LARSON directly represses AGAMOUS during early flower organogenesis in Arabidopsis thaliana

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dc.contributor.advisorLiu, Zhongchien_US
dc.contributor.authorBao, Xiaozhongen_US
dc.contributor.departmentCell Biology & Molecular Geneticsen_US
dc.date.accessioned2004-06-04T05:52:12Z
dc.date.available2004-06-04T05:52:12Z
dc.date.issued2004-04-30en_US
dc.description.abstractHow cells in a multicellular organism assume their developmental fates and form distinct patterns is a fundamental biological question. To address this question, I studied genetic and molecular regulation of Arabidopsis flower organ formation and identity determination. Specifically, how the expression of floral meristem and floral organ identity gene AGAMOUS (AG) was regionalized during flower organogenesis. A novel AG repressor LARSON (LSN) was previously isolated in a genetic screen. lsn loss-of-function mutations caused precocious expression of AG in the inflorescence meristem and ectopic expression of AG in sepal primordia, resulting in partial homeotic transfomation of late inflorescences into floral meristems and strong homeotic transformation of first whorl sepals into carpels. LSN encoded a homeodomain protein that directly bond to AG cis-regulatory elements in vitro. The cis-regulatory elements were conserved in 17 Brassicaceae species. LSN was expressed in a subset of cells located in the peripheral zones of inflorescence and floral meristems. LSN expression was significantly reduced in the sepal and petal primordia in wild-type flowers, indicating that repression of AG in the sepals and petals was independent of LSN transcription. LSN might establish epigenetic AG repression in the ancestral cells in the peripheral zone to specify the identities of descendant cell types in the floral organs. Therefore, floral organ identities were not only dependent upon gene expression in the organs, but were also dependent upon the histories of the cell development. Genetic and molecular analyses showed that LSN acted upstream of a putative repression complex, which, I proposed, was involved in the maintenance of AG repression in flowers. The putative repressive complex consistes of APETALA1 (AP1), LUNIG (LUG) and SEUSS (SEU) known to encode flower specific repressors of AG. Mutations in these three genes enhanced the lsn phenotypes. However, none of their proteins interacted with LSN in yeast. Instead, AP1, SEU, and LUG might form a protein complex. Genetic and molecular analyses suggested that the AG-repressive functions of the putative complex depended upon LSN activity in the peripheral zone of floral meristem. The AG-repressive function of LSN in the inflorescence meristem was independent of AP1/SEU/LUG putative complex.en_US
dc.format.extent38299445 bytes
dc.format.mimetypeapplication/pdf
dc.identifier.urihttp://hdl.handle.net/1903/1487
dc.language.isoen_US
dc.relation.isAvailableAtDigital Repository at the University of Marylanden_US
dc.relation.isAvailableAtUniversity of Maryland (College Park, Md.)en_US
dc.subject.pqcontrolledBiology, Molecularen_US
dc.subject.pqcontrolledBiology, Geneticsen_US
dc.subject.pqcontrolledBiology, Cellen_US
dc.subject.pquncontrolledLARSONen_US
dc.subject.pquncontrolledAGAMOUSen_US
dc.subject.pquncontrolledBELLRINGERen_US
dc.subject.pquncontrolledhomeoticen_US
dc.subject.pquncontrolledfloweren_US
dc.subject.pquncontrolledArabidopsisen_US
dc.titleLARSON directly represses AGAMOUS during early flower organogenesis in Arabidopsis thalianaen_US
dc.typeDissertationen_US

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