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MT-TG

From Wikipedia, the free encyclopedia
Transfer RNA
mitochondrially encoded tRNA glycine
Identifiers
SymbolMT-TG
Alt. symbolsMTTG
NCBI gene4563
HGNC7486
RefSeqNC_001807
Other data
LocusChr. MT[1]

Mitochondrially encoded tRNA glycine also known asMT-TG is atransfer RNA which in humans is encoded by themitochondrialMT-TGgene.[1]

Structure

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TheMT-TG gene is located on thep arm of themitochondrial DNA at position 12 and it spans 68 base pairs.[2] The structure of atRNA molecule is a distinctive folded structure which contains three hairpin loops and resembles a three-leafedclover.[3]

Function

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MT-TG is a small 68 nucleotidetransfer RNA (human mitochondrial map position 9991-10058) that transfers the amino acidglycine to a growingpolypeptide chain at theribosome site ofprotein synthesis duringtranslation.

Clinical significance

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Myoclonic epilepsy with ragged-red fibers (MERRF)

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Mutations intransfer RNAs have been found to lead to marked mitochondrial energy deficiency and a hindrance of mitochondrial proliferation, and defects inoxidative phosphorylation. Such defects may result inmyoclonic epilepsy with ragged-red fibers (MERRF). Myoclonic epilepsy with ragged-red fibers (MERRF) is a raremitochondrial disorder that affects many parts of the body, particularly themuscles andnervous system. In most cases, the signs and symptoms of this disorder appear during childhood or adolescence. The features of MERRF vary widely among affected individuals, even among members of the same family. Common clinical manifestations includemyoclonus,myopathy,spasticity,epilepsy,peripheral neuropathy,dementia,ataxia,atrophy and more.[4][5]

Familial hypertrophic cardiomyopathy

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Mutations in theMT-TG gene has also been associated with familialhypertrophic cardiomyopathy. Familialhypertrophic cardiomyopathy is a heart condition characterized by thickening of the heart, usually in theinterventricular septum. Common phenotypes includechest pain, shortness of breath,physical exertion,palpitations,lightheadedness,dizziness andfainting.[6] A family with a transition mutation of 9997T>C in theMT-TG gene exhibited familial hypertrophic cardiomyopathy.[7]

References

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  1. ^Anderson S, Bankier AT, Barrell BG, de Bruijn MH, Coulson AR, Drouin J, Eperon IC, Nierlich DP, Roe BA, Sanger F, Schreier PH, Smith AJ, Staden R, Young IG (April 1981). "Sequence and organization of the human mitochondrial genome".Nature.290 (5806):457–65.Bibcode:1981Natur.290..457A.doi:10.1038/290457a0.PMID 7219534.S2CID 4355527.
  2. ^"MT-TG mitochondrially encoded tRNA glycine [Homo sapiens (human)] - Gene - NCBI".www.ncbi.nlm.nih.gov.
  3. ^"tRNA / transfer RNA | Learn Science at Scitable".www.nature.com.
  4. ^"Myoclonic epilepsy with ragged-red fibers".Genetics Home Reference. U.S. National Library of Medicine.
  5. ^Graham BH, Waymire KG, Cottrell B, Trounce IA, MacGregor GR, Wallace DC (July 1997). "A mouse model for mitochondrial myopathy and cardiomyopathy resulting from a deficiency in the heart/muscle isoform of the adenine nucleotide translocator".Nature Genetics.16 (3):226–34.doi:10.1038/ng0797-226.PMID 9207786.S2CID 7285265.
  6. ^"Familial hypertrophic cardiomyopathy".Genetics Home Reference. U.S. National Library of Medicine.
  7. ^Merante F, Tein I, Benson L, Robinson BH (September 1994)."Maternally inherited hypertrophic cardiomyopathy due to a novel T-to-C transition at nucleotide 9997 in the mitochondrial tRNA(glycine) gene".American Journal of Human Genetics.55 (3):437–46.PMC 1918404.PMID 8079988.

Further reading

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Mitochondrial proteins
Outer membrane
fatty acid degradation
tryptophan metabolism
monoamine neurotransmitter
metabolism
Intermembrane space
Inner membrane
oxidative phosphorylation
pyrimidine metabolism
mitochondrial shuttle
steroidogenesis
other
Matrix
citric acid cycle
anaplerotic reactions
urea cycle
alcohol metabolism
Other/to be sorted
Mitochondrial DNA
Complex I
Complex III
Complex IV
ATP synthase
tRNA

This article incorporates text from theUnited States National Library of Medicine, which is in thepublic domain.

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