Human Molecular Genetics, Vol 8, 323-330, Copyright © 1999 by Oxford University Press
L Feng, AB Seymour, S Jiang, A To, AA Peden, EK Novak, L Zhen, ME Rusiniak, EM Eicher, MS Robinson, MB Gorin and RT Swank
Lysosomes, melanosomes and platelet-dense granules are abnormal in the
mouse hypopigmentation mutant pearl. The beta3A subunit of the AP-3 adaptor
complex, which likely regulates protein trafficking in the trans - Golgi
network/endosomal compartments, was identified as a candidate for the pearl
gene by a positional/candidate cloning approach. Mutations, including a
large internal tandem duplication and a deletion, were identified in two
respective pearl alleles and are predicted to abrogate function of the
beta3A protein. Significantly lowered expression of altered beta3A
transcripts occurred in kidney of both mutant alleles. The several distinct
pearl phenotypes suggest novel functions for the AP-3 complex in mammals.
These experiments also suggest mutations in AP-3 subunits as a basis for
unique forms of human Hermansky-Pudlak syndrome and congenital night
blindness, for which the pearl mouse is an appropriate animal model.
ARTICLES
The beta3A subunit gene (Ap3b1) of the AP-3 adaptor complex is altered in the mouse hypopigmentation mutant pearl, a model for Hermansky- Pudlak syndrome and night blindness
Department of Molecular and Cell Biology, Roswell Park Cancer Institute, Elm and Carlton Streets, Buffalo NY 14263, USA.
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