Literature DB >> 24577744

VPS53 mutations cause progressive cerebello-cerebral atrophy type 2 (PCCA2).

Miora Feinstein1, Hagit Flusser, Tally Lerman-Sagie, Bruria Ben-Zeev, Dorit Lev, Orly Agamy, Idan Cohen, Rotem Kadir, Sara Sivan, Esther Leshinsky-Silver, Barak Markus, Ohad S Birk.   

Abstract

BACKGROUND: Progressive cerebello-cerebral atrophy (PCCA) leading to profound mental retardation, progressive microcephaly, spasticity and early onset epilepsy, was diagnosed in four non-consanguineous apparently unrelated families of Jewish Moroccan ancestry. Common founder mutation(s) were assumed.
METHODS: Genome-wide linkage analysis and whole exome sequencing were done, followed by realtime PCR and immunofluorescent microscopy.
RESULTS: Genome-wide linkage analysis mapped the disease-associated gene to 0.5 Mb on chromosome 17p13.3. Whole exome sequencing identified only two mutations within this locus, which were common to the affected individuals: compound heterozygous mutations in VPS53, segregating as expected for autosomal recessive heredity within all four families, and common in Moroccan Jews (∼1:37 carrier rate). The Golgi-associated retrograde protein (GARP) complex is involved in the retrograde pathway recycling endocytic vesicles to Golgi; c.2084A>G and c.1556+5G>A VPS53 founder mutations are predicted to affect the C-terminal domain of VPS53, known to be critical to its role as part of this complex. Immunofluorescent microscopy demonstrated swollen and abnormally numerous CD63 positive vesicular bodies, likely intermediate recycling/late endosomes, in fibroblasts of affected individuals.
CONCLUSIONS: Autosomal recessive PCCA type 2 is caused by VPS53 mutations.

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Year:  2014        PMID: 24577744     DOI: 10.1136/jmedgenet-2013-101823

Source DB:  PubMed          Journal:  J Med Genet        ISSN: 0022-2593            Impact factor:   6.318


  27 in total

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Authors:  David C Gershlick; Morié Ishida; Julie R Jones; Allison Bellomo; Juan S Bonifacino; David B Everman
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10.  Post-Golgi anterograde transport requires GARP-dependent endosome-to-TGN retrograde transport.

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