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Abstract
The above-ground structures of a plant are produced by the shoot apical meristem, a collection of undifferentiated cells located at growing shoot tips. Within the shoot apical meristem, two zones can be distinguished by their drastically different rates of cell division. Slow cell divisions in the central zone serve to maintain the central zone and provide daughter cells for the peripheral zone. Cells in the peripheral zone rapidly proliferate to form organ primordia. Along the cell lineage path from the central zone to the developing organ, critical changes in gene activities occur. First, a meristem maintenance program must be down-regulated and an organ proliferation program initiated. The fate of the organ is subsequently imposed by programs that determine organ morphologies. This process continues reiteratively throughout the lifetime of the meristem to give rise to leaves and floral organs at the appropriate times during plant development.
Genes that regulate organogenesis can be identified through the characterization of mutations that either impede the plant's ability to form organs or alter organ morphology. Mutations in the SERRATE (SE ) and ENSALADA (ENS ) genes result in complex phenotypes affecting the initiation and elaboration of lateral organs. Consistent with a role in transcriptional regulation during organogenesis, the SE locus was found to encode a zinc-finger protein whose mRNA accumulates in the meristem and in newly initiated organ primordia. Furthermore, the roles of the SE and ENS genes were studied relative to one another and to previously characterized genes through double mutant analyses. A model consistent with my results proposes that the SE and ENS gene products coordinate changes in gene expression in primordia, emerging from the meristem.
This dissertation contains co-authored materials.
