Unveiling genetics of non-syndromic albinism using whole exome sequencing: A comprehensive study of TYR, TYRP1, OCA2 and MC1R genes in 17 families.

Melanocytes Molecular diagnostics Oculocutaneous albinism Skin depigmentation Whole exome sequencing

Journal

Gene
ISSN: 1879-0038
Titre abrégé: Gene
Pays: Netherlands
ID NLM: 7706761

Informations de publication

Date de publication:
11 Nov 2023
Historique:
received: 20 09 2023
revised: 22 10 2023
accepted: 10 11 2023
medline: 14 11 2023
pubmed: 14 11 2023
entrez: 13 11 2023
Statut: aheadofprint

Résumé

Oculocutaneous albinism (OCA) is a group of skin depigmentation disorders. Clinical presentation of OCA includes defects in melanocyte differentiation, melanin biosynthesis, and melanosome maturation and transport. A molecular diagnostics study of families presenting oculocutaneous albinism. In this study, 17 consanguineous OCA families consisting of 93 patients were investigated. Whole Exome Sequencing (WES) of the index patient in each family were performed. Short listed variants of WES were Sanger validated for Mendelian segregation in obligate carriers and other available family members. Variant prioritization and pathogenicity were classified as per the criteria of American College Medical Genetics and Genomics (ACMG). Comparative computational modelling was performed to predict the potential damaging effect of the altered proteins. 15 pathogenic variations: c.132 T > A, c.346C > T, c.488C > G, c.1037G > A in TYR, c.1211C > T, c.1441G > A, c.1706_1707insT, c.2020C > G, c.2402G > C, c.2430del, in OCA2, c.1067G > A in TYRP1 and c.451C > T, c.515G > T, c.766C > T, c.917G > A in MC1R genes were identified. Three variants in OCA2 gene were characterized: c.1706_1707insT, c.2430del, and c.2402G > C, all of which were not reported before in OCA families. A few studies focusing on mutation screening of OCA patients have been reported before; however, this study has uniquely presents the Pakhtun ethnic population residing on the North-Western boarder. It explains that TYR, OCA2, TYRP1, and MC1R variations lead to non-syndromic OCA phenotype The overlapping phenotypes of OCA can precisely be diagnosed for its molecular pathogenicity using WES. This study recommends WES as a first-line molecular diagnostic tool, and provides a basis for developing customized genetic tests i.e. pre-marital screening to reduce the disease burden in the future generations.

Sections du résumé

BACKGROUND BACKGROUND
Oculocutaneous albinism (OCA) is a group of skin depigmentation disorders. Clinical presentation of OCA includes defects in melanocyte differentiation, melanin biosynthesis, and melanosome maturation and transport.
OBJECTIVES OBJECTIVE
A molecular diagnostics study of families presenting oculocutaneous albinism.
METHODS METHODS
In this study, 17 consanguineous OCA families consisting of 93 patients were investigated. Whole Exome Sequencing (WES) of the index patient in each family were performed. Short listed variants of WES were Sanger validated for Mendelian segregation in obligate carriers and other available family members. Variant prioritization and pathogenicity were classified as per the criteria of American College Medical Genetics and Genomics (ACMG). Comparative computational modelling was performed to predict the potential damaging effect of the altered proteins.
RESULTS RESULTS
15 pathogenic variations: c.132 T > A, c.346C > T, c.488C > G, c.1037G > A in TYR, c.1211C > T, c.1441G > A, c.1706_1707insT, c.2020C > G, c.2402G > C, c.2430del, in OCA2, c.1067G > A in TYRP1 and c.451C > T, c.515G > T, c.766C > T, c.917G > A in MC1R genes were identified. Three variants in OCA2 gene were characterized: c.1706_1707insT, c.2430del, and c.2402G > C, all of which were not reported before in OCA families.
CONCLUSION CONCLUSIONS
A few studies focusing on mutation screening of OCA patients have been reported before; however, this study has uniquely presents the Pakhtun ethnic population residing on the North-Western boarder. It explains that TYR, OCA2, TYRP1, and MC1R variations lead to non-syndromic OCA phenotype The overlapping phenotypes of OCA can precisely be diagnosed for its molecular pathogenicity using WES. This study recommends WES as a first-line molecular diagnostic tool, and provides a basis for developing customized genetic tests i.e. pre-marital screening to reduce the disease burden in the future generations.

