Error in Table
On a recent occasion, we realized that in the original article, there was a mistake in Table 1 as published. The citation numbers in the Table 1 referring to the NDUFAF5 mutations in various ethnic groups did not match the given reference order list in the published article. In Table 1, (1) reference 26 should be reference (1); (2) reference 27 should be reference 30; (3) reference 28 should be reference (2); (4) reference 12 should be reference 31; (5) reference 29 should be reference 32; and (6) reference 13 should be reference (3). The corrected Table 1 appears below.
Table 1
| References | Ethnicity | Sex* | Mutation | Onset age | Clinical features | MRI findings | Outcome |
|---|---|---|---|---|---|---|---|
| Saada et al. (1) | Ashkenazi Jewish | M | c.749G>T, c.749G>T | 12 m | Motor development retardation, ataxia, bilateral ptosis, optic atrophy, diffuse hypotonia | Symmetrical lesions of bilateral basal ganglia, striatum and cortical areas | Death at ~2.5 y |
| Ashkenazi Jewish | M | c.749G>T, c.749G>T | 12 m | Death at ~6 y | |||
| Ashkenazi Jewish | F | c.749G>T, c.749G>T | 12 m | Death at ~4.5 y | |||
| Ashkenazi Jewish | F | c.749G>T, c.749G>T | 12 m | Death at ~6 y | |||
| Ashkenazi Jewish | F | c.749G>T, c.749G>T | 12 m | Death at ~7 y | |||
| Fang et al. (30) | Chinese | c.212C>T, c.698G>T | Developmental delay and regression, seizures | Bilateral lesions of brainstem and basal ganglia | |||
| Sugiana et al. (2) | Egyptian | M | c.719T>C, c.719T>C | Birth | Intrauterine growth retardation, facial dysmorphism, corpus callosum agenesis, ventricular septation, left diaphragmatic hernia, adrenal insufficiency | – | Death at ~7 d |
| Tong et al. (31) | Chinese | F | c.145C>G, c.836T>G | 8 m | Neurodevelopmental delay, swallowing dysfunction, dyspnea | Bilateral medulla oblongata lesions | Death at 21 m |
| Gerards et al. (32) | Moroccan | M | c.477A>C, c.477A>C | 3 y | Dysarthria, dystonic posture, spastic quadriplegia, mental retardation | Caudate, putamen, substantia nigra and peri-aqueductal grey area lesions, bifrontal atrophy | Alive at 23 y |
| Moroccan | M | c.477A>C, c.477A>C | 3 y | Alive at 29 y | |||
| Simon et al. (3) | Taiwanese | F | c.155A>C, c.836T>G | 6 m | Developmental delay, global hypotonia, difficulty swallowing | Symmetrical thalamic and midbrain lesions, corpus callosum dysgenesis | Death at 27 m |
| Taiwanese | F | c.836T>G, c.836T>G | 27 m | Vision loss, strabismus, nystagmus, muscle weakness, inability to walk | Hyperintense lesions in posterior fossa, caudate and cervical spinal cord | Death at 19 y | |
| Caucasian | M | c.327G>C, c.223–907A>C | 3 m | Seizures, hypotonia, loss of vision, feeding difficulty | T2 hyperintensity in thalamus, midbrain, upper spinal cord | Death at 8 m | |
| Ashkenazi Jewish | M | c.327G>C, c.749G>T | 5 m | Torticollis, nystagmus, swallowing and feeding difficulty | Bilateral lesions in thalamus, putamen and frontal lobes | Death at 17 m | |
| This pedigree | Chinese | F | c.425A > C, c.836T > G | 6y | Generalized dystonia, spastic quadriplegia, dysphagia and dysarthria | Alive at 23 y | |
| Chinese | F | c.425A > C, c.836T > G | 6y | Generalized dystonia, optic atrophy, dysphagia and dysarthria | Abnormal symmetric signals in the posterior region of the bilateral putamen | Alive at 20 y | |
| Chinese | F | c.425A > C, c.836T > G | 6y | Generalized dystonia, febrile convulsions (1-3 y), dysphagia and dysarthria | Abnormal symmetric signals in the posterior region of the bilateral putamen | Alive at 18 y |
Clinical features of patients with NDUFAF5 variations reported in literature.
M, Male; F, Female.
Missing Citation
In the original article References 30, 31, and 32 were not cited/included in the published article. The citation has now been inserted in Table 1, under the section Discussion.
New References to be Added in the continuing order:
-
30. Fang F, Shen Y, Shen DM, Liu ZM, Ding CH, Zhang WC, et al. [Clinical and genetic characteristics of children with Leigh syndrome]. Zhonghua er ke za zhi = Chinese J Pediatr. (2017) 55:205–9. doi: 10.3760/cma.j.issn.0578-1310.2017.03.008
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31. Tong W, Wang Y, Lu Y, Ye T, Song C, Xu Y, et al. Whole-exome sequencing helps the diagnosis and treatment in children with neurodevelopmental delay accompanied unexplained dyspnea. Sci Rep. (2018) 8:5214.
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32. Gerards M, Sluiter W, van den Bosch BJ, de Wit LE, Calis CM, Frentzen M, et al. Defective complex I assembly due to C20orf7 mutations as a new cause of Leigh syndrome. J Med Genet. (2010) 47:507–12. doi: 10.1136/jmg.2009.067553
The authors apologize for this error and confirm that it does not change the scientific conclusions of the article in any way. The original article has been updated.
Publisher's Note
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References
1.
Saada A Edvardson S Shaag A Chung WK Segel R Miller C et al . Combined oxphos complex i and iv defect, due to mutated complex i assembly factor c20orf7. J Inherit Metab Dis. (2012) 35:125–31. 10.1007/s10545-011-9348-y
2.
Sugiana C Pagliarini DJ McKenzie M Kirby DM Salemi R Abu-Amero KK et al . Mutation of c20orf7 disrupts complex i assembly and causes lethal neonatal mitochondrial disease. Am J Hum Genet. (2008) 83:468–78. 10.1016/j.ajhg.2008.09.009
3.
Simon MT Eftekharian SS Stover AE Osborne AF Braffman BH Chang RC et al . Novel mutations in the mitochondrial complex i assembly gene ndufaf5 reveal heterogeneous phenotypes. Mol Genet Metab. (2019) 126:53–63. 10.1016/j.ymgme.2018.11.001
Summary
Keywords
bilateral striatal necrosis, NDUFAF5, mitochondrial complex I deficiency, whole-exome sequencing, novel variation
Citation
Bi H, Guo H, Wang Q, Zhang X, Zhao Y, Li J, Zhao W, Tuo H and Zhang Y (2021) Corrigendum: A Novel Variation in the Mitochondrial Complex I Assembly Factor NDUFAF5 Causes Isolated Bilateral Striatal Necrosis in Childhood. Front. Neurol. 12:792230. doi: 10.3389/fneur.2021.792230
Received
10 October 2021
Accepted
11 October 2021
Published
09 November 2021
Approved by
Frontiers Editorial Office, Frontiers Media SA, Switzerland
Volume
12 - 2021
Updates
Copyright
© 2021 Bi, Guo, Wang, Zhang, Zhao, Li, Zhao, Tuo and Zhang.
This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Hongyan Bi hybi1996@sina.com
This article was submitted to Neurogenetics, a section of the journal Frontiers in Neurology
Disclaimer
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.