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So, K. K. H.

Publications and source records attributed to So, K. K. H..

3 recordsLinked to original sources

Integrative multiomic analysis on single-nucleotide variants identifies candidate genes for human craniofacial malformation

Craniofacial malformation (CFM) is a congenital defect encompassing a wide range of phenotypic presentations and is largely driven by genetics. Despite the discovery of more than 300 causal genes, there are a myriad of CFM cases with unknown genetic etiology. The complex gene regulations and heterogeneous cellular interactions in the developing head complicate disease-gene identification and prenatal genetic diagnosis. Recent progress in multiomic profiling of human embryogenesis enables the discovery of novel candidates from established GWAS data. Here, we developed an approach to prioritize GWAS variants using the epigenomes and single-cell transcriptomes of embryonic tissues and progenitor cells by implementing machine learning classifiers and combinatorial analysis. Systematic evaluation revealed significant improvement in the machine learning model performance after integrating transcriptome of neural crest cells (NCCs) and cranial placodes, as well as epigenomic profile of early craniofacial tissues. We identified 249 genes from the best-performing classifier, which include documented CFM-associated genes. Gene regulatory network (GRN) inference showed that 24 candidate genes were involved in NCC- and placode-specific regulons, of which 15 (F11R, ISL1, KANK4, L1TD1, LAMB1, MIA, PRDM1, S100A10, S100A11, STOM, STT3B, TESK2, USP43, WDR86, ZNF439) were novel candidates for human CFM. Motif analysis revealed putative functional SNPs contributing to CFM pathogenesis by disrupting transcription factor binding motifs in neural crest and placodes. Our analyses suggested that PRDM1 and ISL1 are strong candidates for human CFM, as supported by other animal functional studies. This study demonstrates a successful method for disease gene identification using epigenomic and single-cell transcriptomic profiles, and sheds light on the linkage between early cell lineages and the pathogenic process of CFM. Author SummaryCraniofacial malformation is one of the most common congenital disorders that affects food ingestion, speech and social interaction of the patients. The identification of craniofacial disease genes is difficult due to the dynamic gene expression and contribution from multiple cell types during embryonic development. In this study, we combine artificial intelligence with patient genetic and embryo multiomic information to identify new candidate genes for human craniofacial malformation. Using machine learning classifiers and combinatorial analyses, we prioritized single-nucleotide variants from patient datasets and identified 249 candidate genes. Annotation of the variants and candidate genes showed that some of them overlapped with known disease genes, demonstrating the efficacy of our approach. Further analyses using lineage reconstruction and motif analyses revealed a number of promising novel candidates, in particular PRDM1 and ISL1, are likely to be causative genes for human CFM. Our study has demonstrated a translatable approach for disease gene identification utilizing machine learning algorithm and multiomic data, and provides a gene list for improving diagnostic panels and understanding the pathogenic processes of craniofacial disorders.

genetics↗

Irx3/5 define the cochlear sensory domain and regulate vestibular and cochlear sensory patterning in the mammalian inner ear

The mammalian inner ear houses the vestibular and cochlear sensory organs dedicated to sensing balance and sound, respectively. These distinct sensory organs arise from a common prosensory region, but the mechanisms underlying their divergence remain elusive. Here, we showed that two evolutionarily conserved homeobox genes, Irx3 and Irx5, are required for the patterning and segregation of the saccular and cochlear sensory domains, as well as for the formation of auditory sensory cells. Irx3/5 were highly expressed in the cochlea, their deletion resulted in a significantly shortened cochlea with a loss of the ductus reuniens that bridged the vestibule and cochlea. Remarkably, ectopic vestibular hair cells replaced the cochlear non-sensory structure, the Greater Epithelial Ridge. Moreover, most auditory sensory cells in the cochlea were transformed into hair cells of vestibular identity, with only a residual organ of Corti remaining in the mid-apical region of Irx3/5 double knockout mice. Conditional temporal knockouts further revealed that Irx3/5 are essential for controlling cochlear sensory domain formation before embryonic day 14. Our findings demonstrate that Irx3/5 regulate the patterning of vestibular and cochlear sensory cells, providing insights into the separation of vestibular and cochlear sensory organs during mammalian inner ear development.

developmental biology↗

seRNA PAM-1 regulates skeletal muscle satellite cell activation and aging through trans regulation of Timp2 expression synergistically with Ddx5

Muscle satellite cells (SCs) are responsible for muscle homeostasis and regeneration; and lncRNAs play important roles in regulating SC activities. Here in this study, we identify PAM-1 (Pax7 Associated Muscle lncRNA) that is induced in activated SCs to promote SC activation into myoblast cells upon injury. PAM-1 is generated from a myoblast specific super-enhancer (SE); as a seRNA it binds with a number of target genomic loci predominantly in trans. Further studies demonstrate that it interacts with Ddx5 to tether PAM-1 SE to it inter-chromosomal targets Timp2 and Vim to activate the gene expression. Lastly, we show that PAM-1 expression is increased in aging SCs, which leads to enhanced inter-chromosomal interaction and target genes up-regulation. Altogether, our findings identify PAM-1 as a previously unknown lncRNA that regulates both SC activation and aging through its trans gene regulatory activity.

developmental biology↗