A catenin of the plakophilin-subfamily, Pkp3, responds to canonical-Wnt pathway components and signals.

Desmosomal junction Desmosome junction Destruction complex Nucleus Pkp-3 Plakophilin-3 catenin Signaling pool Wnt signaling pathway plakophilin3-catenin

Journal

Biochemical and biophysical research communications
ISSN: 1090-2104
Titre abrégé: Biochem Biophys Res Commun
Pays: United States
ID NLM: 0372516

Informations de publication

Date de publication:
23 07 2021
Historique:
received: 12 05 2021
accepted: 13 05 2021
pubmed: 1 6 2021
medline: 12 11 2021
entrez: 31 5 2021
Statut: ppublish

Résumé

Vertebrate beta-catenin plays a key role as a transducer of canonical-Wnt signals. We earlier reported that, similar to beta-catenin, the cytoplasmic signaling pool of p120-catenin-isoform1 is stabilized in response to canonical-Wnt signals. To obtain a yet broader view of the Wnt-pathway's impact upon catenin proteins, we focused upon plakophilin3 (plakophilin-3; Pkp3) as a representative of the plakophilin-catenin subfamily. Promoting tissue integrity, the plakophilins assist in linking desmosomal cadherins to intermediate filaments at desmosome junctions, and in common with other catenins they perform additional functions including in the nucleus. In this report, we test whether canonical-Wnt pathway components modulate Pkp3 protein levels. We find that in common with beta-catenin and p120-catenin-isoform1, Pkp3 is stabilized in the presence of a Wnt-ligand or a dominant-active form of the LRP6 receptor. Pkp3's levels are conversely lowered upon expressing destruction-complex components such as GSK3β and Axin, and in further likeness to beta-catenin and p120-isoform1, Pkp3 associates with GSK3beta and Axin. Finally, we note that Pkp3-catenin trans-localizes into the nucleus in response to Wnt-ligand and its exogenous expression stimulates an accepted Wnt reporter. These findings fit an expanded model where context-dependent Wnt-signals or pathway components modulate Pkp3-catenin levels. Future studies will be needed to assess potential gene regulatory, cell adhesive, or cytoskeletal effects.

Identifiants

pubmed: 34058472
pii: S0006-291X(21)00814-7
doi: 10.1016/j.bbrc.2021.05.043
pmc: PMC8252864
mid: NIHMS1709723
pii:
doi:

Substances chimiques

PKP3 protein, human 0
Plakophilins 0

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

31-39

Subventions

Organisme : NIMH NIH HHS
ID : R01 MH115717
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA016672
Pays : United States
Organisme : NIDDK NIH HHS
ID : K01 DK092320
Pays : United States
Organisme : NIDDK NIH HHS
ID : R03 DK118771
Pays : United States
Organisme : NIGMS NIH HHS
ID : R01 GM107079
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK115655
Pays : United States
Organisme : NIH HHS
ID : S10 OD024976
Pays : United States

Informations de copyright

Copyright © 2021 Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors have no conflict of interests to report.

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Auteurs

Ji Yeon Hong (JY)

Severance Biomedical Science Institute, Yonsei University College of Medicine, 50 Yonsei-ro, Seodaemun-gu, Seoul, 03722, Republic of Korea. Electronic address: mire1390@gmail.com.

Jessica Zapata (J)

Department of Genetics, University of Texas MD Anderson Cancer Center, Houston TX, 77030, USA.

Alexandria Blackburn (A)

Department of Pediatrics, McGovern Medical School, The University of Texas Health Science Center, Houston TX, 77030, USA; University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences, Houston TX, 77030, USA.

Ryan Baumert (R)

Department of Genetics, University of Texas MD Anderson Cancer Center, Houston TX, 77030, USA; University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences, Houston TX, 77030, USA.

Seung Min Bae (SM)

Department of Psychiatry, Gachon University Gil Medical Center, Gachon College of Medicine, 774 Bun-gil, Namdongdae-ro, Namdong-gu, Incheon, 21565, Republic of Korea.

Hong Ji (H)

Department of Genetics, University of Texas MD Anderson Cancer Center, Houston TX, 77030, USA.

Hee Jin Nam (HJ)

Department of Plastic and Reconstructive Surgery, Seoul National University College of Medicine, 101 Daehak-ro, Jongno-gu, Seoul, 03080, Republic of Korea.

Rachel K Miller (RK)

Department of Genetics, University of Texas MD Anderson Cancer Center, Houston TX, 77030, USA; Department of Pediatrics, McGovern Medical School, The University of Texas Health Science Center, Houston TX, 77030, USA; University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences, Houston TX, 77030, USA.

Pierre D McCrea (PD)

Department of Genetics, University of Texas MD Anderson Cancer Center, Houston TX, 77030, USA; University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences, Houston TX, 77030, USA. Electronic address: pdmccrea@mdanderson.org.

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Classifications MeSH