A novel mutation at ANTXR1 in an Indian patient with growth retardation–alopecia–pseudoanodontia–optic atrophy syndrome
Article Type
Research Article
Publication Title
Oral Surgery, Oral Medicine, Oral Pathology and Oral Radiology
Abstract
Objective Growth retardation–alopecia–pseudoanodontia–optic atrophy (GAPO) syndrome (Online Mendelian Inheritance in Man [OMIM] ID 230740) is one of the rarest autosomal recessive syndromes. It is characterized by many phenotypes, including wide anterior fontanel, frontal bossing of the face, depressed nasal bridge, along with the 4 classic phenotypes contained in the name of the syndrome. Recent reports identified nonsense, missense, and splicing mutations at different exons of ANTXR1 responsible for GAPO syndrome in patients from different ethnic populations. Here, we are reporting a mutation at ANTXR1 in an Indian patient with GAPO syndrome. Study design We describe an inherited mutation at ANTXR1 in a 6-year-old Indian boy with GAPO syndrome. Results Genomic DNA from the patient with the GAPO syndrome and his family members were screened for previously reported mutations at ANTXR1 by sequencing. Novel homozygous and heterozygous mutations in exon-3 of ANTXR1 (c.265 G > A, p.Gly89 Arg) were identified in the patient and in other members of the family, respectively. However, no mutated allele was identified in genomic DNA from unrelated healthy individuals. Bioinformatic analysis by different tools predicted the deleterious, damaging, or aberrant splicing effect of mutation on the protein. Conclusions Functional inefficiency of ANTXR1 as a result of mutation might have led to GAPO syndrome.
First Page
e261
Last Page
e265
DOI
10.1016/j.oooo.2017.07.009
Publication Date
11-1-2017
Recommended Citation
Chattopadhyay, Esita; Ghose, Sandip; Ray, Anindita; Anjum, Nishat; Mazumdar, Anjana; and Roy, Bidyut, "A novel mutation at ANTXR1 in an Indian patient with growth retardation–alopecia–pseudoanodontia–optic atrophy syndrome" (2017). Journal Articles. 2361.
https://digitalcommons.isical.ac.in/journal-articles/2361