The receptor-like kinase SOL2 mediates CLE signaling in Arabidopsis.
Ontology highlight
ABSTRACT:
SUBMITTER: Miwa H
PROVIDER: S-EPMC2582179 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:Cell division is often regulated by extracellular signaling networks to ensure correct patterning during development. In Arabidopsis, the SHORT-ROOT (SHR)/SCARECROW (SCR) transcription factor dimer activates CYCLIND6;1 (CYCD6;1) to drive formative divisions during root ground tissue development. Here, we show plasma-membrane-localized BARELY ANY MERISTEM1/2 (BAM1/2) family receptor kinases are required for SHR-dependent formative divisions and CYCD6;1 expression, but not SHR-dependent ground tissue specification. Root-enriched CLE ligands bind the BAM1 extracellular domain and are necessary and sufficient to activate SHR-mediated divisions and CYCD6;1 expression. Correspondingly, BAM-CLE signaling contributes to the restriction of formative divisions to the distal root region. Additionally, genetic analysis reveals that BAM-CLE and SHR converge to regulate additional cell divisions outside of the ground tissues. Our work identifies an extracellular signaling pathway regulating formative root divisions and provides a framework to explore this pathway in patterning and evolution.
| S-EPMC7768756 | biostudies-literature
Project description:CLAVATA3/EMBRYO SURROUNDING REGION (CLE) peptides are secreted endogenous plant ligands that are sensed by receptor kinases (RKs) to convey environmental and developmental inputs. Typically, this involves an RK with narrow ligand specificity that signals together with a more promiscuous co-receptor. For most CLEs, biologically relevant (co-)receptors are unknown. The dimer of the receptor-like protein CLAVATA 2 (CLV2) and the pseudokinase CORYNE (CRN) conditions perception of so-called root-active CLE peptides, the exogenous application of which suppresses root growth by preventing protophloem formation in the meristem. clv2 as well as crn null mutants are resistant to root-active CLE peptides, possibly because CLV2-CRN promotes expression of their cognate receptors. Here, we have identified the CLE-RESISTANT RECEPTOR KINASE (CLERK) gene, which is required for full sensing of root-active CLE peptides in early developing protophloem. CLERK protein can be replaced by its close homologs, SENESCENCE-ASSOCIATED RECEPTOR-LIKE KINASE (SARK) and NSP-INTERACTING KINASE 1 (NIK1). Yet neither CLERK nor NIK1 ectodomains interact biochemically with described CLE receptor ectodomains. Consistently, CLERK also acts genetically independently of CLV2-CRN We, thus, have discovered a novel hub for redundant CLE sensing in the root.
| S-EPMC6001375 | biostudies-literature
Project description:CLAVATA1 (CLV1), CLV2, CLV3, CORYNE (CRN), BAM1 and BAM2 are key regulators that function at the shoot apical meristem (SAM) of plants to promote differentiation by limiting the size of the organizing center that maintains stem cell identity in neighboring cells. Previous results have indicated that the extracellular domain of the receptor kinase CLV1 binds to the CLV3-derived CLE ligand. The biochemical role of the receptor-like protein CLV2 has remained largely unknown. Although genetic analysis suggested that CLV2, together with the membrane kinase CRN, acts in parallel with CLV1, recent studies using transient expression indicated that CLV2 and CRN from a complex with CLV1. Here, we report detection of distinct CLV2-CRN heteromultimeric and CLV1-BAM multimeric complexes in transient expression in tobacco and in Arabidopsis meristems. Weaker interactions between the two complexes were detectable in transient expression. We also find that CLV2 alone generates a membrane-localized CLE binding activity independent of CLV1. CLV2, CLV1 and the CLV1 homologs BAM1 and BAM2 all bind to the CLV3-derived CLE peptide with similar kinetics, but BAM receptors show a broader range of interactions with different CLE peptides. Finally, we show that BAM and CLV1 overexpression can compensate for the loss of CLV2 function in vivo. These results suggest two parallel ligand-binding receptor complexes controlling stem cell specification in Arabidopsis.
