Abstract：
CONCLUSIONS: BIG regulates ground tissue formative divisions by bridging the auxin gradient with SHR abundance in Arabidopsis roots. The formative divisions of cortex/endodermis initials (CEIs) and CEI daughter cells (CEIDs) in Arabidopsis roots are coordinately controlled by the longitudinal auxin gradient and the radial SHORT ROOT (SHR) abundance. However, the mechanism underlying this coordination remains poorly understood. In this study, we demonstrate that BIG regulates ground tissue formative divisions by bridging the auxin gradient with SHR abundance. Mutations in BIG gene repressed cell cycle progression, delaying the formative divisions within the ground tissues and impairing the establishment of endodermal and cortical identities. In addition, we uncovered auxin\'s suppressive effect on BIG expression, triggering CYCLIND6;1 (CYCD6;1) activation in an SHR-dependent fashion. Moreover, the degradation of RETINOBLASTOMA-RELATED (RBR) is jointly regulated by BIG and CYCD6;1. The loss of BIG function led to RBR protein accumulation, detrimentally impacting the SHR/SCARECROW (SCR) protein complex and the CEI/CEID formative divisions. Collectively, these findings shed light on a fundamental mechanism wherein BIG intricately coordinates the interplay between SHR/SCR and auxin, steering ground tissue patterning within Arabidopsis root tissue.
摘要：
结论：BIG通过桥接拟南芥根中生长素梯度与SHR丰度来调节地面组织形成分裂。拟南芥根中皮质/内胚层缩写（CEI）和CEI子细胞（CEID）的形成分裂受纵向生长素梯度和径向短根（SHR）丰度的协调控制。然而,这种协调背后的机制仍然知之甚少。在这项研究中,我们证明BIG通过桥接生长素梯度与SHR丰度来调节地面组织形成性分裂。BIG基因突变抑制细胞周期进程，延迟地面组织内的形成分裂，并损害内胚层和皮质身份的建立。此外,我们发现生长素对BIG表达的抑制作用，以SHR依赖性方式触发CYCLIND6;1（CYCD6;1）激活。此外，视网膜母细胞瘤相关(RBR)的降解受BIG和CYCD6共同调控;1.BIG功能的丧失导致RBR蛋白积累，不利地影响SHR/SCARECROW(SCR)蛋白复合物和CEI/CEID形成分裂。总的来说，这些发现揭示了一个基本机制，其中BIG错综复杂地协调SHR/SCR和生长素之间的相互作用，转向拟南芥根组织内的地面组织图案。
