Receptor-like cytoplasmic kinases PBL34/35/36 are required for CLE peptide-mediated signaling to maintain shoot apical meristem and root apical meristem homeostasis in Arabidopsis

Author:

Wang Wenping1ORCID,Hu Chong1ORCID,Li Xiaonan1ORCID,Zhu Yafen1ORCID,Tao Liang1ORCID,Cui Yanwei1ORCID,Deng Dingqian1ORCID,Fan Xiaoxuan1ORCID,Zhang Hong1ORCID,Li Jia12ORCID,Gou Xiaoping1ORCID,Yi Jing1ORCID

Affiliation:

1. Ministry of Education Key Laboratory of Cell Activities and Stress Adaptations, School of Life Sciences, Lanzhou University, Lanzhou 730000, China

2. School of Life Sciences, Guangzhou University, Guangzhou 510006, China

Abstract

Abstract 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.

Funder

National Natural Science Foundation of China

111 Project

China Postdoctoral Science Foundation

Fundamental Research Funds for the Central Universities

Lanzhou City’s Scientific Research Funding Subsidy to Lanzhou University

Publisher

Oxford University Press (OUP)

Subject

Cell Biology,Plant Science

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