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Evidence for a possible regulatory gene (Suc-1) controlling sucrase expression in mouse intestine

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Abstract

Assays for sucrase carried out on intestinal sonicates prepared from 18 different strains of mice revealed a threefold variation in specific activity, the values for CBA/Ca mice being significantly less than for any other strain. Further comparison of the CBA/Ca versus the C57BL/6J mouse showed this deficiency, which became established 2–4 weeks after birth, to apply to isomaltase as well as sucrase but not to maltase or trehalase. Backcross experiments indicated that this deficiency in sucrase activity was inherited as a single codominantly expressed genetic factor. The ability of the CBA/Ca mouse to regulate sucrase activity in response to changes in diet was also reduced compared to that of the C57BL/6J mouse. No difference could be detected in the affinity of sucrase for its substrate or in the ability of heat to denature sucrase prepared from CBA/Ca and C57BL/6J mice. It is suggested that part of the regulatory region of the gene coding for sucrase-isomaltase is modified in the CBA/Ca mouse and that this locus should be given the notation Suc-1 for future reference.

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This work supported by an MRC project grant to M. W. Smith.

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James, P.S., Smith, M.W., Butcher, G.W. et al. Evidence for a possible regulatory gene (Suc-1) controlling sucrase expression in mouse intestine. Biochem Genet 24, 169–181 (1986). https://doi.org/10.1007/BF00502786

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  • DOI: https://doi.org/10.1007/BF00502786

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