Erratum: FALS with FUS mutation in Japan, with early onset, rapid progress and basophilic inclusion

Correction to: J Hum Genet 2010; 55, 252–254. doi:10.1038/jhg.2010.16; published online 12 March 2010

Since the publication of this article, the authors of the above paper have noticed an error in the description of mutation. The mutation ‘c.1561C>T; p.R521C’ should have been ‘c.1562G>T; p.R521L’. The authors replaced Figure 1c as attached. The legend of the Figure 1c is changed to ‘(c) sequence of the index case with a missense mutation (G1562T) in exon15 of the FUS gene that substituted cysteine for arginine at residue 521 (R521L)’.

Figure 1

(a) Pedigree of a Japanese family with FALS with FUS mutations. Males are represented by squares, females by circles. Affected members are represented by solid symbols, deceased individuals by diagonals. The proband is indicated by an arrow. Autopsied cases are marked with asterisks. (b–e) Sequence electropherogram of the FUS gene. (b) Sequence of a normal subject; (c) sequence of the index case with a missense mutation (G1562T) in exon15 of the FUS gene that substituted cysteine for arginine at residue 521 (R521L); and (e) sequence of the other case with histidine for proline at residue 517 (H517P). The arrows indicate the substitution site. (f–h) Hematoxylin–eosin staining and immunohistochemistry of the midbrain from the index case. A few basophilic inclusion bodies were present in the neurons of the brain stem (f, arrow). These basophilic bodies were stained with ubiquitin (g, arrow), but not with TDP43 (h, arrow). Scale bar, 50μm. A full color version of this figure is available at the Journal of Human Genetics journal online.

The authors apologize for any inconvenience caused.