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Title: Function of the asymmetric leaves 1 gene in Arabidopsis organ development
Author: Barley, Ross N.
Awarding Body: University of Edinburgh
Current Institution: University of Edinburgh
Date of Award: 2001
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Much of a plants architecture is formed postembryonically by shoot apical meristems (SAMs). SAMs produce lateral organs such as leaves from their flanks whilst maintaining a pool of undifferentiated cells centrally. knox genes are expressed in the SAM but are downregulated in organ founder cells at the time of initiation. The knox genes are implicated in maintaining division or preventing differentiation of SAM cells. Loss-of-function mutations in knox genes are associated with defects in meristem maintenance. Gain-of-function mutations resulting in ectopic knox expression disrupt normal organ development. PHANTASTICA (PHAN) in Antirrhinum and ROUGHSHEATH2 (RS2) in maize encode MYB transcription factors that are expressed in initiating organs and negatively regulate knox genes. phan mutants show variable defects in leaf patterning, affecting both proximodistal and dorsoventral axes whilst rs2 mutations resemble dominant mutations in knox genes. A homologous protein is encoded by AtPHAN in Arabidopsis though its function is not known. asymmetric leaves1 (as1) is a recessive mutation in Arabidopsis that disrupts development of cotyledons, leaves, and floral organs and shares lobing characteristics with transgenic plants mixexpressing knox genes. AtPHAN was found to correspond to as1 by PCR analysis and complementation. AS1 was found to be expressed in initiating organs throughout Arabidopsis development in a domain complementary to knox genes. Molecular and genetic epistasis experiments showed that AS1 negatively regulates the knox genes KNAT1 and KNAT2 in organs. In turn the knox gene SHOOTMERISTEMLESS downregulates AS1expression in the meristem. This genetic pathway defines a mechanism for distinguishing between organ founder cells and meristem cells at the shoot apex and demonstrates that genes expressed in organ primordia interact with meristem genes in regulating morphogenesis.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available