| S-EPMC2974754 | biostudies-literature
Project description:Appropriate flowering time is critical for the reproductive success of plant species. Emerging evidence indicates that calcium may play an important role in the regulation of flowering time. However, the underlying molecular mechanisms remain unclear. In this study, we demonstrate that calcium-dependent protein kinase 32 (CPK32) regulates flowering time by affecting the alternative polyadenylation of FLOWERING CONTROL LOCUS A (FCA) and altering the transcription of FLOWERING LOCUS C (FLC), a central repressor of flowering time. The knockdown of CPK32 results in an obvious late flowering phenotype and dramatically enhanced FLC transcription. CPK32 interacts with FCA, and phosphorylates the serine592 of FCA in a Ca2+-dependent manner. Moreover, the ratio of abundance of the FCA transcripts (FCA-D and FCA-P) changes significantly in the cpk32 mutant, which subsequently affects FLC expression and consequently regulates floral transition. The present evidence demonstrates that CPK32 modulates flowering time by regulating FCA alternative polyadenylation and consequent FLC expression.
| S-EPMC8783668 | biostudies-literature
Project description:Pattern recognition receptors (PRRs) sense microbial patterns and activate innate immunity against attempted microbial invasions. The leucine-rich repeat receptor kinases (LRR-RK) FLS2 and EFR, and the LRR receptor protein (LRR-RP) receptors RLP23 and RLP42, respectively, represent prototypical members of these two prominent and closely related PRR families. We conducted a survey of Arabidopsis thaliana immune signaling mediated by these receptors to address the question of commonalities and differences between LRR-RK and LRR-RP signaling. Quantitative differences in timing and amplitude were observed for several early immune responses, with RP-mediated responses typically being slower and more prolonged than those mediated by RKs. Activation of RLP23, but not FLS2, induced the production of camalexin. Transcriptomic analysis revealed that RLP23-regulated genes represent only a fraction of those genes differentially expressed upon FLS2 activation. Several positive and negative regulators of FLS2-signaling play similar roles in RLP23 signaling. Intriguingly, the cytoplasmic receptor kinase BIK1, a positive regulator of RK signaling, acts as a negative regulator of RP-type immune receptors in a manner dependent on BIK1 kinase activity. Our study unveiled unexpected differences in two closely related receptor systems and reports a new negative role of BIK1 in plant immunity.
| S-EPMC6367016 | biostudies-literature
Project description:Tyrosine kinase receptors represent targets of great interest for cancer therapy. Here we show, for the first time, the importance of the orphan tyrosine kinase receptor, ROR2, in melanoma progression. Using melanoma tissue microarrays, we show that ROR2 is expressed predominantly in metastatic melanoma. As ROR2 has been shown to specifically interact with the non-canonical Wnt ligand, Wnt5A, this corroborates our earlier data implicating Wnt5A as a mediator of melanoma metastasis. We show here that increases in Wnt5A cause increases in ROR2 expression, as well as the PKC-dependent, clathrin-mediated internalization of ROR2. WNT5A knockdown by siRNA decreases ROR2 expression, but silencing of ROR2 has no effect on WNT5A levels. ROR2 knockdown does, however, result in a decrease in signaling downstream of Wnt5A. Using in vitro and in vivo metastasis assays, we show that ROR2 is necessary for the Wnt5A-mediated metastasis of melanoma cells. These data imply that ROR2 may represent a novel target for melanoma therapy.
| S-EPMC2803338 | biostudies-literature
Project description:Smad proteins are critical intracellular mediators of signaling by growth and differentiation factors of the transforming growth factor beta superfamily. We have isolated a member of the Smad family, Smad8, from a rat brain cDNA library and biochemically and functionally characterized its ability to transduce signals from serine kinase receptors. In Xenopus embryo, Smad8 is able to transcriptionally activate a subset of mesoderm target genes similar to those induced by the receptor serine kinase, activin receptor-like kinase (ALK)-2. Smad8 can be specifically phosphorylated by a constitutively active ALK-2 but not the related receptor serine kinase, ALK-4. In response to signaling from ALK-2, Smad8 associates with a common regulatory molecule, Smad4, and this association leads to a synergistic effect on gene transcription. Furthermore, Smad8 is able to rescue the expression of mesoderm genes blocked by truncated ALK-2 in the embryo. These results indicate that Smad8 can function as a downstream signaling mediator of ALK-2.
