Literature DB >> 33824500

Biallelic variants in TMEM222 cause a new autosomal recessive neurodevelopmental disorder.

Daniel L Polla1,2, Mohammad Ali Farazi Fard3, Zahra Tabatabaei3, Parham Habibzadeh3, Olga A Levchenko4, Pooneh Nikuei5, Periklis Makrythanasis6,7, Mureed Hussain1, Sandra von Hardenberg8, Sirous Zeinali9, Mohammad-Sadegh Fallah10, Janneke H M Schuurs-Hoeijmakers1, Mohsin Shahzad11,12,13, Fareeha Fatima14, Neelam Fatima14, Laura Donker Kaat15, Hennie T Bruggenwirth15, Leah R Fleming16, John Condie17, Rafal Ploski18, Agnieszka Pollak18, Jacek Pilch19, Nina A Demina4, Alena L Chukhrova4, Vasilina S Sergeeva4, Hanka Venselaar20, Amira T Masri21, Hanan Hamamy6, Federico A Santoni6,22, Katrin Linda1, Zubair M Ahmed11, Nael Nadif Kasri1, Arjan P M de Brouwer1, Anke K Bergmann8, Sven Hethey23, Majid Yavarian3, Muhammad Ansar6,24, Saima Riazuddin11, Sheikh Riazuddin12,13, Mohammad Silawi3, Gaia Ruggeri25, Filomena Pirozzi25, Ebrahim Eftekhar5, Afsaneh Taghipour Sheshdeh3, Shima Bahramjahan3, Ghayda M Mirzaa25,26,27, Alexander V Lavrov4, Stylianos E Antonarakis6,28, Mohammad Ali Faghihi3,29, Hans van Bokhoven30.   

Abstract

PURPOSE: To elucidate the novel molecular cause in families with a new autosomal recessive neurodevelopmental disorder.
METHODS: A combination of exome sequencing and gene matching tools was used to identify pathogenic variants in 17 individuals. Quantitative reverse transcription polymerase chain reaction (RT-qPCR) and subcellular localization studies were used to characterize gene expression profile and localization.
RESULTS: Biallelic variants in the TMEM222 gene were identified in 17 individuals from nine unrelated families, presenting with intellectual disability and variable other features, such as aggressive behavior, shy character, body tremors, decreased muscle mass in the lower extremities, and mild hypotonia. We found relatively high TMEM222 expression levels in the human brain, especially in the parietal and occipital cortex. Additionally, subcellular localization analysis in human neurons derived from induced pluripotent stem cells (iPSCs) revealed that TMEM222 localizes to early endosomes in the synapses of mature iPSC-derived neurons.
CONCLUSION: Our findings support a role for TMEM222 in brain development and function and adds variants in the gene TMEM222 as a novel underlying cause of an autosomal recessive neurodevelopmental disorder.

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Mesh:

Year:  2021        PMID: 33824500      PMCID: PMC8725574          DOI: 10.1038/s41436-021-01133-w

Source DB:  PubMed          Journal:  Genet Med        ISSN: 1098-3600            Impact factor:   8.864


  38 in total

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Authors:  C Colantuoni; A E Purcell; C M Bouton; J Pevsner
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Journal:  Genet Med       Date:  2011-09       Impact factor: 8.822

6.  Fast, scalable generation of high-quality protein multiple sequence alignments using Clustal Omega.

Authors:  Fabian Sievers; Andreas Wilm; David Dineen; Toby J Gibson; Kevin Karplus; Weizhong Li; Rodrigo Lopez; Hamish McWilliam; Michael Remmert; Johannes Söding; Julie D Thompson; Desmond G Higgins
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7.  Expression of pre-selected TMEMs with predicted ER localization as potential classifiers of ccRCC tumors.

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Journal:  BMC Cancer       Date:  2015-07-14       Impact factor: 4.430

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Journal:  Front Pharmacol       Date:  2018-12-06       Impact factor: 5.810

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Journal:  Nat Cell Biol       Date:  2009-02-01       Impact factor: 28.824

10.  The Pfam protein families database in 2019.

Authors:  Sara El-Gebali; Jaina Mistry; Alex Bateman; Sean R Eddy; Aurélien Luciani; Simon C Potter; Matloob Qureshi; Lorna J Richardson; Gustavo A Salazar; Alfredo Smart; Erik L L Sonnhammer; Layla Hirsh; Lisanna Paladin; Damiano Piovesan; Silvio C E Tosatto; Robert D Finn
Journal:  Nucleic Acids Res       Date:  2019-01-08       Impact factor: 16.971

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