| Summary: | Auxin is a well-studied phytohormone, vital for diverse plant developmental processes. The <i>GH3</i> genes are one of the major auxin responsive genes, whose expression changes lead to modulation of plant development and auxin homeostasis. However, the transcriptional regulation of these <i>GH3</i> genes remains largely unknown. WRI1 is an essential transcriptional regulator governing plant fatty acid biosynthesis. Recently, we identified that the expression of <i>GH3.3</i> is increased in the roots of <i>wri1-1</i> mutant. Nevertheless, in this study we found that AtWRI1 did not activate or repress the promoter of <i>GH3.3</i> (<i>proGH3.3</i>) despite of its binding to <i>proGH3.3</i>. Cross-family transcription factor interactions play pivotal roles in plant gene regulatory networks. To explore the molecular mechanism by which WRI1 controls <i>GH3.3</i> expression, we screened an Arabidopsis transcription factor library and identified TCP20 as a novel AtWRI1-interacting regulator. The interaction between AtWRI1 and TCP20 was further verified by several approaches. Importantly, we found that TCP20 directly regulates <i>GH3.3</i> expression via binding to TCP binding element. Furthermore, AtWRI1 repressed the TCP20-mediated transactivation of <i>proGH3.3</i>. EMSAs demonstrated that AtWRI1 antagonized TCP20 from binding to <i>proGH3.3</i>. Collectively, we provide new insights that WRI1 attenuates <i>GH3.3</i> expression through interaction with TCP20, highlighting a new mechanism that contributes to fine-tuning auxin homeostasis.
|
|---|