Atypical phenotypes in titinopathies explained by second titin mutations

Anni Evilä, Anna Vihola, J. Sarparanta, Olayinka Raheem, Johanna Palmio, Satu Sandell, B. Eymard, Isabel Illa, Ricard Rojas‐García, Karolina Hankiewicz,

Annals of Neurology · 2014 · 91 citations · 24 references

Abstract

The unequal expression levels of TTN transcripts in 5 probands suggested severely reduced expression of the frameshift mutated allele, probably through nonsense-mediated decay, explaining the more severe phenotypes. The Iberian TMD mutation may cause a more severe TMD rather than LGMD2J when homozygous. The Finnish patient compound heterozygous for the FINmaj TMD mutation and the novel A-band titin missense mutation showed a phenotype completely different from previously described titinopathies. Our results further expand the complexity of muscular dystrophies caused by TTN mutations and suggest that the coexistence of second mutations may constitute a more common general mechanism explaining phenotype variability.

References

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