Identifiants

pubmed: 37956964
pii: S0378-1119(23)00827-2
doi: 10.1016/j.gene.2023.147986
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

147986

Informations de copyright

Copyright © 2023 Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Qaiser Zaman (Q)

Department of Zoology, Government Postgraduate College Dargai, Malakand 23050, Pakistan; Higher Education Department, Peshawar 25120, Government of Khyber Pakhtunkhwa, Pakistan; Department of Zoology, Abdul Wali Khan University, Mardan 23200, Pakistan.

Jamshid Khan (J)

Department of Zoology, Government Postgraduate College Dargai, Malakand 23050, Pakistan.

Mashal Ahmad (M)

Department of Zoology, Government Postgraduate College Dargai, Malakand 23050, Pakistan.

Hamza Khan (H)

Department of Zoology, Government Postgraduate College Dargai, Malakand 23050, Pakistan; Department of Zoology, Islamia College, Peshawar 25120, Pakistan.

Hammad Tufail Chaudhary (HT)

Department of Pathology, Medical College, Taif University, Taif, Saudi Arabia.

Gauhar Rehman (G)

Department of Zoology, Abdul Wali Khan University, Mardan 23200, Pakistan.

Obaid Ur Rahman (OU)

Department of Biochemistry, Swat Medical College, Swat 19200, Pakistan.

Muhammad M Shah (MM)

Department of Zoology, Government Postgraduate College Dargai, Malakand 23050, Pakistan.

Javeria Hussain (J)

Department of Zoology, Government Postgraduate College Dargai, Malakand 23050, Pakistan.

Qaisar Jamal (Q)

Department of Zoology, University of Peshawar, Peshawar 25120, Pakistan.

Bakht Tareen Khan (BT)

Department of Zoology, University of Peshawar, Peshawar 25120, Pakistan.

Muhammad A Khan (MA)

Department of Zoology, Government Postgraduate College Dargai, Malakand 23050, Pakistan.
Department of Zoology, Government Postgraduate College Dargai, Malakand 23050, Pakistan.

Kalsoom Sahar (K)

Department of Zoology, Government Postgraduate College Dargai, Malakand 23050, Pakistan.

Muhammad Idrees (M)

Department of Zoology, Government Postgraduate College Dargai, Malakand 23050, Pakistan.

Raees Ahmad (R)

Department of Zoology, Government Postgraduate College Timergara, Dir Lower 18300, Pakistan.

Mohammad Shah Faisal (MS)

Department of Zoology, Islamia College, Peshawar 25120, Pakistan.

Muhammad Ismail Khan (MI)

Department of Zoology, Islamia College, Peshawar 25120, Pakistan.

Muhammad Khisroon (M)

Department of Zoology, University of Peshawar, Peshawar 25120, Pakistan.

Angham Abdulrhman Abdulkareem (AA)

Center of Excellence in Genomic Medicine Research, King Abdulaziz University, Jeddah, Saudi Arabia; Faculty of Science, Department of Biochemistry, King Abdulaziz University, Jeddah, Saudi Arabia.

Eugene Lee (E)

3billion Inc., Seoul, Republic of Korea.

Seung Woo Ryu (SW)

3billion Inc., Seoul, Republic of Korea.

Nousheen Bibi (N)

Department of Bioinformatics, Shaheed Benazir Bhutto Women University, Peshawar 25120, Pakistan.

Osama Yousef Muthaffar (OY)

Department of Pediatrics, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia.

Musharraf Jelani (M)

Rare Diseases Genetics and Genomics, Centre for Omic Sciences, Islamia College, Peshawar 25120, Pakistan. Electronic address: mjelani@icp.edu.pk.

Muhammad Imran Naseer (MI)

Center of Excellence in Genomic Medicine Research, King Abdulaziz University, Jeddah, Saudi Arabia; Department of Medical Laboratory Technology, Faculty of Applied Medical Sciences, King Abdulaziz University, Jeddah, Saudi Arabia. Electronic address: minaseer@kau.edu.sa.

Classifications MeSH