Verlee Maxim, D'haenens Erika, De Cock Laurenz, Muiño Mosquera Laura, De Groote Katya, Vandekerckhove Kristof, Panzer Joseph, Roets Ellen, Menten Björn, Symoens Sofie, Coucke Paul, Van Damme Tim, Vergult Sarah, Callewaert Bert
Center for Medical Genetics, Ghent University Hospital, Ghent, Belgium.
Department of Biomolecular Medicine, Ghent University, Ghent, Belgium.
Eur J Hum Genet. 2025 Jan 27. doi: 10.1038/s41431-025-01788-y.
The etiology of congenital heart disease (CHD) is complex, comprising both genetic and environmental factors. Despite documented familial occurrences, the genetic etiology remains largely elusive. Trio exome sequencing identified a heterozygous FLT4 splice site variant in two families with respectively tetralogy of Fallot (TOF), and variable CHD comprising both the TOF spectrum and aortic coarctation. In the first family, Sanger sequencing on cDNA confirmed aberrant splicing for the c.985+1G > A variant. In the second family, transcriptome sequencing uncovered altered splicing for the c.1657+6T > C variant, despite normal targeted Sanger sequencing. In conclusion, our study establishes FLT4 splice site variants as a molecular cause of both left and right-sided isolated CHD, with incomplete penetrance. RNA-sequencing emerges as a valuable technique in unraveling the missing inheritability of CHD.
先天性心脏病(CHD)的病因复杂,包括遗传和环境因素。尽管有家族发病的记录,但遗传病因在很大程度上仍不清楚。三联体全外显子测序在两个家庭中分别发现了一个杂合的FLT4剪接位点变异,一个家庭患有法洛四联症(TOF),另一个家庭患有包括TOF谱系和主动脉缩窄在内的多种先天性心脏病。在第一个家庭中,对cDNA进行的桑格测序证实了c.985+1G>A变异的异常剪接。在第二个家庭中,尽管靶向桑格测序正常,但转录组测序发现c.1657+6T>C变异存在剪接改变。总之,我们的研究确定FLT4剪接位点变异是左右侧孤立性先天性心脏病的分子病因,外显率不完全。RNA测序成为揭示先天性心脏病缺失遗传性的一项有价值的技术。