A novel DLG4 variant causes DLG4-related synaptopathy with intellectual regression.


Journal

Human genome variation
ISSN: 2054-345X
Titre abrégé: Hum Genome Var
Pays: England
ID NLM: 101652445

Informations de publication

Date de publication:
05 Jan 2024
Historique:
received: 25 08 2023
accepted: 21 11 2023
revised: 09 11 2023
medline: 6 1 2024
pubmed: 6 1 2024
entrez: 5 1 2024
Statut: epublish

Résumé

DLG4-related synaptopathy is a neurodevelopmental disorder caused by a DLG4 variant. We identified a novel de novo heterozygous frameshift variant, NM_001321075.3(DLG4):c.554_563del, in a Japanese girl. Intellectual regression without motor delay was observed at 2 years of age, and she was diagnosed with autism spectrum disorder and attention-deficit/hyperactivity disorder. Recognizing the possibility of DLG4-related synaptopathy in patients with intellectual regression is important for ensuring an accurate diagnosis.

Identifiants

pubmed: 38182567
doi: 10.1038/s41439-023-00260-x
pii: 10.1038/s41439-023-00260-x
doi:

Types de publication

Journal Article

Langues

eng

Pagination

1

Informations de copyright

© 2024. The Author(s).

Références

Sheng, M. & Kim, E. The postsynaptic organization of synapses. Cold Spring Harb. Perspect. Biol. 3, a005678 (2011).
doi: 10.1101/cshperspect.a005678 pubmed: 22046028 pmcid: 3225953
Rodríguez-Palmero, A. et al. DLG4-related synaptopathy: a new rare brain disorder. Genet. Med. 23, 888–899 (2021).
doi: 10.1038/s41436-020-01075-9 pubmed: 33597769
Kaplanis, J. et al. Evidence for 28 genetic disorders discovered by combining healthcare and research data. Nature 586, 757–762 (2020).
doi: 10.1038/s41586-020-2832-5 pubmed: 33057194 pmcid: 7116826
Rauch, A. et al. Range of genetic mutations associated with severe non-syndromic sporadic intellectual disability: an exome sequencing study. Lancet 380, 1674–1682 (2012).
doi: 10.1016/S0140-6736(12)61480-9 pubmed: 23020937
Lelieveld, S. H. et al. Meta-analysis of 2,104 trios provides support for 10 new genes for intellectual disability. Nat. Neurosci. 19, 1194–1196 (2016).
doi: 10.1038/nn.4352 pubmed: 27479843
Moutton, S. et al. Truncating variants of the DLG4 gene are responsible for intellectual disability with marfanoid features. Clin. Genet. 93, 1172–1178 (2018).
doi: 10.1111/cge.13243 pubmed: 29460436
Fitzgerald, T. W., Gerety, S. S., Jones, W. D. & van Kogelenberg, M. Large-scale discovery of novel genetic causes of developmental disorders. Nature 519, 223–228 (2015).
doi: 10.1038/nature14135
Xing, J. et al. Resequencing and association analysis of six PSD-95-related genes as possible susceptibility genes for schizophrenia and autism spectrum disorders. Sci. Rep. 6, 27491 (2016).
doi: 10.1038/srep27491 pubmed: 27271353 pmcid: 4895433
Bosch, D. G. et al. Novel genetic causes for cerebral visual impairment. Eur. J. Hum. Genet. 24, 660–665 (2016).
doi: 10.1038/ejhg.2015.186 pubmed: 26350515
Amor, D. J. Investigating the child with intellectual disability. J. Paediatr. Child Health 54, 1154–1158 (2018).
doi: 10.1111/jpc.14202 pubmed: 30294993
Moeschler, J. B. & Shevell, M., Committee on Genetics. Comprehensive evaluation of the child with intellectual disability or global developmental delays. Pediatrics 134, e903–e918 (2014).
doi: 10.1542/peds.2014-1839 pubmed: 25157020
Gordon, A. S. et al. Frequency of genomic secondary findings among 21,915 eMERGE network participants. Genet. Med. 22, 1470–1477 (2020).
doi: 10.1038/s41436-020-0810-9 pmcid: 7713503
Wozniak-Mielczarek, L. et al. How to distinguish Marfan syndrome from Marfanoid habitus in a physical examination—comparison of external features in patients with Marfan syndrome and Marfanoid habitus. Int. J. Environ. Res. Public Health 19, 772 (2022).
doi: 10.3390/ijerph19020772 pubmed: 35055593 pmcid: 8775541
Chen, X. et al. PSD-95 family MAGUKs are essential for anchoring AMPA and NMDA receptor complexes at the postsynaptic density. Proc. Natl Acad. Sci. USA 112, E6983–E6992 (2015).
doi: 10.1073/pnas.1517045112 pubmed: 26604311 pmcid: 4687590

Auteurs

Sachi Tokunaga (S)

Department of Pediatrics, Hyogo Medical University School of Medicine, Nishinomiya, Hyogo, Japan. sa-tokunaga@hyo-med.ac.jp.

Hideki Shimomura (H)

Department of Pediatrics, Hyogo Medical University School of Medicine, Nishinomiya, Hyogo, Japan.

Naoko Taniguchi (N)

Department of Pediatrics, Hyogo Medical University School of Medicine, Nishinomiya, Hyogo, Japan.

Kumiko Yanagi (K)

Department of Genome Medicine, National Center for Child Health and Development, Tokyo, Japan.

Tadashi Kaname (T)

Department of Genome Medicine, National Center for Child Health and Development, Tokyo, Japan.

Nobuhiko Okamoto (N)

Department of Medical Genetics, Osaka Women's and Children's Hospital, Osaka, Japan.

Yasuhiro Takeshima (Y)

Department of Pediatrics, Hyogo Medical University School of Medicine, Nishinomiya, Hyogo, Japan.

Classifications MeSH