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Pontocerebellar hypoplasia type 1B (PCH1B) describes an autosomal recessive neurological condition that involves hypoplasia or atrophy of the cerebellum and pons, resulting in neurocognitive impairments. Although there is phenotypic variability, this is often an infantile lethal condition, and most cases have been described to be congenital and neurodegenerative. PCH1B is caused by mutations in the gene EXOSC3, which encodes exosome component 3, a subunit of the human RNA exosome complex. A range of pathogenic variants with some correlation to phenotype have been reported. The most commonly reported pathogenic variant in EXOSC3 is c.395A>C, p.(Asp132Ala); homozygosity for this variant has been proposed to lead to milder phenotypes than compound heterozygosity. In this case, we report two siblings with extraordinarily mild presentations of PCH1B who are compound heterozygous for variants in EXOSC3 c.155delC and c.80T>G. These patients drastically expand the phenotypic variability of PCH1B and raise questions about genotype-phenotype associations.
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http://dx.doi.org/10.1136/bcr-2020-236732 | DOI Listing |
bioRxiv
July 2025
Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, IN.
Charge-changing perturbations are notoriously difficult to investigate with alchemical free energy calculations. The routine use of periodic boundary conditions and electrostatic approximations, such as particle-mesh Ewald (PME), may produce finite-size effect errors that become non-negligible as a perturbation changes a simulation cell's net charge away from zero. Two prevalent strategies exist to correct for these errors: the analytic correction (AC) and co-alchemical ion (CI) methods.
View Article and Find Full Text PDFbioRxiv
June 2025
Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, IN.
Missense variants in EXOSC3, an RNA exosome subunit, have been identified in patients with PCH1b. We investigated three missense variants in the S1 domain of EXOSC3, including one variant of uncertain significance (VUS) and two pathogenic variants (hence S1 variants). EXOSC3 S1 variant cell lines were generated using CRISPR-Cas9 resulting in widespread proteome changes including decreases in some RNA exosome subunits paired with increases in the catalytic subunit DIS3.
View Article and Find Full Text PDFGenes (Basel)
May 2025
Department of Neurology and CMT Program at Yale, Yale School of Medicine, New Haven, CT 06510, USA.
Pontocerebellar hypoplasia is a rare neurodegenerative syndrome characterized by severe hypoplasia or atrophy of pons and cerebellum that may be associated with other brain malformations, microcephaly, optic nerve atrophy, dystonia, ataxia and neuromuscular disorders. At this time, there are 17 variants of PCH distinguished by clinical presentation and distinctive radiological and biochemical features in addition to pontine and cerebellar hypoplasia. PCH1 is defined as PCH variant associated with anterior horn degeneration in the spinal cord with muscle weakness and hypotonia, and is associated with recessive variants in genes VRK1, EXOSC3, EXOSC8, EXOSC9 and SLC25A46.
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June 2025
Department of Biochemistry, Emory University School of Medicine, Atlanta, Georgia 30322, USA
The RNA exosome is a multisubunit, evolutionarily conserved ribonuclease complex that is essential for processing, decay, and surveillance of many cellular RNAs. Missense mutations in genes encoding the structural subunits of the RNA exosome complex cause a diverse range of diseases, collectively known as RNA exosomopathies, often involving neurological and developmental defects. The varied symptoms suggest that different mutations lead to distinct in vivo consequences.
View Article and Find Full Text PDFOxysterol-binding protein-like protein 9 () is a member of a large eukaryotic gene lipid transport protein family that mediates the exchange of sterols and phospholipids between the trans-Golgi network and the endoplasmic reticulum. Denovo missense mutations in the gene have been previously reported to be associated with intellectual disability. Herein, we report for the first time, to the best of our knowledge, a novel homozygous nonsense variant in the gene in a consanguineous family with two fetuses with cerebral ventriculomegaly, cerebellar hypoplasia, and arthrogryposis multiplex.
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