Lessons from the root apex - Intercellular Communication in Plants - page 213

two-hybrid assays showed that WER is able to interact with a bHLH-type protein
to control epidermal cell patterning during Arabidopsis root development (Lee &
Schiefelbein, 1999).
The GL2 gene encodes a homeodomain-containing protein (Rerie et al. , 1994).
It is preferentially expressed in the N cells (Masucci et al. , 1996) already early
during embryogenesis (Lin & Schiefelbein, 2001; Costa & Dolan, 2003). It is first
expressed in the future epidermis in the heart stage embryo and its expression is
progressively restricted to those cells that will acquire an N identity at the transition
between torpedo and mature stage (Costa & Dolan, 2003).
CPC encodes a small protein with a MYB-like DNA-binding domain, but it does
not have a typical transcriptional activation domain (Wada et al. , 1997). It is pref-
erentially expressed in the differentiating N cells (Wada et al. , 1997, 2002). CPC
has been suggested either to work together with the TTG gene product or in an
independent pathway that controls the number of root hairs upstream of GL2 in the
developmental pathway of root hair formation. (Wada et al. , 1997). Interestingly,
CPC protein is able to move to the hair-forming cells and repress gene expression
(Wada et al. , 2002). These studies indicate that transcriptional feedback loops be-
tween the WER , CPC and GL2 genes help to establish position-dependent epidermal
patterning (Lee & Schiefelbein, 2002; Costa & Dolan, 2003).
Various gene expression studies have shown that WER positively regulates GL2
expression in the N cells (Lee & Schiefelbein, 1999) and is thus required to specify
the positional information for GL2 expression (Hung et al. , 1998; Lin & Schiefel-
bein, 2001). The WER gene is also required for positive regulation of CPC tran-
scription in the developing N cells, and CPC acts as a negative regulator of GL2
(Wada et al. , 1997; Schellmann et al. , 2002; Wada et al. , 2002), WER and itself in
the developing H cells (Lee & Schiefelbein, 2002).
Based on GL2 promoter-reporter gene expression studies, it was proposed that
the epidermal cell patterning mechanism in the root initiates during the early heart
stage and that it occurs before the establishment of a functional meristem (Lin &
Schiefelbein, 2001). Lee and Schiefelbein (2002) have proposed a simple model for
the origin of the epidermal cell pattern. In this model, the specification of an H or
N cells relies on the relative activity of two competing transcription factors, WER
and CPC. In heart stage embryos, all epidermal cells express WER and GL2 and, in
the absence of positional cues, use CPC to inhibit their neighbours from expressing
these genes. In the growing root the pattern is established by positional cues from the
underlying tissue that break the symmetry of the inhibition and cause greater WER
transcription in the cells overlying a single cortical cell (Fig. 8.5). This leads to a high
level of GL2 and CPC expression and to the N cell fate. In the alternate cell position,
the CPC protein produced by the developing N cell is proposed to accumulate by
virtue of its cell-to-cell trafficking and it represses GL2 , WER and CPC expression,
permitting H cell differentiation to proceed (Lee & Schiefelbein, 2002).
Recently, a different model for the establishment of the root epidermal pattern
has been proposed based on more detailed examination of GL2 , WER and CPC
gene expression during embryogenesis (Costa & Dolan, 2003). According to this
model the development of cell patterning in the root epidermis is also initiated