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Repression of flowering under a noninductive photoperiod by the HDA 9 ‐ AGL 19 ‐ FT module in Arabidopsis
Author(s) -
Kang MinJeong,
Jin HongShi,
Noh YooSun,
Noh Bosl
Publication year - 2015
Publication title -
new phytologist
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.742
H-Index - 244
eISSN - 1469-8137
pISSN - 0028-646X
DOI - 10.1111/nph.13161
Subject(s) - flowering locus c , arabidopsis , biology , agamous , chromatin immunoprecipitation , histone , mutant , chromatin , acetylation , phytochrome a , activator (genetics) , genetics , photoperiodism , microbiology and biotechnology , gene expression , gene , promoter , botany
Summary Posttranslational acetylation of histones is reversibly regulated by histone deacetylases ( HDAC s). Despite the evident significance of HDAC s in Arabidopsis development, the biological roles and underlying molecular mechanisms of many HDAC s are yet to be elucidated. By a reverse‐genetic approach, we isolated an hda9 mutant and performed phenotypic analyses on it. In order to address the role of HDA 9 in flowering, genetic, molecular, and biochemical approaches were employed. hda9 flowered early under noninductive short‐day ( SD ) conditions and had increased expression of the floral integrator FLOWERING LOCUS T ( FT ) and the floral activator AGAMOUS ‐ LIKE 19 ( AGL 19 ) compared with the wild‐type. The hda9 mutation increased histone acetylation and RNA polymerase II occupancy at AGL 19 but not at FT during active transcription, and the HDA 9 protein directly targeted AGL 19 . AGL 19 expression was higher under SD than under inductive long‐day (LD) conditions, and an AGL 19 overexpression caused a strong up‐regulation of FT . A genetic analysis showed that an agl19 mutation is epistatic to the hda9 mutation, masking both the early flowering and the increased FT expression of hda9 . Taken together, our data indicate that HDA 9 prevents precocious flowering under SD conditions by curbing the hyperactivation of AGL 19 , an upstream activator of FT , through resetting the local chromatin environment.