Regulation of epidermal cell production by the suppressor of erecta and erecta genes in Arabidopsis thaliana
Abstract
Despite many scientific studies on plant epidermal cell development and differentiation, the knowledge on molecular regulation of the ontogeny of plant epidermal cells is still very limited. The biggest breakthrough is the establishment of signaling pathways for stomatal lineage formation in Arabidopsis, which start from extracellular signaling peptides to their transmembrane receptor kinase complexes to mitogen-activated protein kinase (MAPK) cascades and eventually to transcription factors. Several leucine-rich repeat receptor kinases (LRR-RKs), including the ERECTA (ER) protein, are known to be involved in this signaling process. ER regulates stomatal patterning and proliferation of epidermal cells. To identify additional mutations affecting epidermal cell production in the ecotype of Landsberg erecta (Ler, containing the er-1 mutation), our lab looked for DNA polymorphisms that were linked to the Ler-like epidermal phenotype in the F2 progeny of a cross between Ler and Col-0 (wild type). We identified a deletion of two adjacent LRR-RKs in a region of approximately 21kb on chromosome 2 in Ler that may be involved in epidermal cell production. My thesis research primarily focused on the functional characterization of this deleted region and one of the candidate genes, At2G29000. I found that mutations of At2G29000 partially suppressed the increased epidermal cell phenotype of er mutants, which were thus named suppressor of erecta (sue). The heterozygous er-1 mutation together with a heterozygous sue-1 mutation also resulted in a Ler-like epidermal phenotype. The suppression of sue on er is stronger on the adaxial epidermis than on the abaxial epidermis, which seemed to correlate with the stronger SUE expression in the adaxial epidermis than in the abaxial epidermis based on GUS-reporter gene studies for SUE. The interaction between sue and erecta on epidermal cell production was neither additive nor epistatic and the outcomes suggested a dosage effect between them. Both the sue and er mutations were found to suppress trichome production. The phenotypic and genotypic results suggested that the other candidate gene At2G28990 also played a role similar to that of SUE in the regulation of epidermal cell production. This research has provided evidence that two novel LRR-RK genes regulate epidermal development, and novel observations of the effect of er mutations on epidermal cell production.
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- OSU Theses [15752]