Coordinatore | THE HEBREW UNIVERSITY OF JERUSALEM.
Organization address
address: GIVAT RAM CAMPUS contact info |
Nazionalità Coordinatore | Israel [IL] |
Totale costo | 100˙000 € |
EC contributo | 100˙000 € |
Programma | FP7-PEOPLE
Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013) |
Code Call | FP7-PEOPLE-2009-RG |
Funding Scheme | MC-IRG |
Anno di inizio | 2010 |
Periodo (anno-mese-giorno) | 2010-01-01 - 2013-12-31 |
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THE HEBREW UNIVERSITY OF JERUSALEM.
Organization address
address: GIVAT RAM CAMPUS contact info |
IL (JERUSALEM) | coordinator | 100˙000.00 |
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'A central question in biology is how cell fates are established and maintained. In general, the cellular phenotype is determined by the transcriptional program, which is orchestrated by transcription factors (TFs) – proteins that bind specific DNA sequences to activate or repress transcription. Often, expression of a single transcription factor can lead to a radical alteration in cell fate. Although a number of such crucial TFs have been identified, we know relatively little about TF-regulated genes that determine the cellular phenotype. This is especially true in plants. The dome-shaped shoot apical meristem (SAM) of plant is a highly structured organ composed of multiple, functionally distinct zones. The SAM sustains plant growth by continuously producing new lateral organs throughout the life cycle. This unique capacity is achieved by a pool of self-renewing pluripotent stem cells reside at the tip of the SAM and by their daughter cells, which remain undifferentiated to proliferate before being incorporated into organs. Many of the TFs required to pattern the SAM are known, but their target genes, and thus their mechanisms of action, are almost completely unknown. Here I propose to use genomic and genetic tools to map in Arabidopsis thaliana the direct targets of two TF's crucial for proper meristem formation and maintenance. WUS which is required for stem cell specification and STM that function to suppress differentiation and to promote cell proliferation. Loss-of-function mutations in WUS or STM result in a lack of a self-maintaining meristem. I will combine affinity purification mediated by in vivo protein biotinylation together with high-throughput sequencing to map binding sites of WUS and STM. I will integrate the data to construct functional network required for carrying out stem cell and meristematic cell fate. I will use loss- and gain- of function approach to study the role of WUS and STM-binding in regulating expression and function of their targets'
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