Regulation of root epidermal cell fate specification in <italic>Arabidopsis</italic>.

Abstract

The formation of the root epidermis in <italic>Arabidopsis </italic> provides a simple and elegant model for the study of cell fate specification. An epidermal cell develops as a root hair cell when it overlies two cortical cells, and develops as a root non-hair cell when it overlies a single cortical cell. A network of transcription factor proteins, <italic>WEREWOLF</italic> (<italic>WER</italic>), <italic>GLABRA3</italic> (<italic>EGL3</italic>), <italic> ENHANCER OF GLABRA3</italic> (<italic>EGL3</italic>), and <italic>TRANSPARENT TESTA GLABRA1</italic> (<italic>TTG1</italic>), promote the non-hair cell fate through the activation of <italic>GLABRA2</italic> (<italic>GL2</italic>) gene expression in the non-hair cell position, and promote the hair cell fate through the activation of <italic>CAPRICE</italic> (<italic>CPC</italic>) gene expression in the non-hair cell position. The CPC protein acts through a mechanism of lateral inhibition to regulate gene expression in the neighboring hair cells by the direct movement of the CPC protein from non-hair cells to hair cells and throughout the epidermis. We have identified four CPC homologs, TRIPTYCHON (TRY), ENHANCER OF TRY AND CPC 1, 2 and 3 (ETC1, ETC2 and ETC3), that are able to functionally substitute for the CPC in root epidermal patterning. <italic> CPC, TRY</italic> and <italic>ETC1</italic> are expressed in the non-hair cell position and act in a partially redundant manner to regulate cell fate specification in the root, whereas <italic>ETC2</italic> and <italic>ETC3 </italic> are not expressed in the root and do not have a role in root epidermal patterning. We identify a new regulator of root epidermal patterning, <italic> TRANSPARENT TESTA GLABRA2</italic> (<italic>TTG2</italic>), that enhances a <italic>cpc</italic> mutant phenotype. We find that the <italic>TTG2</italic> and <italic>GL2</italic> and genes positively regulate <italic>TRY</italic> gene expression, but do not regulate <italic>CPC</italic> or <italic>ETC1 </italic> gene expression in the non-hair cell position. Thus, we propose that <italic>TTG2</italic> and <italic>GL2</italic> act in a secondary step to initiate and maintain lateral inhibition signaling through the regulation of <italic>TRY</italic> gene expression in the root epidermis.