Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Connexin31 cannot functionally replace connexin43 during cardiac morphogenesis in mice.

Qingyi Zheng-Fischhöfer1, Alexander Ghanem, Jung-Sun Kim

  • 1Institut für Genetik, Universität Bonn, 53117 Bonn, Germany.

Journal of Cell Science
|February 2, 2006
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Lymphatic mimicry of spiral arteries is impaired by human sFLT1 overexpression in a preeclampsia mouse model.

Placenta·2025
Same author

Impact of initial rhythm, rhythm at hospital admission and cause of arrest on the outcome of extracorporeal cardiopulmonary resuscitation in out-of-hospital cardiac arrest.

The American journal of emergency medicine·2025
Same author

Percutaneous Valvular and Structural Heart Disease Interventions.2024 Core Curriculum of the European Association of Percutaneous Cardiovascular Interventions (EAPCI) of the ESC in collaboration with the European Association of Cardiovascular Imaging (EACVI) and the Cardiovascular Surgery Working Group (WG CVS) of the European Society of Cardiology.

EuroIntervention : journal of EuroPCR in collaboration with the Working Group on Interventional Cardiology of the European Society of Cardiology·2024
Same author

Percutaneous Valvular and Structural Heart Disease Interventions. 2024 Core Curriculum of the European Association of Percutaneous Cardiovascular Interventions (EAPCI) of the ESC in collaboration with the European Association of Cardiovascular Imaging (EACVI) and the Cardiovascular Surgery Working Group (WG CVS) of the European Society of Cardiology.

EuroIntervention : journal of EuroPCR in collaboration with the Working Group on Interventional Cardiology of the European Society of Cardiology·2024
Same author

Self-management for physicians: an interview with Professor Alexander Ghanem.

European heart journal. Acute cardiovascular care·2024
Same author

Overexpression of Human sFLT1 in the Spongiotrophoblast Is Sufficient to Induce Placental Dysfunction and Fetal Growth Restriction in Transgenic Mice.

International journal of molecular sciences·2024
Same journal

Establishing MS2-MCP-based single-molecule RNA visualization in Schizosaccharomyces pombe.

Journal of cell science·2026
Same journal

LGI1-ADAM22 complex organizes PSD93 clustering at the axon initial segment.

Journal of cell science·2026
Same journal

Potential role of myeloid bodies in protection against photo-oxidative damage of the retinal pigment epithelium.

Journal of cell science·2026
Same journal

From the FAZ to the TAC: Widespread cytoskeletal engagement of T. brucei KMP11.

Journal of cell science·2026
Same journal

Branched actin segregates endocytic cargo to control sorting and fission.

Journal of cell science·2026
Same journal

FAM122A inhibition of PP2A-B55 through a bipartite binding mechanism.

Journal of cell science·2026
See all related articles

Connexin43 and connexin31 incompatibility does not affect embryonic development. However, connexin31 cannot replace connexin43 in heart development, leading to cardiac malformations in knock-in mice.

Area of Science:

  • Developmental Biology
  • Cell Biology
  • Genetics

Background:

  • Connexin43 (Cx43) and connexin31 (Cx31) are gap junction proteins with distinct expression patterns during mouse embryonic development.
  • Previous studies suggested Cx43 and Cx31 incompatibility might segregate embryonic and extraembryonic tissues.

Purpose of the Study:

  • To investigate the functional consequences of replacing connexin43 with connexin31 during mouse embryonic development.
  • To determine if connexin31 can functionally substitute for connexin43 in cardiac morphogenesis.

Main Methods:

  • Generation of connexin43 knock-in connexin31 mice, where the Cx43 gene's coding region is replaced by Cx31.
  • Analysis of embryonic development, survival rates, and cardiac morphology and function in homozygous knock-in mice.

Related Experiment Videos

Main Results:

  • Homozygous connexin43 knock-in connexin31 mice were born at expected Mendelian frequencies but did not survive to adulthood.
  • Neonatal homozygous knock-in mouse hearts exhibited malformations in the right ventricle and significantly low QRS complex voltage on electrocardiograms.
  • These cardiac defects were similar to connexin43-deficient mice, unlike hearts where Cx43 was replaced by connexin40.

Conclusions:

  • The incompatibility of connexin43 and connexin31 does not impede overall embryonic development.
  • Connexin31 cannot functionally replace connexin43 during cardiac morphogenesis, leading to severe heart defects.
  • Gap junction protein function is critical for normal heart development and requires specific connexin types.