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Abstract
We are using the model of the developing mouse embryo to elucidate the pattern of
arginase expression in mammalian cells in normal animals and in arginase I (AI) deficiency
during development by digoxigenin-labeled RNA in situ hybridization. Our goal is to
understand the regulation of these isozymes, with the expectation that this knowledge
will help patients suffering from AI deficiency. We found that AI mRNA was widely
and strongly expressed in the normal developing mouse embryo; in contrast, a relatively
strong AII mRNA signal was found only in the intestine. In the AI knockout mouse embryo,
no AII overexpression was found. These results indicated that arginases are needed
in mouse embryonic development and AI is the principal form required. The strong AI
expression in the peripheral nervous system suggests that the pathogenesis of the
neurological retardation in AI deficiency may be conditioned by AI deficiency in the
nervous system during embryonic development.