Ministry of Education Key Laboratory of Cell Activities and Stress Adaptations, School of Life Sciences, Lanzhou University, Lanzhou 730000, China.
School of Life Sciences, Guangzhou University, Guangzhou 510006, China.
Plant Cell. 2022 Mar 29;34(4):1289-1307. doi: 10.1093/plcell/koab315.
Shoot apical meristem (SAM) and root apical meristem (RAM) homeostasis is tightly regulated by CLAVATA3 (CLV3)/EMBRYO SURROUNDING REGION-related (CLE) peptide signaling. However, the intracellular signaling components after CLV3 is perceived by the CLV1-CLV3-INSENSITIVE KINASE (CIK) receptor complex and CLE25/26/45 are sensed by the BARELY ANY MERISTEM (BAM)-CIK receptor complex are unknown. Here, we report that PBS1-LIKE34/35/36 (PBL34/35/36), a clade of receptor-like cytoplasmic kinases, are required for both CLV3-mediated signaling in the SAM and CLE25/26/45-mediated signaling in the RAM. Physiological assays showed that the SAM and RAM of pbl34 pbl35 pbl36 were resistant to CLV3 and CLE25/26/45 treatment, respectively. Genetic analyses indicated that pbl34 pbl35 pbl36 greatly enhanced the SAM defects of clv2 and rpk2 but not clv1, and did not show additive effects with bam3 and cik2 in the RAM. Further biochemical assays revealed that PBL34/35/36 interacted with CLV1, BAM1/3, and CIKs, and were phosphorylated by CLV1 and BAM1. All these results suggest that PBL34/35/36 act downstream of CLV1 and BAM1/3 to mediate the CLV3 and CLE25/26/45 signals in maintaining SAM and RAM homeostasis, respectively. Our findings shed light on how CLE signals are transmitted intracellularly after being perceived by cell surface receptor complexes.
茎尖分生组织 (SAM) 和根端分生组织 (RAM) 的稳态由 CLAVATA3 (CLV3)/EMBRYO SURROUNDING REGION-related (CLE) 肽信号严格调控。然而,CLV3 被 CLV1-CLV3-INSENSITIVE KINASE (CIK) 受体复合物感知后,以及 CLE25/26/45 被 BARELY ANY MERISTEM (BAM)-CIK 受体复合物感知后的细胞内信号成分尚不清楚。在这里,我们报告 PBS1-LIKE34/35/36 (PBL34/35/36),一组受体样细胞质激酶,对于 SAM 中的 CLV3 介导的信号传导和 RAM 中的 CLE25/26/45 介导的信号传导都是必需的。生理测定表明,pbl34 pbl35 pbl36 的 SAM 和 RAM 分别对 CLV3 和 CLE25/26/45 处理具有抗性。遗传分析表明,pbl34 pbl35 pbl36 极大地增强了 clv2 和 rpk2 的 SAM 缺陷,但不是 clv1,并且在 RAM 中与 bam3 和 cik2 没有相加效应。进一步的生化测定表明,PBL34/35/36 与 CLV1、BAM1/3 和 CIKs 相互作用,并被 CLV1 和 BAM1 磷酸化。所有这些结果表明,PBL34/35/36 在 CLV1 和 BAM1/3 下游发挥作用,分别介导 CLV3 和 CLE25/26/45 信号,以维持 SAM 和 RAM 的稳态。我们的发现揭示了 CLE 信号在被细胞表面受体复合物感知后如何在细胞内传递。