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Zinc accumulation in heterozygous mutants of fumble , the pantothenate kinase homologue of Drosophila
Author(s) -
Gutiérrez Lucia,
Sabaratnam Narmatha,
Aktar Rubina,
Bettedi Lucia,
Mandilaras Konstantinos,
Missirlis Fanis
Publication year - 2010
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2010.05.029
Subject(s) - mutant , zinc , neurodegeneration , biology , biochemistry , enzyme , coenzyme a , kinase , wild type , chemistry , gene , medicine , disease , organic chemistry , reductase
Coenzyme A (CoA) functions in the intracellular trafficking of acetyl groups. In humans, mutations in the pantothenate kinase‐2 gene, which encodes a key enzyme in CoA biosynthesis, are associated with neurodegeneration and premature death. Diagnosis is based on iron accumulation in the globus pallidus observed by magnetic resonance imaging. We investigated the elemental composition of the fumble mutant, a model of the human disease. Surprisingly, flies carrying a fumble loss‐of‐function allele had a three‐fold increase in total zinc levels per dry weight when compared to control strains, but no change in total iron, copper or manganese levels. Accordingly, zinc supplementation had an adverse impact on the development of fumble mutant larvae, but zinc chelation failed to protect.