98%
921
2 minutes
20
Orofacial clefts are among the most common birth defects and result in an improper formation of the mouth or the roof of the mouth. Monosomy of the distal aspect of human chromosome 6p has been recognized as causative in congenital malformations affecting the brain and cranial skeleton including orofacial clefts. Among the genes located in this region is PAK1IP1, which encodes a nucleolar factor involved in ribosomal stress response. Here, we report the identification of a novel mouse line that carries a point mutation in the Pak1ip1 gene. Homozygous mutants show severe developmental defects of the brain and craniofacial skeleton, including a median orofacial cleft. We recovered this line of mice in a forward genetic screen and named the allele manta-ray (mray). Our findings prompted us to examine human cases of orofacial clefting for mutations in the PAK1IP1 gene or association with the locus. No deleterious variants in the PAK1IP1 gene coding region were recognized, however, we identified a borderline association effect for SNP rs494723 suggesting a possible role for the PAK1IP1 gene in human orofacial clefting.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3723895 | PMC |
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0069333 | PLOS |
Hum Mutat
September 2025
State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan, China.
Over the past decade, genome-wide association studies (GWASs) have found genetic variants associated with elevated risk for nonsyndromic orofacial cleft (NSOFC). In the post-GWAS era of NSOFC genetic research, an important aim is to identify the pathogenic variants that influence craniofacial development processes, towards understanding how they lead to disease manifestation. However, two major challenges hinder the translation of GWAS results into a mechanistic understanding.
View Article and Find Full Text PDFOral Dis
September 2025
Department of Oral Diagnosis, School of Dentistry, University of Campinas (FOP/UNICAMP), Piracicaba, Brazil.
Oral Dis
September 2025
Department of Second Clinical Medical School, Guangdong Medical University, Dongguan, China.
ALTEX
August 2025
Department of Biomedical Engineering, Institute for Quantitative Health Science and Engineering, Michigan State University, East Lansing, MI, USA.
Sonic hedgehog (SHH) is a major intercellular signaling pathway involved in the orchestration of embryogenesis, including orofacial morphogenesis. The SHH pathway is sensitive to disruption, including both genetic predisposition and chemical-induced disruption at multiple molecular targets including antagonism of the SHH signal transducer Smoothened (SMO). Here we report the adverse outcome pathway (AOP) 460 describing the linkage between antagonism of the SMO receptor, a key intermediate in the hedgehog signaling, and orofacial clefts (OFCs).
View Article and Find Full Text PDFZhonghua Kou Qiang Yi Xue Za Zhi
September 2025
Department of Cleft Lip and Palate Surgery, West China Hospital of Stomatology, Sichuan University & State Key Laboratory of Oral Diseases & National Center for Stomatology & National Clinical Research Center for Oral Diseases, Chengdu 610041, China.
This study aims to preliminarily investigate the role of methylation in the epigenetic regulation of the pathogenesis of non-syndromic orofacial clefts (NSOC), to address the gaps in previous explorations of susceptibility genes associated with NSOC. We conducted an association analysis of single nucleotide polymorphisms (SNPs) and genes related to methylation using data from a large-scale genome-wide association study involving Han Chinese patients with non-syndromic orofacial clefts and healthy controls. A significant association was found between NSOC and the DNA methylation gene TET1, as well as the histone methylation gene NSD1.
View Article and Find Full Text PDF