Galactosyltransferase defects in reeler mouse brains.

Abstract:

:Galactosyltransferase activities were examined in the cerebellum, cerebral cortex, and brain stem of reeler and wild-type mice. Galactosyltransferase assays were optimal for all required substrates, linear with incubation time, and proportional to protein concentration. In brain areas affected by the reeler mutation (i.e., cerebral cortex and cerebellum), galactosylation of both endogenous and exogenous glycoprotein acceptors was greatly reduced in reeler relative to controls. On the other hand, glycosylation of endogenous glycolipids was low, and equal between reeler and wild-type. Galactosyltransferase activities were similar, though not identical, in reeler and wild-type brain stems, which are phenotypically normal in reeler mice. Glucosyltransferase, beta-galactosidase, beta-N-acetylglucosaminidase, acid phosphatase, and lactate dehydrogenase specific activities were all unaffected in reeler cerebella, while galactosyltransferase activity was 52% of control. Inhibition of either UDPgalactose hydrolysis or beta-galactosidase had no effect on galactosyltransferase activity. The spectrum or galactosyltransferase deficiencies in reeler suggests that this enzyme is associated with the development of young granule cells.

journal_name

J Neurochem

authors

Shur BD

doi

10.1111/j.1471-4159.1982.tb04719.x

subject

Has Abstract

pub_date

1982-07-01 00:00:00

pages

201-9

issue

1

eissn

0022-3042

issn

1471-4159

journal_volume

39

pub_type

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