Control of plant cell fate transitions by transcriptional and hormonal signals

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The aim of our computational modeling is twofold. First, we seek to understand the relative contribution of cell proliferation, fate transition and respecification in mediating the pCLV3:HEC1-GR phenotype. We use the model to check which hypothetical scenarios are compatible with our experimental observations. Second, we aim to get insights into the hec1,2,3 phenotype which admits only limited experimental manipulations. Taking into account the functions of HEC derived from experiments and simulations of HEC-gain-offunction scenarios, we use the model to conclude how changes in cell proliferation, fate transition and respecification might contribute to the hec1,2,3 mutant phenotype.

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تاریخ انتشار 2017