背景回顾：Shoot apical meristem (SAM) and root apical meristem (RAM) homeostasis is tightly regulated by CLAVATA3 (CLV3)/EMBRYO SURROUNDING REGION (ESR)-related (CLE) peptide signaling.

提出问题：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. 

主要发现：Here, we report that PBS1-LIKE34/35/36 (PBL34/35/36), a clade of receptor-like cytoplasmic kinases (RLCKs), are required for both CLV3-mediated signaling in the SAM and CLE25/26/45-mediated signaling in the RAM. 

结果1-生理试验：Physiological assays showed that the SAM and RAM of pbl34 pbl35 pbl36 were resistant to CLV3 and CLE25/26/45 treatment, respectively. 

结果2-遗传试验：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. 

结果3-生化试验：Further biochemical assays revealed that PBL34/35/36 interacted with CLV1, BAM1/3, and CIKs, and were phosphorylated by CLV1 and BAM1. 

结论：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 maintainingSAM and RAM homeostasis, respectively. 

总结：Our findings shed light on how CLE signals are transmitted intracellularly after being perceived by cell surface receptor complexes.

 摘 要 

茎尖分生组织（SAM）和根尖分生组织（RAM）内稳态受到CLE多肽信号转导的严格调控。但是，CLV3被CLV1–CIK受体复合体感知以及CLE25/26/45被BAM-CIK受体复合体感知，接着下游的胞内信号转导组分还是未知的。本文中，作者报道了类受体胞质激酶PBL34/35/36对于SAM中CLV3介导的信号转导和RAM中CLE25/26/45介导的信号转导都是必需的。生理试验显示，pbl34 pbl35 pbl36突变体的SAM对于CLV3处理不敏感，RAM对于CLE25/26/45处理不敏感。遗传分析显示，pbl34 pbl35 pbl36突变极大地增强了clv2和rpk2突变体的缺陷，但是不会增强clv1的缺陷，同时并不会与bam3和cik2在RAM中表现出加性效应。进一步的生化试验显示，PBL34/35/36能够与CLV1、BAM1/3以及CIKs发生互作，并且会被CLV1和BAM1所磷酸化。这些结果表明PBL34/35/36作用于CLV1和BAM1/3的下游，介导CLV3和CLE25/26/45的信号转导，从而分别作用于SAM和RAM的内稳态。本文的发现揭示了CLE信号在被细胞表面受体复合体感知后，是如何在细胞内被传递的。