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Abstract

Total activity, pH optimum and heat inactivation of arylsulfatase A (EC 3.1.6.1) were followed during development in brain, liver, kidney and heart of normal and myelin deficient jimpy mice. The pH optimum and heat inactivation did not change during postnatal development and were the same for normal and mutant mice in all tissues studied. In prenatal brain and liver the arylsulfatase A was less stable to heat inactivation than during postnatal development, although the pH optimum was the same. The developmental activity patterns were different for each tissue, but no difference between normal and jimpy mice could be found except for brain, where arylsulfatase A activity was lower after the 15th day of life until death of the animal around 25 days. In normal, but not in jimpy brains, the activity of arylsulfatase A correlates well with reported rates of sulfatide synthesis in vivo and with cerebroside sulfotransferase activity.The tissue characteristic developmental activity patterns of arylsulfatase A suggest that this enzyme is regulated on the tissue level. The change of heat inactivation properties, found in pre- and postnatal brain and liver, may reflect a structural modification of the enzyme protein around birth. The apparent developmental coordination of synthesizing and degrading enzyme activities of sulfatide in brains of normal mice seems to be of functional significance for normal brain maturation. The absence of this coordination in developing jimpy brains indicates that synthesis and degradation of sulfatide may be regulated rather by epigenetic control factors than by a direct genetic link.