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J. Cell Biol., Volume 141, Number 5, June 1, 1998 1267-1275

Enhanced Secretion of Amylase from Exocrine Pancreas of Connexin32-deficient Mice

Marc Chanson,* Marjorie Fanjul,§ Domenico Bosco,Dagger Eric Nelles,par Susanne Suter,* Klaus Willecke,par and Paolo MedaDagger

* Department of Pediatrics, Dagger  Department of Morphology, University of Geneva, Switzerland; § Laboratory of Cell Biology, University Paul Sabatier, France; and par  Institute for Genetics, University of Bonn, Germany

To determine whether junctional communication between pancreatic acinar cells contributes to their secretory function in vivo, we have compared wild-type mice, which express the gap junctional proteins connexin32 (Cx32) and connexin26, to mice deficient for the Cx32 gene. Pancreatic acinar cells from Cx32 (-/-) mice failed to express Cx32 as evidenced by reverse transcription-PCR and immunolabeling and showed a marked reduction (4.8- and 25-fold, respectively) in the number and size of gap junctions. Dye transfer studies showed that the extent of intercellular communication was inhibited in Cx32 (-/-) acini. However, electrical coupling was detected by dual patch clamp recording in Cx32 (-/-) acinar cell pairs. Although wild-type and Cx32 (-/-) acini were similarly stimulated to release amylase by carbamylcholine, Cx32 (-/-) acini showed a twofold increase of their basal secretion. This effect was caused by an increase in the proportion of secreting acini, as detected with a reverse hemolytic plaque assay. Blood measurements further revealed that Cx32 (-/-) mice had elevated basal levels of circulating amylase. The results, which demonstrate an inverse relationship between the extent of acinar cell coupling and basal amylase secretion in vivo, support the view that the physiological recruitment of secretory acinar cells is regulated by gap junction mediated intercellular communication.


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