Convergence of auxin and gibberellin signaling on the regulation of the GATA transcription factors GNC and GNL in Arabidopsis thaliana

被引:129
|
作者
Richter, Rene [1 ]
Behringer, Carina [1 ]
Zourelidou, Melina [1 ]
Schwechheimer, Claus [1 ]
机构
[1] Tech Univ Munich, D-85354 Freising Weihenstephan, Germany
关键词
LATERAL ROOT-FORMATION; FACTOR GENE FAMILY; PHYTOCHROME-INTERACTING FACTORS; RESPONSE ELEMENTS; LIGHT; DOWNSTREAM; EXPRESSION; CYTOKININ; ARF19; AUXIN-RESPONSE-FACTOR-2;
D O I
10.1073/pnas.1304250110
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Plant growth is regulated by a complex network of signaling events. Points of convergence for the signaling cross-talk between the phytohormones auxin and gibberellin (GA), which partly control overlapping processes during plant development, are largely unknown. At the cellular level, auxin responses are controlled by members of the AUXIN RESPONSE FACTOR (ARF) family of transcription factors as well as AUXIN/INDOLE-3-ACETIC ACID INDUCIBLE (AUX/IAA) proteins that repress the activity of at least a subset of ARFs. Here, we show that the two paralogous GATA transcription factors GATA, NITRATE-INDUCIBLE, CARBON-METABOLISM INVOLVED (GNC) and GNC-LIKE (GNL)/CYTOKININ-RESPONSIVE GATA FACTOR1 (CGA1) are direct and critical transcription targets downstream from ARF2 in the control of greening, flowering time, and senescence. Mutants deficient in the synthesis or signaling of the phytohormone GA are also impaired in greening, flowering, and senescence, and interestingly, GNC and GNL were previously identified as important transcription targets of the GA signaling pathway. In line with a critical regulatory role for GNC and GNL downstream from both auxin and GA signaling, we show here that the constitutive activation of GA signaling is sufficient to suppress arf2 mutant phenotypes through repression of GNC and GNL. In addition, we show that GA promotes ARF2 protein abundance through a translation-dependent mechanism that could serve to override the autoinhibitory negative feedback regulation of ARF2 on its own transcription and thereby further promote GA signaling.
引用
收藏
页码:13192 / 13197
页数:6
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