Mapping protein expression in XXXX pancreatic islets by immunolabeling and electron energy loss spectrum-imaging.

@entity3007 @entity1568 @entity19 @entity5072 @entity10338 @entity72715 @entity141 @entity599
A combination of immuno-electron microscopy and electron energy-loss spectrum-imaging was used to map the distributions of endocrine polypeptide hormones and proteins in @entity19 pancreatic islet of Langerhans. Tissue was analyzed from control animals and from @entity19 that were heterozygous for the @entity72715 gene, which defines a @entity141 / @entity3007 -dependent membrane fusion and ion channel protein. The heterozygous @entity72715 (+/-) @entity19 displays defects in @entity10338 mediated @entity141 signaling and insulin secretion. Therefore, information was obtained about the distributions of the hormones insulin and glucagon, as well as the proteins @entity72715 and the @entity10338 . Insulin secretion appears to be defective in the mutants. It was found from immunolabeling experiments that expression of the @entity10338 is reduced in mutant islets compared to control islets. Subcellular distributions of @entity599 and @entity1568 obtained by electron energy-loss spectrum-imaging showed that the insulin concentrations of beta granules were essentially the same in control and mutant islets. By contrast, immunogold labeling of mutant islets shows more insulin immunoreactivity in the beta granules. It follows that insulin may be packaged differently in mutant islets, making antigenic determinants more available to the labeling antibody. The increased rate of insulin secretion in the @entity5072 mutant islets can be explained by compensatory increases in islet size, rather than by an increased insulin concentration in the beta cells. The results indicate that reduced @entity72715 expression leads to defects in the @entity10338 expression in the endocrine cells of the mutant @entity19 . Increased size of the islet or of adrenal medulla may be a compensatory mechanism for secretion defect by individual endocrine cells. Defects in @entity10338 expression, and documented consequences of a @entity141 signaling defect, lead to other changes in organelles such as the mitochondrial number in islet beta-cells. The effects and consequences of reduced @entity72715 expression on mitochondria are evident in ultrastructural observations.
