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Hormonal regulation of temperature‐induced growth in Arabidopsis
Author(s) -
Stavang Jon A.,
GallegoBartolomé Javier,
Gómez María D.,
Yoshida Shigeo,
Asami Tadao,
Olsen Jorunn E.,
GarcíaMartínez José L.,
Alabadí David,
Blázquez Miguel A.
Publication year - 2009
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/j.1365-313x.2009.03983.x
Subject(s) - auxin , hypocotyl , arabidopsis , gibberellin , repressor , mutant , microbiology and biotechnology , elongation , phytochrome , transcription factor , plant hormone , biology , chemistry , biochemistry , botany , gene , materials science , red light , ultimate tensile strength , metallurgy
Summary Successful plant survival depends upon the proper integration of information from the environment with endogenous cues to regulate growth and development. We have investigated the interplay between ambient temperature and hormone action during the regulation of hypocotyl elongation, and we have found that gibberellins (GAs) and auxin are quickly and independently recruited by temperature to modulate growth rate, whereas activity of brassinosteroids (BRs) seems to be required later on. Impairment of GA biosynthesis blocked the increased elongation caused at higher temperatures, but hypocotyls of pentuple DELLA knockout mutants still reduced their response to higher temperatures when BR synthesis or auxin polar transport were blocked. The expression of several key genes involved in the biosynthesis of GAs and auxin was regulated by temperature, which indirectly resulted in coherent variations in the levels of accumulation of nuclear GFP–RGA (repressor of GA1) and in the activity of the DR5 reporter. DNA microarray and genetic analyses allowed the identification of the transcription factor PIF4 (phytochrome‐interacting factor 4) as a major target in the promotion of growth at higher temperature. These results suggest that temperature regulates hypocotyl growth by individually impinging on several elements of a pre‐existing network of signaling pathways involving auxin, BRs, GAs, and PIF4.