Literature DB >> 30448479

Phosphorylation of Cx43 residue Y313 by Src contributes to blocking the interaction with Drebrin and disassembling gap junctions.

Li Zheng1, Hanjun Li1, Andrew Cannon1, Andrew J Trease1, Gaelle Spagnol1, Hong Zheng2, Stanley Radio3, Kaushik Patel2, Surinder Batra1, Paul L Sorgen4.   

Abstract

Phosphorylation regulates connexin43 (Cx43) function from assembly/disassembly to coupling at the plaque. Src is a tyrosine kinase known to both phosphorylate Cx43 (residues Y247 and Y265) and affect gap junction intercellular communication. However, the Cx43 carboxyl-terminal (CT) domain contains additional tyrosine residues and proteomic discovery mass spectrometry data identified Y313 as a potential phosphorylation target. Based upon the study of Lin et al. (2001) J. Cell Biol., which still observed tyrosine phosphorylation by Src when using a Cx43 Y247/Y265F mutant, we addressed the possibility of Y313 phosphorylation (pY313) by Src. In vitro Src phosphorylation of purified Cx43CT followed by mass spectroscopy revealed that Src also phosphorylates Y313. This observation was confirmed by repeating the in vitro phosphorylation using different combinations of Cx43CT Y → F mutants and a general anti-pTyr antibody. Next, a phospho-specific antibody was generated to help characterize the importance of pY313. We established an in cyto experimental system by stably expressing Cx43 WT and mutants (Y247F, Y265F, Y313F, Y247/265F, Y247/313F, Y265/313F, or Y247/265/313F) in Cx43-deficient HeLa cells. Cx43 WT and mutants, in the absence of v-Src, localized to the plasma membrane and formed gap junctions. When v-Src was over-expressed, Cx43 WT localized intracellularly, while all of the single and double mutants remained able to form plaques and transfer dye, albeit variable in number and amount, respectively. Complete Src-resistance was only achieved with the Cx43 Y247/265/313F mutant. Furthermore, Cx43 Y265F inhibited the ability of v-Src to phosphorylate Y247 and Y313 as well as phosphorylation at both Y265 and Y313 was necessary to inhibit the Cx43 interaction with Drebrin. Finally, we observed in diseased cardiac tissue, in which Src is active, an increase in intercalated disc and intracellular localized Cx43 pY313.
Copyright © 2018 Elsevier Ltd. All rights reserved.

Entities:  

Keywords:  Connexin43; Drebrin; Gap junctions; Intercellular communication; Phosphorylation; Src

Mesh:

Substances:

Year:  2018        PMID: 30448479      PMCID: PMC8961861          DOI: 10.1016/j.yjmcc.2018.11.008

Source DB:  PubMed          Journal:  J Mol Cell Cardiol        ISSN: 0022-2828            Impact factor:   5.000


  56 in total

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Authors:  C D Cooper; J L Solan; M K Dolejsi; P D Lampe
Journal:  Methods       Date:  2000-02       Impact factor: 3.608

Review 2.  Structural basis for the selective permeability of channels made of communicating junction proteins.

Authors:  Jose F Ek-Vitorin; Janis M Burt
Journal:  Biochim Biophys Acta       Date:  2012-02-10

3.  TC-PTP directly interacts with connexin43 to regulate gap junction intercellular communication.

Authors:  Hanjun Li; Gaelle Spagnol; Naava Naslavsky; Steve Caplan; Paul L Sorgen
Journal:  J Cell Sci       Date:  2014-05-20       Impact factor: 5.285

Review 4.  Specific Cx43 phosphorylation events regulate gap junction turnover in vivo.

Authors:  Joell L Solan; Paul D Lampe
Journal:  FEBS Lett       Date:  2014-02-04       Impact factor: 4.124

5.  Connexin 43, angiotensin II, endothelin 1, and type III collagen alterations in heart of rats having undergone fatal electrocution.

Authors:  Quan-Yong Huang; Yu-Chuan Chen; Shui-Ping Liu
Journal:  Am J Forensic Med Pathol       Date:  2012-09       Impact factor: 0.921

6.  GJA1-20k Arranges Actin to Guide Cx43 Delivery to Cardiac Intercalated Discs.

Authors:  Wassim A Basheer; Shaohua Xiao; Irina Epifantseva; Ying Fu; Andre G Kleber; TingTing Hong; Robin M Shaw
Journal:  Circ Res       Date:  2017-09-18       Impact factor: 17.367

Review 7.  Gap junctions: structure and function (Review).

Authors:  W Howard Evans; Patricia E M Martin
Journal:  Mol Membr Biol       Date:  2002 Apr-Jun       Impact factor: 2.857

Review 8.  The effects of connexin phosphorylation on gap junctional communication.

Authors:  Paul D Lampe; Alan F Lau
Journal:  Int J Biochem Cell Biol       Date:  2004-07       Impact factor: 5.085

9.  v-Src-mediated phosphorylation of connexin43 on tyrosine disrupts gap junctional communication in mammalian cells.

Authors:  R Lin; B J Warn-Cramer; W E Kurata; A F Lau
Journal:  Cell Commun Adhes       Date:  2001

10.  Differential phosphorylation of the gap junction protein connexin43 in junctional communication-competent and -deficient cell lines.

Authors:  L S Musil; B A Cunningham; G M Edelman; D A Goodenough
Journal:  J Cell Biol       Date:  1990-11       Impact factor: 10.539

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  6 in total

1.  [SRC kinase inhibitor PP2 inhibits invasion and metastasis of lung cancer A549 cells by upregulating connexin43 expression].

Authors:  Daoxin Wang; Yaming Liu; Wanchen Zhao; Ru Wang; Xuhui Tong; Guojun Jiang
Journal:  Nan Fang Yi Ke Da Xue Xue Bao       Date:  2019-07-30

Review 2.  Recent advances in connexin gap junction biology.

Authors:  Paul D Lampe; Dale W Laird
Journal:  Fac Rev       Date:  2022-05-27

Review 3.  The Structural and the Functional Aspects of Intercellular Communication in iPSC-Cardiomyocytes.

Authors:  Eva Kiss; Carolin Fischer; Jan-Mischa Sauter; Jinmeng Sun; Nina D Ullrich
Journal:  Int J Mol Sci       Date:  2022-04-18       Impact factor: 6.208

4.  Src Regulation of Cx43 Phosphorylation and Gap Junction Turnover.

Authors:  Joell L Solan; Paul D Lampe
Journal:  Biomolecules       Date:  2020-11-24

Review 5.  Connexins-Therapeutic Targets in Cancers.

Authors:  Magdalena Nalewajska; Małgorzata Marchelek-Myśliwiec; Martyna Opara-Bajerowicz; Violetta Dziedziejko; Andrzej Pawlik
Journal:  Int J Mol Sci       Date:  2020-11-30       Impact factor: 5.923

6.  Calmodulin Directly Interacts with the Cx43 Carboxyl-Terminus and Cytoplasmic Loop Containing Three ODDD-Linked Mutants (M147T, R148Q, and T154A) that Retain α-Helical Structure, but Exhibit Loss-of-Function and Cellular Trafficking Defects.

Authors:  Li Zheng; Sylvie Chenavas; Fabien Kieken; Andrew Trease; Sarah Brownell; Asokan Anbanandam; Paul L Sorgen; Gaelle Spagnol
Journal:  Biomolecules       Date:  2020-10-17
  6 in total

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