| Literature DB >> 32562828 |
Mingjie Li1, Xinxin Lu1, Jian Dong1, Zuwu Yao2, Yinlong Wu1, Huiying Rao3, Xiaoli Huang1, Xijun Chen1, Yi Huang1, Yan'an Wu4.
Abstract
Marfan syndrome is a heritable autosomal-dominant connective tissue disorder and it was typically caused by mutations in FBN1. However, the synonymous mutation was seldom recorded to be related to Marfan syndrome. Hereon, Multiplex ligation-dependent probe amplification failed to detect a copy number variant involving FBN1 but a synonymous mutation c.4773A > G (p.Gly1591Gly) was identified by NGS in exon 39. RNA was extracted from patient's aortic tissue and reverse polymerase chain reaction demonstrated the presence of a shortened mRNA transcript. Results of minigene models indicated that c.4773A > G was bona fide responsibility for the aberrant splicing pattern, and artificial mutations of c.4773A > C and c.4773A > T also gave rise to fragments with exon 39 entire skipped. Together, the novel synonymous mutations in c.4773 position (A > G, C, T), middle of exon 39 of FBN1 gene, was found to be associated with Marfan syndrome by altering the splicing pattern of pre-mRNA.Entities:
Keywords: Marfan syndrome; Skip; Splicing; Synonymous mutation
Year: 2020 PMID: 32562828 DOI: 10.1016/j.ygeno.2020.06.024
Source DB: PubMed Journal: Genomics ISSN: 0888-7543 Impact factor: 5.736