TUBA1A mutations: from isolated lissencephaly to familial polymicrogyria

Neurology. 2011 Mar 15;76(11):988-92. doi: 10.1212/WNL.0b013e31821043f5.

Abstract

Background: Mutations in the TUBA1A gene have been reported in patients with lissencephaly and perisylvian pachygyria.

Methods: Twenty-five patients with malformations of cortical development ranging from lissencephaly to polymicrogyria were screened for mutations in TUBA1A.

Results: Two novel heterozygous missense mutations in TUBA1A were identified: c.629A>G (p.Tyr210Cys) occurring de novo in a boy with lissencephaly, and c.13A>C (p.Ile5Leu) affecting 2 sisters with polymicrogyria whose mother presented somatic mosaicism for the mutation.

Conclusions: Mutations in TUBA1A have been described in patients with lissencephaly and pachygyria. We report a mutation in TUBA1A as a cause of polymicrogyria. So far, all mutations in TUBA1A have occurred de novo, resulting in isolated cases. This article describes familial recurrence of TUBA1A mutations due to somatic mosaicism in a parent. These findings broaden the phenotypic spectrum associated with TUBA1A mutations and have implications for genetic counseling.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Cerebral Cortex / abnormalities*
  • Child
  • Female
  • Genetic Testing
  • Humans
  • Infant
  • Male
  • Malformations of Cortical Development / genetics*
  • Malformations of Cortical Development / pathology
  • Mutation, Missense
  • Tubulin / genetics*

Substances

  • TUBA1A protein, human
  • Tubulin