The role of the SCRAMBLED receptor-like kinase in patterning the Arabidopsis root epidermis

Abstract

Cell-type patterning in the Arabidopsis root epidermis is achieved by a network of transcription factors and influenced by a position-dependent mechanism. The SCRAMBLED receptor-like kinase is required for the normal pattern to arise, but its precise role is not understood. Here we describe genetic and molecular studies to define the spatial and temporal role of SCM in epidermal patterning and its relationship to the transcriptional network. Our results suggest that SCM helps unspecified epidermal cells interpret their position in relation to the underlying cortical cells and establish distinct cell identities. Furthermore, SCM loss-of-function and overexpression analyses suggest that SCM influences cell fate through its negative transcriptional regulation of the WEREWOLF MYB gene in epidermal cells at the H position. We also find that SCM function is specifically required for patterning the post-embryonic root epidermis and not for the analogous epidermal cell-type patterning during embryogenesis or hypocotyl development. In addition, we show that two closely related SCM-like genes in Arabidopsis (SRF1 and SRF3) are not required alone or together with SCM for proper epidermal patterning. These findings help define the developmental and mechanistic role of SCM and suggest a new model for its action in root epidermal cell patterning.

Steroids are required for epidermal cell fate establishment in Arabidopsis roots

“…The root epidermal phenotype observed in bri1 and BRZtreated plants was reminiscent of cpc mutants, where a large number of cells in the H position adopt the N cell fate (7,18). Like GL2, CPC expression is WER-dependent (4,19).…”

“…Genetic and molecular studies demonstrate that CPC plays a largely additive role with SCM in repressing WER expression and promoting hair cell fate in H cells (7). The conversion of N cells to hair cell fate observed in scm single mutants is almost completely eliminated in scm cpc double mutants (7), suggesting that ectopic hair cell fate requires CPC activity.…”

“…The identification of a receptor-like kinase, SCRAMBLED (SCM), has led to a model where an asymmetrically distributed positional signal activates SCM in epidermal cells located between 2 cortical cells (6). Activated SCM promotes hair cell fate by decreasing the abundance of WER (7). Laterally translocated CPC promotes the preferential accumulation of SCM in the H cell position, thus reinforcing hair cell fate in epidermal cells located between 2 cortical cells (8).…”

TheMYB23Gene Provides a Positive Feedback Loop for Cell Fate Specification in theArabidopsisRoot Epidermis

“…Root hair cells are formed over the anticlinal wall of underlying cortical cells (H position) and nonhair cells over the periclinal wall of underlying cortical cells (N position) (Dolan et al, 1993(Dolan et al, , 1994Galway et al, 1994). This pattern is dependent on SCRAMBLED (SCM), a leucine-rich repeat receptor-like kinase, which appears to detect positional cues and preferentially inhibit WER expression in the H cell position (Kwak et al, 2005;Kwak and Schiefelbein, 2007). As a result, the WER-GL3/EGL3-TTG1 complex is preferentially active in the N cell position, which causes these cells to adopt the non-hair fate and, via lateral inhibition mediated by the onerepeat MYBs, prevents cells in the H cell position from adopting this fate (Schiefelbein and Lee, 2006;Ishida et al, 2008).…”

Arabidopsis TRANSPARENT TESTA GLABRA2Is Directly Regulated by R2R3 MYB Transcription Factors and Is Involved in Regulation ofGLABRA2Transcription in Epidermal Differentiation

“…The primers used were as follows: WER-qRTPCRf and WER-qRTPCRr for WER, CPC-qRTPCRf and CPC-R1 for CPC, GL3-qRTPCRf and GL3-qRTPCRr for GL3, EGL3-qRTPCRf and EGL3-qRTPCRr for EGL3, TTG1-qRTPCRf and TTG1-qRTPCRr for TTG1, TTG2en-qRTPCRf and TTG2-BB for endogenous TTG2, GL2-F and GL2-qRTPCRr for GL2, and RT-EF1a-F1 and RT-EF1a-R1 for EF1a (see Supplemental Table 2 online; Czechowski et al, 2004;Kwak and Schiefelbein, 2007).…”