Author/Authors :
Alfredo Cruz-Ramirez، نويسنده , , Sara D?az-Trivi?o، نويسنده , , Ikram Blilou، نويسنده , , Verônica A. Grieneisen، نويسنده , , Rosangela Sozzani، نويسنده , , Christos Zamioudis، نويسنده , , P?l Miskolczi، نويسنده , , Jeroen Nieuwland، نويسنده , , René Benjamins، نويسنده , , Pankaj Dhonukshe، نويسنده , , Juan Caballero-Pérez، نويسنده , , Beatrix Horvath، نويسنده , , Yuchen Long، نويسنده , , Ari Pekka M?h?nen، نويسنده , , Hongtao Zhang، نويسنده , , Jian Xu، نويسنده , , James AH Murray، نويسنده , , Philip N. Benfey، نويسنده , , Laszlo Bako، نويسنده , , Athanasius F.M. Marée، نويسنده , , et al.، نويسنده ,
Abstract :
In plants, where cells cannot migrate, asymmetric cell divisions (ACDs) must be confined to the appropriate spatial context. We investigate tissue-generating asymmetric divisions in a stem cell daughter within the Arabidopsis root. Spatial restriction of these divisions requires physical binding of the stem cell regulator SCARECROW (SCR) by the RETINOBLASTOMA-RELATED (RBR) protein. In the stem cell niche, SCR activity is counteracted by phosphorylation of RBR through a cyclinD6;1-CDK complex. This cyclin is itself under transcriptional control of SCR and its partner SHORT ROOT (SHR), creating a robust bistable circuit with either high or low SHR-SCR complex activity. Auxin biases this circuit by promoting CYCD6;1 transcription. Mathematical modeling shows that ACDs are only switched on after integration of radial and longitudinal information, determined by SHR and auxin distribution, respectively. Coupling of cell-cycle progression to protein degradation resets the circuit, resulting in a “flip flop” that constrains asymmetric cell division to the stem cell region.
