One of the most exciting aspects of modern cell biology is the potential to make connections between disparate areas of research, and thus open up new lines of enquiry. Two recent papers have done just this (Kanazawa et al. 2000; Im et al. 2001, this issue). Building on the biochemical defect in an inherited metabolic disease (Suzuki 1998), these papers reveal an unexpected connection between lipid mediators, G protein–coupled receptor (GPCR) signaling, and cytokinesis mechanism.
Globoid cell leukodystrophy (GLD), or Krabbe's disease, is a severe, inherited, metabolic disorder in which normal myelin formation is blocked, and multinucleate “globoid cells” accumulate in the brain. The primary defect is an absence of the lipid-degrading enzyme galactoceramidase, which cleaves the galactose headgroup from galactoceramide (Fig. 1). Galactoceramidase-deficient mice and dogs provide models for human GLD...
