Auxin promotion of seedling growth via ARF5 is dependent on the brassinosteroid-regulated transcription factors BES1 and BEH4
Auxin promotion of seedling growth via ARF5 is dependent on the brassinosteroid-regulated transcription factors BES1 and BEH4
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DOI：
10.1002/pld3.166
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发表时间：
2019-09-01
期刊：
影响因子：
3
通讯作者：
Nemhauser, Jennifer L.
中科院分区：
文献类型：
--
作者：
Galstyan, Anahit;Nemhauser, Jennifer L.
幼苗必须不断调整其生长以适应环境。生长素和油菜素类固醇（BR）是植物激素，共同控制光形态建成过程中的生长反应。我们使用我们以前的分析启动子结构的生长素和BR靶基因，以指导我们的调查更广泛的分子基础和生物相关性的转录共调节这些激素。我们发现，生长素调节的转录因子生长素反应因子5（ARF 5）和油菜素类固醇调节的转录因子BRI 1-EMS-抑制子1/阿喹唑耐药2（BES 1）通过保守的二分顺式调控元件共调控一个子集的生长促进基因。此外，通过增加BES 1水平，可以富集与DNA结合的ARF 5。启动子中二分元件的进化丢失导致激素反应性的丧失。我们还鉴定了BES 1/BZR 1家族的另一个成员BEH 4，它与BES 1部分冗余地调节幼苗生长。双突变体分析表明，BEH 4，而不是BZR 1需要旁边的BES 1在早期幼苗发育过程中正常的生长素反应。我们认为ARF 5-BES 1/BEH 4转录模块通过调节多种生长相关基因来促进生长。
Seedlings must continually calibrate their growth in response to the environment. Auxin and brassinosteroids (BRs) are plant hormones that work together to control growth responses during photomorphogenesis. We used our previous analysis of promoter architecture in an auxin and BR target gene to guide our investigation into the broader molecular bases and biological relevance of transcriptional co-regulation by these hormones. We found that the auxin-regulated transcription factor Auxin Responsive Factor 5 (ARF5) and the brassinosteroid-regulated transcription factor BRI1-EMS-Suppressor 1/Brassinazole Resistant 2 (BES1) co-regulated a subset of growth-promoting genes via conserved bipartite cis-regulatory elements. Moreover, ARF5 binding to DNA could be enriched by increasing BES1 levels. The evolutionary loss of bipartite elements in promoters results in loss of hormone responsiveness. We also identified another member of the BES1/BZR1 family called BEH4 that acts partially redundantly with BES1 to regulate seedling growth. Double mutant analysis showed that BEH4 and not BZR1 were required alongside BES1 for normal auxin response during early seedling development. We propose that an ARF5-BES1/BEH4 transcriptional module acts to promote growth via modulation of a diverse set of growth-associated genes.