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J. Cell Biol.,
Volume 141, Number 5, June 1, 1998 1267-1275
* Department of Pediatrics, 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 ( Department of Morphology, University of Geneva, Switzerland; § Laboratory of Cell Biology,
University Paul Sabatier, France; and Institute for Genetics, University of Bonn, Germany
/) 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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