The GATA-type transcription factors GNC and GNL/CGA1 repress gibberellin signaling downstream from DELLA proteins and PHYTOCHROME-INTERACTING FACTORS

被引:180
作者
Richter, Rene [1 ,2 ]
Behringer, Carina [1 ]
Mueller, Isabel Karin [1 ,2 ]
Schwechheimer, Claus [1 ,2 ]
机构
[1] Tech Univ Munich, Ctr Life & Food Sci Weihenstephan, D-85354 Freising Weihenstephan, Germany
[2] Univ Tubingen, Ctr Plant Mol Biol, D-72076 Tubingen, Germany
关键词
Arabidopsis thaliana; DELLA protein; GATA factor; gibberellin; LLM domain; phytochrome-interacting factor; PIF; ARABIDOPSIS SEED-GERMINATION; CHLOROPLAST DEVELOPMENT; FUNCTIONAL-ANALYSIS; CHLOROPHYLL-A; RECEPTOR GID1; LIGHT; GENE; DEGRADATION; THALIANA; GAI;
D O I
10.1101/gad.594910
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The phytohormone gibberellin (GA) regulates various developmental processes in plants such as germination, greening, elongation growth, and flowering time. DELLA proteins, which are degraded in response to GA, repress GA signaling by inhibitory interactions with PHYTOCHROME-INTERACTING FACTOR (PIF) family transcription factors. How GA signaling is controlled downstream from the DELLA and PIF regulators is, at present, unclear. Here, we characterize GNC (GATA, NITRATE-INDUCIBLE, CARBON-METABOLISM INVOLVED) and GNL/CGA1 (GNC-LIKE/CYTOKININ-RESPONSIVE GATA FACTOR1), two homologous GATA-type transcription factors from Arabidopsis thaliana that we initially identified as GA-regulated genes. Our genetic analyses of loss-of-function mutants and overexpression lines establish that GNC and GNL are functionally redundant regulators of germination, greening, elongation growth and flowering time. We further show by chromatin immunoprecipitation that both genes are potentially direct transcription targets of PIF transcription factors, and that their expression is up-regulated in pif mutant backgrounds. In line with a key role of GNC or GNL downstream from DELLA and PIF signaling, we find that their overexpression leads to gene expression changes that largely resemble those observed in a ga1 biosynthesis mutant or a pif quadruple mutant. These findings, together with the fact that gnc and gnl loss-of-function mutations suppress ga1 phenotypes, support the hypothesis that GNC and GNL are important repressors of GA signaling downstream from the DELLA and PIF regulators.
引用
收藏
页码:2093 / 2104
页数:12
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