Literature DB >> 32488467

Autozygosity-driven genetic diagnosis in consanguineous families from Italy and the Greater Middle East.

Flavia Palombo1,2, Claudio Graziano1, Nadia Al Wardy3, Nayereh Nouri4,5, Caterina Marconi6, Pamela Magini1, Giulia Severi1, Chiara La Morgia2,7, Gaetano Cantalupo8,9, Duccio Maria Cordelli6,10, Simone Gangarossa11, Mohammed Nasser Al Kindi3, Mazin Al Khabouri3,12, Mansoor Salehi4, Elisa Giorgio13, Alfredo Brusco13, Francesco Pisani14, Giovanni Romeo6, Valerio Carelli2,7, Tommaso Pippucci15, Marco Seri1,6.   

Abstract

Autozygosity-driven exome analysis has been shown effective for identification of genes underlying recessive diseases especially in countries of the so-called Greater Middle East (GME), where high consanguinity unravels the phenotypic effects of recessive alleles and large family sizes facilitate homozygosity mapping. In Italy, as in most European countries, consanguinity is estimated low. Nonetheless, consanguineous Italian families are not uncommon in publications of genetic findings and are often key to new associations of genes with rare diseases. We collected 52 patients from 47 consanguineous families with suspected recessive diseases, 29 originated in GME countries and 18 of Italian descent. We performed autozygosity-driven exome analysis by detecting long runs of homozygosity (ROHs > 1.5 Mb) and by prioritizing candidate clinical variants within. We identified a pathogenic synonymous variant that had been previously missed in NARS2 and we increased an initial high diagnostic rate (47%) to 55% by matchmaking our candidate genes and including in the analysis shorter ROHs that may also happen to be autozygous. GME and Italian families contributed to diagnostic yield comparably. We found no significant difference either in the extension of the autozygous genome, or in the distribution of candidate clinical variants between GME and Italian families, while we showed that the average autozygous genome was larger and the mean number of candidate clinical variants was significantly higher (p = 0.003) in mutation-positive than in mutation-negative individuals, suggesting that these features influence the likelihood that the disease is autozygosity-related. We highlight the utility of autozygosity-driven genomic analysis also in countries and/or communities, where consanguinity is not widespread cultural tradition.

Entities:  

Year:  2020        PMID: 32488467     DOI: 10.1007/s00439-020-02187-7

Source DB:  PubMed          Journal:  Hum Genet        ISSN: 0340-6717            Impact factor:   4.132


  3 in total

1.  Novel NARS2 variant causing leigh syndrome with normal lactate levels.

Authors:  Ryosuke Tanaka; Ryo Takeguchi; Mami Kuroda; Nao Suzuki; Yoshio Makita; Kumiko Yanagi; Tadashi Kaname; Satoru Takahashi
Journal:  Hum Genome Var       Date:  2022-05-04

2.  De novo and bi-allelic variants in AP1G1 cause neurodevelopmental disorder with developmental delay, intellectual disability, and epilepsy.

Authors:  Muhammad A Usmani; Zubair M Ahmed; Pamela Magini; Victor Murcia Pienkowski; Kristen J Rasmussen; Rebecca Hernan; Faiza Rasheed; Mureed Hussain; Mohsin Shahzad; Brendan C Lanpher; Zhiyv Niu; Foong-Yen Lim; Tommaso Pippucci; Rafal Ploski; Verena Kraus; Karolina Matuszewska; Flavia Palombo; Jessica Kianmahd; Julian A Martinez-Agosto; Hane Lee; Emma Colao; M Mahdi Motazacker; Karlla W Brigatti; Erik G Puffenberger; S Amer Riazuddin; Claudia Gonzaga-Jauregui; Wendy K Chung; Matias Wagner; Matthew J Schultz; Marco Seri; Anneke J A Kievit; Nicola Perrotti; J S Klein Wassink-Ruiter; Hans van Bokhoven; Sheikh Riazuddin; Saima Riazuddin
Journal:  Am J Hum Genet       Date:  2021-06-07       Impact factor: 11.025

Review 3.  Novel phenotype and genotype spectrum of NARS2 and literature review of previous mutations.

Authors:  Mohammad Vafaee-Shahi; Mohammad Farhadi; Ehsan Razmara; Saeid Morovvati; Saeide Ghasemi; Seyedeh Sedigheh Abedini; Zohreh Bagher; Rafieh Alizadeh; Masoumeh Falah
Journal:  Ir J Med Sci       Date:  2021-08-10       Impact factor: 2.089

  3 in total

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