Lessons from leaf epidermal patterning in plants - Intercellular Communication in Plants - page 228

trichome initiation; the absence of positive factors reduces or abolishes trichome
formation and the absence of negative regulators results in an increase in trichomes
number.
9.3.3.1 Positive regulators of trichome initiation
Mutations in two genes, GLABRA1 ( GL1 ) and TRANSPARENT TESTA GLABRA1
( TTG 1), lead to the complete absence of trichomes. In gl1 mutants, all trichomes on
the leaf surface are absent. Only a few trichomes at the leaf margin are not affected.
The GL1 gene encodes an R2-R3 MYB related transcription factor (Oppenheimer
et al. , 1991). GL1 protein is found in the nucleus, indicating that GL1 acts as a tran-
scription factor (Szymanski et al. , 1998). GL1 is expressed initially ubiquitously
in all epidermal cells of the young developing leaf. Then trichome precursor cells
show increasingly higher expression levels and, eventually, expression is found only
in developing trichomes but not in the surrounding epidermis cells (Larkin et al. ,
1993). In addition to the trichome phenotype, mutations in the TTG 1 gene result
in a number of additional defects, including the initiation of ectopic root hairs, the
lack of seed coat mucilage and reduced anthocyanin production (Koornneef, 1981;
Galway et al. , 1994). The control of these different processes is mediated by a set
of MYB-related and MYC-related transcription factors such that a distinct combi-
nation of them controls one specific process (Zhang et al. , 2003). TTG 1 encodes a
protein containing WD40 repeats, which are known to function as protein-protein
interaction domains in a variety of processes (Walker et al. , 1999).
A less severe phenotype is found in GLABRA3 ( GL3 ) mutants. In gl3 mutants,
trichome number and size is drastically reduced. The GL3 gene encodes a basic helix-
loop-helix (bHLH)-like transcription factor (Payne et al. , 2000) and, as the protein
is found in the nucleus (Esch et al. , 2003), it is likely to function as a transcription
factor. The low importance of GL3 in trichome patterning, as suggested by the
weak phenotype of the gl3 mutation, turned out to be misleading because of gene
redundancy. A close homologue of GL3 , the ENHANCER OF GLABRA3 (EGL3)
gene, turned out to act redundantly with GL3 . While the single e gl3 mutant exhibits
no trichome phenotype, the e gl3 gl3 double mutant is completely glabrous (Zhang
et al. , 2003).
In addition to the above-described genes, the GLABRA2 ( GL2 ) gene appears to
be involved in trichome patterning. The phenotype of GL2 mutants is pleiotropic
and includes the reduction of seed coat mucilage, the overproduction of root hairs
and a reduction of trichome growth (Rerie et al. , 1994; Cristina et al. , 1996). The
reduced trichome phenotype suggested that GL2 plays a role in the differentiation
and morphogenesis of trichomes but not in patterning. Misexpression studies sug-
gested an additional role in trichome patterning (Ohashi et al. , 2002). Ubiquitous
expression of GL2 appeared to be lethal but the introduction of additional copies of
GL2 under its own promoter resulted in an increased number of trichomes and the
formation of trichome clusters. These findings suggest that GL2 can also promote
trichome formation and can, therefore, be considered to be a positive regulator of
trichome initiation.