| Summary: | 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. <i>knox</i> genes are expressed in the SAM but are downregulated in organ founder cells at the time of initiation. The <i>knox</i> genes are implicated in maintaining division or preventing differentiation of SAM cells. Loss-of-function mutations in <i>knox</i> genes are associated with defects in meristem maintenance. Gain-of-function mutations resulting in ectopic <i>knox</i> expression disrupt normal organ development. <i>PHANTASTICA (PHAN) </i>in <i>Antirrhinum </i>and <i>ROUGHSHEATH2</i> <i>(RS2) </i>in maize encode MYB transcription factors that are expressed in initiating organs and negatively regulate <i>knox</i> genes. <i>phan</i> mutants show variable defects in leaf patterning, affecting both proximodistal and dorsoventral axes whilst <i>rs</i>2 mutations resemble dominant mutations in <i>knox</i> genes. A homologous protein is encoded by <i>AtPHAN</i> in <i>Arabidopsis</i> though its function is not known. <i>asymmetric leaves1 </i>(<i>as1</i>) is a recessive mutation in <i>Arabidopsis </i>that disrupts development of cotyledons, leaves, and floral organs and shares lobing characteristics with transgenic plants mixexpressing <i>knox</i> genes. <i>AtPHAN</i> was found to correspond to <i>as1</i> by PCR analysis and complementation. <i>AS1</i> was found to be expressed in initiating organs throughout <i>Arabidopsis </i>development in a domain complementary to <i>knox</i> genes. Molecular and genetic epistasis experiments showed that <i>AS1</i> negatively regulates the <i>knox</i> genes <i>KNAT1 </i>and <i>KNAT2</i> in organs. In turn the <i>knox</i> gene <i>SHOOTMERISTEMLESS</i> downregulates <i>AS1</i>expression 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.
|
|---|