| S-EPMC24242 | biostudies-literature
Project description:The shoot apical meristem is maintained by the intercellular factor, CLV3, a dodecapeptide in Arabidopsis. CLV3 belongs to the CLE family and putative CLE genes have been found in various plants, even in the moss Physcomitrella patens. Here, we report that a pteridophyte, Selaginella moelendorffii, also has 15 putative CLE genes in its genome. On the other hand, CLV1 is reported to function as a receptor for the CLV3 peptide, and other CLE peptides might be recognized by CLV1 homologues in various plants. Recent genetic studies of the crn and sol2 mutants of Arabidopsis have revealed that SOL2/CRN encodes a receptor-like kinase protein. SOL2/CRN functions together with CLV2 independently of CLV1 in the CLE signaling pathway. Phylogenetic analysis of CLV1, CLV2 and SOL2/CRN revealed that Arabidopsis, rice, Populus trichocarpa and Vitis vinifera have one copy of the SOL2/CRN and CLV2 homologues, and Selaginella moelendorffii and Physcomitrella patens have no homologues. In contrast, a number of CLV1 homologues were identified in the genomic databases of Arabidopsis, rice, Populus trichocarpa, Vitis vinifera, and even a pteridophyte, Selaginella moelendorffii, and a moss, Physcomitrella patens. These results indicate that CLV1 and its homologues play multiple roles in plant development and environmental responses, whereas SOL2/CRN and CLV2 have more specific roles in vascular plants.
| S-EPMC2688290 | biostudies-literature
Project description:Shoot apical meristem is a well organized undifferentiated tissue which produces plant body. CLV3 peptide hormone regulates SAM homeostasis, and is perceived by several receptor complexes, CLV1, CLV2-SOL2/CRN, and RPK2. CLV1 homologues are encoded in various plants genome. However CLV2 and SOL2/CRN homologues are found only in higher plants. Here we show that the RPK2 homologues were found not only in moss, Physcomitrella patens, but also in liverwort, Marchantia polymorpha. Although CLV2-SOL2/CRN might have specific function in SAM homeostasis, CLV1 and RPK2 may regulate various plant physiological events during plant evolution.
| S-EPMC3122013 | biostudies-literature
Project description:Chondrosarcomas are primary cancers of cartilaginous tissue and capable of alteration to highly aggressive, metastatic, and treatment-refractory states, leading to a poor prognosis with a five-year survival rate at 11 months for dedifferentiated subtype. At present, the surgical resection of chondrosarcoma is the only effective treatment, and no other treatment options including targeted therapies, conventional chemotherapies, or immunotherapies are available for these patients. Here, we identify a signal pathway way involving EZH2/SULF1/cMET axis that contributes to malignancy of chondrosarcoma and provides a potential therapeutic option for the disease. A non-biased chromatin immunoprecipitation sequence, cDNA microarray analysis, and validation of chondrosarcoma cell lines identified sulfatase 1 (SULF1) as the top EZH2-targeted gene to regulate chondrosarcoma progression. Overexpressed EZH2 resulted in downregulation of SULF1 in chondrosarcoma cell lines, which in turn activated cMET pathway. Pharmaceutical inhibition of cMET or genetically silenced cMET pathway significantly retards the chondrosarcoma growth and extends mice survival. The regulation of EZH2/SULF1/cMET axis were further validated in patient samples with chondrosarcoma. The results not only established a signal pathway promoting malignancy of chondrosarcoma but also provided a therapeutic potential for further development of effective target therapy to treat chondrosarcoma.
| S-EPMC9829410 | biostudies-literature