic phenotype of phyA requires PIF1. PIF1 directly binds to gene promoters that displayed PIF1-mediated enhanced response to red light. Expression of mutant PIF1 deficient in interactions with phyA and phyB enhanced the long-term growth response to red light but reduced the expression of selected genes in response to red light. We propose that phytochrome-mediated degradation of PIF1 prevents over-activation of photomorphogenesis during early seedling development.

KEYWORDS:

PIF1; de-etiolation; light (gene expression); light (growth).; phyA

PMID:
25009301
DOI:
10.1093/mp/ssu078
[Indexed for MEDLINE]
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