Neuronal connexin-36 can functionally replace connexin-45 in mouse retina but not in the developing heart

Marina Frank, Britta Eiberger, Ulrike Janssen-Bienhold, Luis Pérez De Sevilla Müller, Antje Tjarks, Jung Sun Kim, Stefan Maschke, Radoslaw Dobrowolski, Philipp Sasse, Reto Weiler, Bernd K. Fleischmann, Klaus Willecke

Research output: Contribution to journalArticlepeer-review

20 Scopus citations

Abstract

The gap junction protein connexin-45 (Cx45) is expressed in the conduction system of the heart and in certain neurons of the retina and brain. General and cardiomyocyte-directed deficiencies of Cx45 in mice lead to lethality on embryonic day 10.5 as a result of cardiovascular defects. Neuron-directed deletion of Cx45 leads to defects in transmission of visual signals. Connexin-36 (Cx36) is co-expressed with Cx45 in certain types of retinal interneurons. To determine whether these two connexins have similar functions and whether Cx36 can compensate for Cx45, we generated knock-in mice in which DNA encoding Cx45 was replaced with that encoding Cx36. Neuron-directed replacement of Cx45 with Cx36 resulted in viable animals. Electroretinographic and neurotransmitter coupling analyses demonstrated functional compensation in the retina. By contrast, general and cardiomyocyte-directed gene replacement led to lethality on embryonic day 11.5. Mutant embryos displayed defects in cardiac morphogenesis and conduction. Thus, functional compensation of Cx45 by Cx36 did not occur during embryonic heart development. These data suggest that Cx45 and Cx36 have similar functions in the retina, whereas Cx45 fulfills special functions in the developing heart that cannot be compensated by Cx36.

Original languageEnglish (US)
Pages (from-to)3605-3615
Number of pages11
JournalJournal of cell science
Volume123
Issue number20
DOIs
StatePublished - Oct 15 2010

Keywords

  • Connexin-36
  • Connexin-45
  • Embryonic heart
  • Knock-in mice
  • Retina
  • Rod-cone pathway

ASJC Scopus subject areas

  • Cell Biology

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