ArticleMolecular neurobiology2017
MARK2/Par1b Insufficiency Attenuates DVL Gene Transcription via Histone Deacetylation in Lumbosacral Spina Bifida.
Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 19 citations in OpenAlex.
- Pathophysiological roles of neural stem cells in neuropsychiatric diseases: from plasticity to pharmacological targeting.Acta pharmacologica Sinica · 2026Review
- Excessive DNA Double-Strand Breaks-Associated 3D Genome Reorganization Contributes to Neural Tube Defects with Folate Deficiency.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Epigenetic dysregulation and the etiology of spina bifida.Neurochemistry international · 2025Review
- Neuronal connectivity, behavioral, and transcriptional alterations associated with the loss of MARK2.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Role of MARK2 in the nervous system and cancer.Cancer gene therapy · 2024Review
- Genetic mutations in ribosomal biogenesis gene TCOF1 identified in human neural tube defects.Molecular genetics & genomic medicine · 2023Article
- Identification of the Key Regulators of Spina Bifida Through Graph-Theoretical Approach.Frontiers in genetics · 2021Article
- Association between rare variants in specific functional pathways and human neural tube defects multiple subphenotypes.Neural development · 2020Article
- Identification of histone acetylation markers in human fetal brains and increased H4K5ac expression in neural tube defects.Molecular genetics & genomic medicine · 2019Article
- Genetic screening and functional analysis of CASP9 mutations in a Chinese cohort with neural tube defects.CNS neuroscience & therapeutics · 2018Article
- Formate rescues neural tube defects caused by mutations inProceedings of the National Academy of Sciences of the United States of America · 2018Article
- Genetic contribution of retinoid-related genes to neural tube defects.Human mutation · 2018Article
- Folate deficiency facilitates recruitment of upstream binding factor to hot spots of DNA double-strand breaks of rRNA genes and promotes its transcription.Nucleic acids research · 2017Article
- Dishevelled Paralogs in Vertebrate Development: Redundant or Distinct?Frontiers in cell and developmental biology · 2017Review
- Spina Bifida: Pathogenesis, Mechanisms, and Genes in Mice and Humans.Scientifica · 2017Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Dishevelled (DVL/Dvl) genes play roles in canonical and noncanonical Wnt signaling, both of which are essential in neural tube closing and are involved in balancing neural progenitor growth and differentiation, or neuroepithelial cell polarity, respectively. In mouse Dvl haploinsufficiency leads to neural tube defects (NTDs), which represent the second most common birth defects. However, DVL genes' genetic contributions in human NTDs are modest. We sought to explore the molecular impact on such genes in human NTDs in a Han Chinese cohort. In 47 cases with NTDs and 61 matched controls, in brain tissues, the DVL1/2 mRNA levels were correlated with the levels of a serine/threonine protein kinase MARK2, and in 20 cases with lumbosacral spina bifida, the mRNA levels of DVL1 and MARK2 were significantly decreased; by contrast, only an intronic rare variant was found. Moreover, in an extended population, we found merely three novel rare missense variants in 1 % of individuals with NTDs. In cell-based assays, Mark2 depletion indeed reduces Dvl gene expression and interrupts neural stem cell (NSCs) growth and differentiation, which are likely to be mediated through a decrease in class IIa HDAC phosphorylation and reduced H3K4ac and H3K27ac occupancies at the Dvl1/2 promoters. Finally, the detections of folate concentration in human brain tissue and NSCs and MEF cells indicates that folate deficiency contributes to the observed decreases in Mark2 and Dvl1 expression. Our present study raises a potential common pathogenicity mechanism in human lumbosacral spina bifida about DVL genes rather than their genetic pathogenic role.
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