Connexin45 provides optimal atrioventricular nodal conduction in the adult mouse heart.

Rationale: The gap junctional protein connexin (Cx) 45 is strongly expressed in the early embryonic myocardium. In the adult hearts of mice and humans, the expression mainly is restricted to the cardiac conduction system. Cx45 plays an essential role for development and function of the embryonic heart because general and cardiomyocyte-directed deficiencies of Cx45 in mice lead to embryonic lethality attributable to morphological and functional cardiovascular defects.

Expression and modulation of connexin 30.2, a novel gap junction protein in the mouse retina.

Mammalian retinae express multiple connexins that mediate the metabolic and electrical coupling of various cell types. In retinal neurons, only connexin 36, connexin 45, connexin 50, and connexin 57 have been described so far. Here, we present an analysis of a novel retinal connexin, connexin 30.

C-terminal tagging with eGFP yields new insights into expression of connexin45 but prevents rescue of embryonic lethal connexin45-deficient mice.

Connexin45 (Cx45) is a member of the connexin family which can form gap junction channels and is known to be expressed in several cell types in the embryonic as well as adult mouse including working cardiomyocytes and certain types of neurons. Until now its subcellular localization could not be unequivocally determined in certain tissues due to the lack of sensitive and specific antibodies. In order to investigate the localization of Cx45, we have generated a transgenic mouse expressing a fusion protein composed of Cx45 and eGFP under control of the endogenous Cx45 promoter using a bacterial artificial chromosome (BAC).

Normal impulse propagation in the atrioventricular conduction system of Cx30.2/Cx40 double deficient mice.

Connexin (Cx) 30.2, Cx40 and Cx45 containing gap junctional channels contribute to electrical impulse propagation through the mouse atrioventricular node (AV-node). The cross talk in between these Cxs may be of great importance for AV-nodal conduction.

The TSG101 protein binds to connexins and is involved in connexin degradation.

Gap junctions mediate electrical and metabolic communication between cells in almost all tissues and are proposed to play important roles in cellular growth control, differentiation and embryonic development. Gap junctional communication and channel assembly were suggested to be regulated by interaction of connexins with different proteins including kinases and phosphatases. Here, we identified the tumor susceptibility gene 101 (TSG101) protein to bind to the carboxyterminal tail of connexin45 in a yeast two-hybrid protein interaction screen.

Human connexin31.9, unlike its orthologous protein connexin30.2 in the mouse, is not detectable in the human cardiac conduction system.

In the human heart connexin(Cx)40, Cx43 and Cx45-containing gap junctional channels electrically couple cardiomyocytes, forming a functional syncytium. In the mouse heart, additionally, Cx30.2-containing gap junctions have been detected in the atrioventricular node where they are implicated, together with Cx45, in impulse delay.

Neurogenesis and widespread forebrain migration of distinct GABAergic neurons from the postnatal subventricular zone.

Most forebrain GABAergic interneurons in rodents are born during embryonic development in the ganglionic eminences (GE) and migrate tangentially into the cortical plate. A subset, however, continues to be generated postnatally in the subventricular zone (SVZ). These interneurons populate the olfactory bulb (OB) reached via migration in the rostral migratory stream (RMS).

Expression of connexin30.2 in interneurons of the central nervous system in the mouse.

Electrical synapses, particularly gap junctions composed of connexin (Cx) 36, have been suggested to synchronize neuronal network oscillations. Recently, we generated Cx30.2-deficient mice which express beta-galactosidase under control of Cx30.

Gating properties of heterotypic gap junction channels formed of connexins 40, 43, and 45.

Connexins (Cxs) 40, 43, and 45 are expressed in many different tissues, but most abundantly in the heart, blood vessels, and the nervous system. We examined formation and gating properties of heterotypic gap junction (GJ) channels assembled between cells expressing wild-type Cx40, Cx43, or Cx45 and their fusion forms tagged with color variants of green fluorescent protein. We show that these Cxs, with exception of Cxs 40 and 43, are compatible to form functional heterotypic GJ channels.

Connexin-mediated cardiac impulse propagation: connexin 30.2 slows atrioventricular conduction in mouse heart.

In mouse heart, four connexins (Cxs), Cx30.2, Cx40, Cx43, and Cx45, form gap junction (GJ) channels for electric and metabolic cell-to-cell signaling. Extent and pattern of Cx isoform expression together with cytoarchitecture and excitability of cells determine the velocity of excitation spread in different regions of the heart.

Properties of mouse connexin 30.2 and human connexin 31.9 hemichannels: implications for atrioventricular conduction in the heart.

Four connexins (Cxs), mouse (m)Cx30.2, Cx40, Cx43, and Cx45, determine cell-cell electrical signaling in mouse heart, and Cx43 and Cx45 are known to form unapposed hemichannels. Here we show that mCx30.

Connexin30.2 containing gap junction channels decelerate impulse propagation through the atrioventricular node.

In the mammalian heart, gap junction channels between electrically coupled cardiomyocytes are necessary for impulse propagation and coordinated contraction of atria and ventricles. Recently, mouse connexin30.2 (Cx30.

Functional properties of mouse connexin30.2 expressed in the conduction system of the heart.

Gap junction channels composed of connexin (Cx) 40, Cx43, and Cx45 proteins are known to be necessary for impulse propagation through the heart. Here, we report mouse connexin30.2 (mCx30.