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Related Concept Videos

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The ability of a drug to produce structural deformations and functional abnormalities in the developing embryo or the fetus is called teratogenicity, and the drug producing this effect is known as a teratogen. Teratogenic effects include stillbirth, miscarriage, intrauterine growth restriction, and neurocognitive delay. A teratogen may affect the embryo at different stages of development, which is important in determining the type and extent of the damage. During blastocyst formation, the early...
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Diploid organisms inherit genetic material through chromosomes from both parents. Copies of the same gene are known as alleles. In most cases, both alleles are simultaneously expressed and allow various cellular processes to function optimally. If one of the alleles is missing or mutated, the expression of the other allele can compensate; however, this is not true for all genes.
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Related Experiment Video

Updated: Nov 26, 2025

Author Spotlight: Studying the Impact of Maternal Dietary Deficiencies on Long-Term Offspring Health Outcomes
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Author Spotlight: Studying the Impact of Maternal Dietary Deficiencies on Long-Term Offspring Health Outcomes

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Gestational folate deficiency alters embryonic gene expression and cell function.

R S Seelan1, P Mukhopadhyay1, J Philipose1

  • 1Department of Oral Immunology and Infectious Diseases, Division of Craniofacial Development & Anomalies, University of Louisville Dental School, 501 S. Preston St., Louisville, KY, 40292, USA.

Differentiation; Research in Biological Diversity
|December 10, 2020
PubMed
Summary

Folate deficiency impacts embryonic development by altering gene expression and cellular functions. This study highlights compromised development in Folate receptor 1 knockout embryos, affecting cell migration and tissue formation.

Keywords:
ApoptosisCell migrationF-actinFolr1Neural crest cellsProliferation

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Area of Science:

  • Developmental biology
  • Genetics
  • Molecular biology

Background:

  • Folic acid is crucial for embryonic development, preventing birth defects.
  • Folate receptor 1 (Folr1) is essential for cellular folate uptake.
  • Folr1 deficiency can lead to embryonic lethality and developmental anomalies.

Purpose of the Study:

  • To investigate the molecular mechanisms underlying developmental defects caused by folate deficiency.
  • To compare gene expression profiles in Folr1 knockout embryos versus wild-type embryos.
  • To identify biological functions and pathways affected by Folr1 deficiency during embryogenesis.

Main Methods:

  • Gene expression profiling of gestational day 9.5 Folr1 knockout and wild-type embryos.
  • Ingenuity Pathway Analysis of differentially expressed genes.
  • In vitro studies on neural crest cell migration under folate-deficient conditions.

Main Results:

  • 837 genes/ESTs showed differential expression in Folr1 knockout embryos.
  • Key affected functions include digestive and cardiovascular system development, tissue and cellular development, and cell growth/differentiation.
  • Affected pathways involve blood coagulation, embryonic stem cell transcription, and cardiomyocyte differentiation.
  • Folate deficiency impaired cranial neural crest cell migration due to cytoskeletal alterations.

Conclusions:

  • Folate deficiency, mediated by Folr1, significantly disrupts multiple embryonic developmental processes.
  • Compromised cell migration and altered cytoskeleton are key consequences of folate deficiency.
  • Folr1 plays a critical role in maintaining normal embryonic development through folate transport and downstream signaling.