TY - JOUR
T1 - Molecular basis of infantile reversible cytochrome c oxidase deficiency myopathy
AU - Horvath, Rita
AU - Kemp, John P.
AU - Tuppen, Helen A. L.
AU - Hudson, Gavin
AU - Oldfors, Anders
AU - Marie, Suely K. N.
AU - Moslemi, Ali-Reza
AU - Servidei, Serenella
AU - Holme, Elisabeth
AU - Shanske, Sara
AU - Kollberg, Gittan
AU - Jayakar, Parul
AU - Pyle, Angela
AU - Marks, Harold M.
AU - Holinski-Feder, Elke
AU - Scavina, Mena
AU - Walter, Maggie C.
AU - Oku, Jorida
AU - Günther-Scholz, Andrea
AU - Smith, Paul M.
AU - Mcfarland, Robert
AU - Chrzanowska-Lightowlers, Zofia M. A.
AU - Lightowlers, Robert N.
AU - Hirano, Michio
AU - Lochmüller, Hanns
AU - Taylor, Robert W.
AU - Chinnery, Patrick F.
AU - Tulinius, Mar
AU - Dimauro, Salvatore
PY - 2009
Y1 - 2009
N2 - Childhood-onset mitochondrial encephalomyopathies are usually severe, relentlessly progressive conditions that have a fatal outcome. However, a puzzling infantile disorder, long known as 'benign cytochrome c oxidase deficiency myopathy' is an exception because it shows spontaneous recovery if infants survive the first months of life. Current investigations cannot distinguish those with a good prognosis from those with terminal disease, making it very difficult to decide when to continue intensive supportive care. Here we define the principal molecular basis of the disorder by identifying a maternally inherited, homoplasmic m.14674T>C mt-tRNA(Glu) mutation in 17 patients from 12 families. Our results provide functional evidence for the pathogenicity of the mutation and show that tissue-specific mechanisms downstream of tRNA(Glu) may explain the spontaneous recovery. This study provides the rationale for a simple genetic test to identify infants with mitochondrial myopathy and good prognosis.
AB - Childhood-onset mitochondrial encephalomyopathies are usually severe, relentlessly progressive conditions that have a fatal outcome. However, a puzzling infantile disorder, long known as 'benign cytochrome c oxidase deficiency myopathy' is an exception because it shows spontaneous recovery if infants survive the first months of life. Current investigations cannot distinguish those with a good prognosis from those with terminal disease, making it very difficult to decide when to continue intensive supportive care. Here we define the principal molecular basis of the disorder by identifying a maternally inherited, homoplasmic m.14674T>C mt-tRNA(Glu) mutation in 17 patients from 12 families. Our results provide functional evidence for the pathogenicity of the mutation and show that tissue-specific mechanisms downstream of tRNA(Glu) may explain the spontaneous recovery. This study provides the rationale for a simple genetic test to identify infants with mitochondrial myopathy and good prognosis.
KW - Cytochrome-c Oxidase Deficiency
KW - Infant, Newborn
KW - Mitochondria
KW - Mitochondrial Encephalomyopathies
KW - Cytochrome-c Oxidase Deficiency
KW - Infant, Newborn
KW - Mitochondria
KW - Mitochondrial Encephalomyopathies
UR - http://hdl.handle.net/10807/14862
U2 - 10.1093/brain/awp221
DO - 10.1093/brain/awp221
M3 - Article
SN - 0006-8950
VL - 132
SP - 3165
EP - 3174
JO - Brain
JF - Brain
ER -