Patterned cell wall deposition is crucial for cell shapes and functions. In Arabidopsis xylem vessels, ROP11 GTPase locally inhibits cell wall deposition through microtubule disassembly, inducing pits in cell walls. Here, we show that an additional ROP signaling pathway promotes cell wall growth at pit boundaries. Two proteins, Boundary of ROP domain1 (BDR1) and Wallin (WAL), localize to pit boundaries and regulate cell wall growth. WAL interacts with F-actin and promotes actin assembly at pit boundaries while BDR1 is a ROP effector. BDR1 interacts with WAL, suggesting that WAL could be recruited to the plasma membrane by a ROP-dependent mechanism. These results demonstrate that BDR1 and WAL mediate a ROP-actin pathway that shapes pit boundaries. The study reveals a distinct machinery in which two closely associated ROP pathways oppositely regulate cell wall deposition patterns for the establishment of tiny but highly specialized cell wall domains.

图案化的细胞壁沉积对于细胞形状和功能至关重要。在拟南芥木质部的血管中，ROP11 GTPase通过微管拆卸局部抑制细胞壁沉积，从而在细胞壁上产生凹坑。在这里，我们显示了一个额外的ROP信号通路可促进细胞壁在凹坑边界处的生长。ROP domain1的边界（BDR1）和Wallin（WAL）的两种蛋白质定位于坑边界并调节细胞壁的生长。当BDR1是ROP效应子时，WAL与F-肌动蛋白相互作用并促进在核边界处的肌动蛋白组装。BDR1与WAL相互作用，表明WAL可以通过ROP依赖性机制募集到质膜。这些结果表明，BDR1和WAL介导了形成凹坑边界的ROP-肌动蛋白途径。