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J. Biol. Chem., Vol. 266, Issue 24, 15999-15606, Aug, 1991
KW Choi, RF Smith, RM Buratowski and WG Quinn
The Drosophila mutant turnip was initially isolated based on poor learning
performance (Quinn, W.G., Sziber, P.P., and Booker, R. (1979) Nature 277,
212-214). Here we show that turnip is dramatically reduced in protein
kinase C (PKC) activity. In addition, turnip flies are deficient in
phosphorylation of a 76-kDa head membrane protein (hereafter pp76) which is
a major substrate for protein kinase C in homogenates of wild-type flies.
Reduced PKC activity, defective pp76 phosphorylation, and most of turnip's
learning deficiency co-map genetically to a region on the X-chromosome,
18A5-18D1-2, spanned by the deletion Df(1)JA27. Apparently turnip+ is not a
structural gene for PKC because Drosophila PKC genes map elsewhere in the
genome. Our results suggest that turnip gene product is required for
activation of PKC and that PKC plays a role in associative learning in
Drosophila.
Deficient protein kinase C activity in turnip, a Drosophila learning mutant
Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge 02139.
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