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Transcriptional and functional targets of SCHIZORIZA in root development

  • van Liere, Sabine
Publication Date
Jan 01, 2017
Wageningen University and Researchcenter Publications
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In this thesis I focus on SCHIZORIZA, a gene involved in tissue specification and cell fate segregation in the Arabidopsis root. Chapter 1 describes asymmetric cell division, Arabidopdis embryo development and root meristem development. In more detail we describe the maintenance of quiescent centre and columella stem cells, the development of ground tissue and epidermis/ lateral root cap. Finally we introduce SCHIZORIZA (SCZ) as a factor involved in radial patterning and the maintenance of cortex identity. In Chapter 2, we study the interaction between the SCZ and SHORTROOT/ SCARECROW pathways that are required in parallel during stem cell niche specification in embryogenesis for the maintenance of tissue fates. Here we investigate the strong synergy of shr and scz mutants and show that at late torpedo stage scz;shr double mutant embryos lose both ground tissue and meristem marker expression. Chapter 3 describes the use of a transcriptomics approach to identify genes differentially regulated by SCZ. These differentially regulated genes can be divided into two distinct tissue enriched groups. Upregulated genes are enriched for root cap expression and cortex expressed genes are overrepresented in the downregulated set of genes. A subset of the upregulated genes has a HSE associated with their promoter and therefore possibly represents direct SCZ targets. In Chapter 4 we describe a mutagenesis screen to identify functional downstream targets of SCZ. Using a cortex and lateral root cap tissue marker, we identified two suppressors of the scz mutant. Both restore the fate segregation phenotype of scz mutants. We used whole genome deep sequencing to map the causal suppressor mutations in the LBD12 gene. The analysis of LBD12 function is described in Chapter 5. We show that the single lbd12 mutant has a QC and columella phenotype. In addition, we show that ectopic expression of LBD12 induces ectopic divisions. Chapter 6 summarizes and discusses the work described in this thesis and gives suggestions for future research.

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