ArticleReproductive toxicology (Elmsford, N.Y.)2021
Prenatal alcohol exposure disrupts Sonic hedgehog pathway and primary cilia genes in the mouse neural tube.
Article in Reproductive toxicology (Elmsford, N.Y.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 23 citations in OpenAlex.
- Developmental Neurotoxicity of Alcohol from Neuronal Basis to Behavioural Outcomes: A Comprehensive Review.Neurology international · 2026Review
- The Role of the Hedgehog Pathway in Alcohol-Induced Birth Defects.Advances in experimental medicine and biology · 2026Review
- Melanin-Concentrating Hormone (MCH): Role in Mediating Reward-Motivated and Emotional Behavior and the Behavioral Disturbances Produced by Repeated Exposure to Reward Substances.International journal of molecular sciences · 2025Review
- Nonconceptus Mechanisms of Prenatal Alcohol Exposure That Disrupt Embryo-Fetal Development: An Integrative View.Alcohol research : current reviews · 2025Review
- Efcab7 deletion sensitizes mice to the teratogenic effects of gastrulation-stage alcohol exposure.Reproductive toxicology (Elmsford, N.Y.) · 2024Article
- Alcohol exposure suppresses ribosome biogenesis and causes nucleolar stress in cranial neural crest cells.PloS one · 2024Article
- Gastrulation-stage alcohol exposure induces similar rates of craniofacial malformations in male and female C57BL/6J mice.Birth defects research · 2024Article
- Review
- A direct interaction between CENTLEIN and RABIN8 is required for primary cilium formation.Acta biochimica et biophysica Sinica · 2023Article
- Fetal alcohol spectrum disorders.Nature reviews. Disease primers · 2023Review
- High-throughput detection of craniofacial defects in fluorescent zebrafish.Birth defects research · 2023Article
- Short-term transcriptomic changes in the mouse neural tube induced by an acute alcohol exposure.Alcohol (Fayetteville, N.Y.) · 2023Article
- Alcohol induces neural tube defects by reducing retinoic acid signaling and promoting neural plate expansion.Frontiers in cell and developmental biology · 2023Article
- Gene-environment interactions in birth defect etiology: Challenges and opportunities.Current topics in developmental biology · 2023Review
- Gene-alcohol interactions in birth defects.Current topics in developmental biology · 2023Article
- The ameliorative effects of choline on ethanol-induced cell death in the neural tube of susceptible BXD strains of mice.Frontiers in neuroscience · 2023Article
- The pro-apoptotic Bax gene modifies susceptibility to craniofacial dysmorphology following gastrulation-stage alcohol exposure.Birth defects research · 2022Article
- Fetal Alcohol Spectrum Disorders: Awareness to Insight in Just 50 Years.Alcohol research : current reviews · 2022Article
- The impact of prenatal alcohol, synthetic cannabinoid and co-exposure on behavioral adaptations in adolescent offspring and alcohol self-administration in adulthood.Neurotoxicology and teratologyArticle
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Neurulation-stage alcohol exposure (NAE; embryonic day [E] 8-10) is associated with midline craniofacial and CNS defects that likely arise from disruption of morphogen pathways, such as Sonic hedgehog (Shh). Notably, midline anomalies are also a hallmark of genetic ciliopathies such as Joubert syndrome. We tested whether NAE alters Shh pathway signaling and the number and function of primary cilia, organelles critical for Shh pathway transduction. Female C57BL/6 J mice were administered two doses of alcohol (2.9 g/kg/dose) or vehicle on E9. Embryos were collected 6, 12, or 24 h later, and changes to Shh, cell cycle genes, and primary cilia were measured in the rostroventral neural tube (RVNT). Within the first 24 h post-NAE, reductions in Shh pathway and cell cycle gene expression and the ratio of Gli3 forms in the full-length activator state were observed. RVNT volume and cell layer width were reduced at 12 h. In addition, altered expression of multiple cilia-related genes was observed at 6 h post-NAE. As a further test of cilia gene-ethanol interaction, mice heterozygous for Kif3a exhibited perturbed behavior during adolescence following NAE compared to vehicle-treated mice, and Kif3a heterozygosity exacerbated the hyperactive effects of NAE on exploratory activity. These data demonstrate that NAE downregulates the Shh pathway in a region of the neural tube that gives rise to alcohol-sensitive brain structures and identifies disruption of primary cilia function, or a "transient ciliopathy", as a possible cellular mechanism of prenatal alcohol pathogenesis.
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