Receptor Kinase Signaling in Arabidopsis root meristem maintenance

Plant development continues after embryogenesis through the activity of small groups of continuously dividing cells, the meristems. Meristems generate the majority of plant organs through balanced cell proliferation and differentiation during the whole lifespan of the plant. Within the root meristem of Arabidopsis thaliana, four mitotically less active cells, the quiescent center (QC), are surrounded by the stem cells responsible for setting of the cells that make up the root. It has been shown that the QC promotes stem cell fat in the cells surrounding it (van den Berg et al 1997; Sabatini et al 2003). The aim of this thesis was to identify signaling components required for root meristem maintenance. In chapter 2 we described that overexpression of a CLV3 like gene (LLP1) under a root meristem specific promoter, causes root meristem differentiation, suggesting that a CLV- like pathway might be responsible for root meristem maintenance. In addition, this presumed CLV-like root pathway acts independently of SHR and SCR without primarily affecting QC specification or stem cell maintenance. To identify the genes involved in these signaling pathway we performed an EMS mutagenesis suppressor screen on the LLP1 ectopic expression line. Mutations in two different loci, sol1 and sol2, have been identified as suppressors of ectopic LLP1 expression. We cloned SOL1 and shown it encodes a putative Zn2+-carboxypeptidases, which may have a role in ligand processing. sol2 mutants show floral phenotypes which resemble clv weak alleles, suggesting some components of the pathway might be shared among shoots and roots. In chapter 3 we used a reverse genetic approach to investigate whether CLV1-like receptors are involved in root meristem maintenance. We studied a clade of 5 leucine-rich-repeat receptor like kinases (LRR-RLKs), two of which are specifically expressed in roots: RCH1 and RCH2, for putative roles of these genes in root development. We performed expression studies combined with single and double mutant loss-of-function analysis. No phenotype could be found in any of the loss-of-function combinations, possibly due to a high level of redundancy in the clade