ArticleAmerican journal of kidney diseases : the official journal of the National Kidney Foundation2024
A Deep Intronic PKHD1 Variant Identified by SpliceAI in a Deceased Neonate With Autosomal Recessive Polycystic Kidney Disease.
Article in American journal of kidney diseases : the official journal of the National Kidney Foundation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 9 citations in OpenAlex.
- A deep intronic IFT172 variant causing pseudoexon inclusion identified by whole-genome sequencing in nephronophthisis.CEN case reports · 2026Article
- SpliceTransformer predicts tissue-specific splicing linked to human diseases.Nature communications · 2024Article
- Combining full-length gene assay and SpliceAI to interpret the splicing impact of all possible SPINK1 coding variants.Human genomics · 2024Article
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25 authors at 13 institutions in 1 country.
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Abstract
The etiologies of newborn deaths in neonatal intensive care units usually remain unknown, even after genetic testing. Whole-genome sequencing, combined with artificial intelligence-based methods for predicting the effects of non-coding variants, provide an avenue for resolving these deaths. Using one such method, SpliceAI, we identified a maternally inherited deep intronic PKHD1 splice variant (chr6:52030169T>C), in trans with a pathogenic missense variant (p.Thr36Met), in a newborn who died of autosomal recessive polycystic kidney disease at age 2 days. We validated the deep intronic variant's impact in maternal urine-derived cells expressing PKHD1. Reverse transcription polymerase chain reaction followed by Sanger sequencing showed that the variant causes inclusion of 147bp of the canonical intron between exons 29 and 30 of PKHD1 into the mRNA, including a premature stop codon. Allele-specific expression analysis at a heterozygous site in the mother showed that the mutant allele completely suppresses canonical splicing. In an unrelated healthy control, there was no evidence of transcripts including the novel splice junction. We returned a diagnostic report to the parents, who underwent in vitro embryo selection.
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