Journal of inherited metabolic disease · 2012
Pontocerebellar hypoplasia type 6 caused by mutations in RARS2: definition of the clinical spectrum and molecular findings in five patients.
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Cassandrini Denise, Cilio Maria Roberta, Bianchi Marzia, Doimo Mara, Balestri Martina, Tessa Alessandra, Rizza Teresa, Sartori Geppo, Meschini Maria Chiara, Nesti Claudia, Tozzi Giulia, Petruzzella Vittoria, Piemonte Fiorella, Bisceglia Luigi, Bruno Claudio, Dionisi-Vici Carlo, D'Amico Adele, Fattori Fabiana, Carrozzo Rosalba, Salviati Leonardo, Santorelli Filippo M, Bertini Enrico
Аннотация
Recessive mutations in the mitochondrial arginyl-transfer RNA synthetase (RARS2) gene have been associated with early onset encephalopathy with signs of oxidative phosphorylation defects classified as pontocerebellar hypoplasia 6. We describe clinical, neuroimaging and molecular features on five patients from three unrelated families who displayed mutations in RARS2. All patients rapidly developed a neonatal or early-infantile epileptic encephalopathy with intractable seizures. The long-term follow-up revealed a virtual absence of psychomotor development, progressive microcephaly, and feeding difficulties. Mitochondrial respiratory chain enzymes in muscle and fibroblasts were normal in two. Blood and CSF lactate was abnormally elevated in all five patients at early stages while appearing only occasionally abnormal with the progression of the disease. Cerebellar vermis hypoplasia with normal aspect of the cerebral and cerebellar hemispheres appeared within the first months of life at brain MRI. In three patients follow-up neuroimaging revealed a progressive pontocerebellar and cerebral cortical atrophy. Molecular investigations of RARS2 disclosed the c.25A>G/p.I9V and the c.1586+3A>T in family A, the c.734G>A/p.R245Q and the c.1406G>A/p.R469H in family B, and the c.721T>A/p.W241R and c.35A>G/p.Q12R in family C. Functional complementation studies in Saccharomyces cerevisiae showed that mutation MSR1-R531H (equivalent to human p.R469H) abolished respiration whereas the MSR1-R306Q strain (corresponding to p.R245Q) displayed a reduced growth on non-fermentable YPG medium. Although mutations functionally disrupted yeast we found a relatively well preserved arginine aminoacylation of mitochondrial tRNA. Clinical and neuroimaging findings are important clues to raise suspicion and to reach diagnostic accuracy for RARS2 mutations considering that biochemical abnormalities may be absent in muscle biopsy.
Предметные рубрики MeSH
Arginine-tRNA LigaseCerebellumChild, PreschoolFemaleFollow-Up StudiesHumansInfantInfant, NewbornIntellectual DisabilityLactic AcidLennox Gastaut SyndromeMagnetic Resonance ImagingMaleMicrocephalyMitochondriaMutationNeuroimagingOlivopontocerebellar AtrophiesPsychomotor DisordersSeizuresSpasms, Infantile