Cristina Dallabona, Truus E. M. Abbink, Rosalba Carrozzo, Alessandra Torraco, Andrea Legati, Carola G. M. van Berkel, Marcello Niceta, Tiziana Langella, Daniela Verrigni, Teresa Rizza, Daria Diodato, Fiorella Piemonte, Eleonora Lamantea, Mingyan Fang, Jianguo Zhang, Diego Martinelli, Elsa Bevivino, Carlo Dionisi-Vici, Adeline Vanderver, Sunny G. Philip, Manju A. Kurian, Ishwar C. Verma, Sunita Bijarnia-Mahay, Sandra Jacinto, Fatima Furtado, Patrizia Accorsi, Anna Ardissone, Isabella Moroni, Ileana Ferrero, Marco Tartaglia, Paola Goffrini, Daniele Ghezzi, Marjo S. van der Knaap and Enrico Bertini. LYRM7 mutations cause a multifocal cavitating leukoencephalopathy with distinct MRI appearance. Brain 2016; 139: 782–794. doi:.
The authors apologize for mixing the mutations of Patients 5 and 7 on pages 788 and 789 in Figure 2 and its legend, in the main text and the online Supplementary Tables. This has now been corrected online.
On page 788, the text should read:
Sanger sequencing of the entire coding sequence of LYRM7 and intron-exon boundaries was performed in three additional patients. Patient 5 was found homozygous for the c.37delA (p.Thr13Hisfs*17) mutation, which is predicted to dramatically affect recognition of the splice donor motif of exon 4 and likely impair proper RNA splicing (Fig. 2M and N), while Patients 6 and 7 were found to be homozygous for the c.214C>T (p.Q72*) (Fig. 2L), and c.243_244+2delGAGT (p.?) (Fig. 2H) mutations, respectively. The Supplementary Tables have been corrected online.
![Genetic features. Electropherograms of the genomic region encompassing the mutation c.244+5insG, homozygous in Patient 1 (A, Pt.1) and heterozygous in both parents (B). The mutation produces a skipping of exon 4 in the LYRM7 transcript of Patient 1 (C and D). Sequencing analysis displayed in Patient 2 (Pt.2) a TTA c.193_195 duplication (E), and in Patient 4 (Pt.4) a homozygous c.73G>A change (F); the latter was heterozygous in the parents (G). Patient 7 (Pt.7) was homozygous for a 4-bp deletion, c.37delA (H), heterozygous in both parents (I). Patient 6 (Pt.6) was homozygous for the missense mutation c.214C>T [p.Q72*] (L). Patient 5 (Pt.5) was homozygous for the c.37delA mutation (M), heterozygous in both parents (N).](https://oup.silverchair-cdn.com/oup/backfile/Content_public/Journal/brain/141/11/10.1093_brain_awy194/2/m_awy194f1.jpeg?Expires=1749458296&Signature=hsdHCCCCZ38lqe7seATq1y-isJDeltsIXkypLtLCeMOW-p0SpJTcrE7kSKL3XHjG-u0tYxNNz5ULFsFRCtESFdcN4fDIB9d5lHaN1HbLDNcNMtE3Nom0LkjUY1b62c1genqcAUwoeegDQmWNTjIsx8VwiMPiFruukVEmnfSqtwVscUdwl1~u9xWs-qkURqlXdNlCFvAiWiseJbeh5RO~ndmNkiKgDsokDlFnmpENV0ho2Nk8jPxfCoDrisFIu2ATYtolwky2qU~x1f1SvQF5umlbKHpxmxBaf7t~K1ZwLzigQeQQSgfzIT20FI3~7MmSMLlJGloEgx1u0-aBecZ5jw__&Key-Pair-Id=APKAIE5G5CRDK6RD3PGA)
Genetic features. Electropherograms of the genomic region encompassing the mutation c.244+5insG, homozygous in Patient 1 (A, Pt.1) and heterozygous in both parents (B). The mutation produces a skipping of exon 4 in the LYRM7 transcript of Patient 1 (C and D). Sequencing analysis displayed in Patient 2 (Pt.2) a TTA c.193_195 duplication (E), and in Patient 4 (Pt.4) a homozygous c.73G>A change (F); the latter was heterozygous in the parents (G). Patient 7 (Pt.7) was homozygous for a 4-bp deletion, c.37delA (H), heterozygous in both parents (I). Patient 6 (Pt.6) was homozygous for the missense mutation c.214C>T [p.Q72*] (L). Patient 5 (Pt.5) was homozygous for the c.37delA mutation (M), heterozygous in both parents (N).
On page 789, Figure 2 and legend should be as follows:
