GLABRA2 regulates gene expression via its own EAR-motif mediated recruitment of the TPL/TPR corepressors

GL2 binds L1 box elements in the promoters of its target genes; however, the mechanisms by which it controls gene expression remain elusive. GL2 contains two putative ethylene-responsive element-binding factor-associated amphiphilic repression (EAR) motifs proximal to its N- and C-termini.

The N-terminal EAR motif is highly conserved among GL2 orthologs that form a distinct clade of HD-Zip IV transcription factors in monocots and dicots. We demonstrate that deletion or alanine substitution of this N-terminal EAR motif results in a partial loss-of-function phenotypes in trichomes, non-hair root cells, and seed coat mucilage. In contrast, mutations affecting the C-terminal EAR motif display improper nuclear localization, likely due to protein misfolding.