Genetic origin of sporadic cases and RNA toxicity in neuronal intranuclear inclusion disease.


Journal

Journal of medical genetics
ISSN: 1468-6244
Titre abrégé: J Med Genet
Pays: England
ID NLM: 2985087R

Informations de publication

Date de publication:
05 2022
Historique:
received: 19 12 2020
revised: 10 02 2021
accepted: 10 03 2021
pubmed: 27 3 2021
medline: 27 4 2022
entrez: 26 3 2021
Statut: ppublish

Résumé

GGC repeat expansion in Multiple genetic screenings were performed on NIID individuals and their available family members. Methylation status of blood DNA, NOTCH2NLC mRNA level from muscle biopsies and RNA foci from skin biopsies of NIID individuals or asymptomatic carriers were evaluated and compared. In two sporadic NIID families, we identified two clinically and pathologically asymptomatic fathers carrying large GGC repeat expansion, above 300 repeats, with offspring repeat numbers of 172 and 148, respectively. Further evaluation revealed that the GGC repeat numbers in the sperm from two asymptomatic fathers were only 63 and 98, respectively. The CpG island in Our study suggested the GGC repeat expansion in NOTCH2NLC might have a disease-causing number ranging from ~41 to ~300 repeats. The contraction of GGC repeat expansion in sperm could be a possible mechanism for the paternal-biased origin in some sporadic or recessive inherited NIID individuals. The toxic RNA gain-of-function mechanism was identified to be involved in the pathogenicity of this disease.

Sections du résumé

BACKGROUND
GGC repeat expansion in
METHODS
Multiple genetic screenings were performed on NIID individuals and their available family members. Methylation status of blood DNA, NOTCH2NLC mRNA level from muscle biopsies and RNA foci from skin biopsies of NIID individuals or asymptomatic carriers were evaluated and compared.
RESULTS
In two sporadic NIID families, we identified two clinically and pathologically asymptomatic fathers carrying large GGC repeat expansion, above 300 repeats, with offspring repeat numbers of 172 and 148, respectively. Further evaluation revealed that the GGC repeat numbers in the sperm from two asymptomatic fathers were only 63 and 98, respectively. The CpG island in
CONCLUSION
Our study suggested the GGC repeat expansion in NOTCH2NLC might have a disease-causing number ranging from ~41 to ~300 repeats. The contraction of GGC repeat expansion in sperm could be a possible mechanism for the paternal-biased origin in some sporadic or recessive inherited NIID individuals. The toxic RNA gain-of-function mechanism was identified to be involved in the pathogenicity of this disease.

Identifiants

pubmed: 33766934
pii: jmedgenet-2020-107649
doi: 10.1136/jmedgenet-2020-107649
doi:

Substances chimiques

RNA, Messenger 0
RNA 63231-63-0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

462-469

Informations de copyright

© Author(s) (or their employer(s)) 2022. No commercial re-use. See rights and permissions. Published by BMJ.

Déclaration de conflit d'intérêts

Competing interests: None declared.

Auteurs

Jianwen Deng (J)

Department of Neurology, Peking University First Hospital, Beijing, China.
Beijing Key Laboratory of Neurovascular Disease Discovery, Beijing, China.

Binbin Zhou (B)

Department of Neurology, First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.

Jiaxi Yu (J)

Department of Neurology, Peking University First Hospital, Beijing, China.
Beijing Key Laboratory of Neurovascular Disease Discovery, Beijing, China.

Xiaochen Han (X)

Department of Neurology, Sixth Medical Center of PLA General Hospital, Beijing, China.

Jianhui Fu (J)

Department of Neurology, Huashan Hospital Fudan University, Shanghai, China.

Xiaobin Li (X)

Department of Neurology, First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.

Xufang Xie (X)

Department of Neurology, First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.

Min Zhu (M)

Department of Neurology, First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.

Yilei Zheng (Y)

Department of Neurology, First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.

Xueyu Guo (X)

Grandomics Biosciences, Beijing, China.

Pidong Li (P)

Grandomics Biosciences, Beijing, China.

Qingqing Wang (Q)

Department of Neurology, Peking University First Hospital, Beijing, China.
Beijing Key Laboratory of Neurovascular Disease Discovery, Beijing, China.

Jing Liu (J)

Department of Neurology, Peking University First Hospital, Beijing, China.
Beijing Key Laboratory of Neurovascular Disease Discovery, Beijing, China.

Wei Zhang (W)

Department of Neurology, Peking University First Hospital, Beijing, China.
Beijing Key Laboratory of Neurovascular Disease Discovery, Beijing, China.

Yun Yuan (Y)

Department of Neurology, Peking University First Hospital, Beijing, China.
Beijing Key Laboratory of Neurovascular Disease Discovery, Beijing, China.

Sheng Yao (S)

Department of Neurology, Sixth Medical Center of PLA General Hospital, Beijing, China bjyaosheng@sina.com drwangzx@163.com hongdaojun@hotmail.com.

Zhaoxia Wang (Z)

Department of Neurology, Peking University First Hospital, Beijing, China bjyaosheng@sina.com drwangzx@163.com hongdaojun@hotmail.com.
Beijing Key Laboratory of Neurovascular Disease Discovery, Beijing, China.

Daojun Hong (D)

Department of Neurology, First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China bjyaosheng@sina.com drwangzx@163.com hongdaojun@hotmail.com.
Department of Neurology, Peking University People's Hospital, Beijing, China.

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