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DOI 10.1016/j.ajhg.2019.09.025

Медицинская библиотека · American journal of human genetics · 2019

Homozygous Missense Variants in NTNG2, Encoding a Presynaptic Netrin-G2 Adhesion Protein, Lead to a Distinct Neurodevelopmental Disorder.

Dias Caroline M, Punetha Jaya, Zheng Céline, Mazaheri Neda, Rad Abolfazl, Efthymiou Stephanie, Petersen Andrea, Dehghani Mohammadreza, Pehlivan Davut, Partlow Jennifer N, Posey Jennifer E, Salpietro Vincenzo, Gezdirici Alper, Malamiri Reza Azizi, Al Menabawy Nihal M, Selim Laila A, Vahidi Mehrjardi Mohammad Yahya, Banu Selina, Polla Daniel L, Yang Edward, Rezazadeh Varaghchi Jamileh, Mitani Tadahiro, van Beusekom Ellen, Najafi Maryam, Sedaghat Alireza, Keller-Ramey Jennifer, Durham Leslie, Coban-Akdemir Zeynep, Karaca Ender, Orlova Valeria, Schaeken Lieke L M, Sherafat Amir, Jhangiani Shalini N, Stanley Valentina, Shariati Gholamreza, Galehdari Hamid, Gleeson Joseph G, Walsh Christopher A, Lupski James R, Seiradake Elena, Houlden Henry, van Bokhoven Hans, Maroofian Reza

СтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАПеревод в очереди

Аннотация

NTNG2 encodes netrin-G2, a membrane-anchored protein implicated in the molecular organization of neuronal circuitry and synaptic organization and diversification in vertebrates. In this study, through a combination of exome sequencing and autozygosity mapping, we have identified 16 individuals (from seven unrelated families) with ultra-rare homozygous missense variants in NTNG2; these individuals present with shared features of a neurodevelopmental disorder consisting of global developmental delay, severe to profound intellectual disability, muscle weakness and abnormal tone, autistic features, behavioral abnormalities, and variable dysmorphisms. The variants disrupt highly conserved residues across the protein. Functional experiments, including in silico analysis of the protein structure, in vitro assessment of cell surface expression, and in vitro knockdown, revealed potential mechanisms of pathogenicity of the variants, including loss of protein function and decreased neurite outgrowth. Our data indicate that appropriate expression of NTNG2 plays an important role in neurotypical development.

Для цитирования: Dias Caroline M, Punetha Jaya, Zheng Céline, Mazaheri Neda, Rad Abolfazl, Efthymiou Stephanie, Petersen Andrea, Dehghani Mohammadreza, Pehlivan Davut, Partlow Jennifer N, Posey Jennifer E, Salpietro Vincenzo, Gezdirici Alper, Malamiri Reza Azizi, Al Menabawy Nihal M, Selim Laila A, Vahidi Mehrjardi Mohammad Yahya, Banu Selina, Polla Daniel L, Yang Edward, Rezazadeh Varaghchi Jamileh, Mitani Tadahiro, van Beusekom Ellen, Najafi Maryam, Sedaghat Alireza, Keller-Ramey Jennifer, Durham Leslie, Coban-Akdemir Zeynep, Karaca Ender, Orlova Valeria, Schaeken Lieke L M, Sherafat Amir, Jhangiani Shalini N, Stanley Valentina, Shariati Gholamreza, Galehdari Hamid, Gleeson Joseph G, Walsh Christopher A, Lupski James R, Seiradake Elena, Houlden Henry, van Bokhoven Hans, Maroofian Reza. Homozygous Missense Variants in NTNG2, Encoding a Presynaptic Netrin-G2 Adhesion Protein, Lead to a Distinct Neurodevelopmental Disorder.. American journal of human genetics. 2019. DOI: 10.1016/j.ajhg.2019.09.025.

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