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Related Concept Videos

Teratogenicity01:07

Teratogenicity

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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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Among all the organelles in an animal cell, only mitochondria have their own independent genomes. Animal mitochondrial DNA is a double-stranded, closed-circular molecule with around 20,000 base pairs. Mitochondrial DNA is unique in that one of its two strands, the heavy, or H, -strand is guanine rich, whereas the complementary strand is cytosine rich and called the light, or L, -strand. Compared to nuclear DNA, mitochondrial DNA has a very low percentage of non-coding regions and is marked by...
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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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Nondisjunction is the failure of homologous chromosomes or sister chromatids to separate correctly and move to the opposite poles of the cells. This produces daughter cells with abnormal chromosome numbers.  Nondisjunction is common during anaphase I or anaphase II of meiosis.  Mutations in synaptonemal complex proteins that attach homologous chromosomes increase the chances of nondisjunction in anaphase I of meiosis I. In contrast, mutations in topoisomerases and condensins that hold...
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Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
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Related Experiment Video

Updated: Feb 27, 2026

Mouse In Vivo Placental Targeted CRISPR Manipulation
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Maternal placenta modulates a deleterious fetal mutation.

Hongen Xu1, Hubert Pausch2, Heli Venhoranta3

  • 1Department of Bioinformatics, Wissenschaftszentrum Weihenstephan, Technische Universität München, Freising, Germany.

Biology of Reproduction
|July 7, 2017
PubMed
Summary

Maternal placental tissue influences the severity of fetal intrauterine growth restriction (IUGR) caused by a paternally inherited gene mutation. This study reveals maternal effects on IUGR penetrance, highlighting placental communication in cattle.

Keywords:
PEG3cattledevelopmental biologyepigeneticsfetal developmentgenomic imprintingimprinted genesintrauterine growth restrictionplacenta

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Area of Science:

  • Reproductive biology
  • Genetics
  • Developmental biology

Background:

  • Intrauterine growth restriction (IUGR) is linked to placental metabolic issues, with fetal mutations impacting maternal physiology.
  • Maternal placental influence on fetal IUGR severity, particularly with paternally inherited mutations, remains unclear in ruminants.

Purpose of the Study:

  • To investigate early molecular events in fetal and maternal placentomes related to a paternally inherited MIMT1 deletion causing IUGR in cattle.
  • To identify how maternal placental components affect the variable severity of IUGR.

Main Methods:

  • Comparative transcriptome and genomic imprinting analysis of fetal and maternal placentomes from wild-type and MIMT1Del/WT cattle fetuses.
  • Focus on early developmental stages before IUGR manifestation.

Main Results:

  • Fewer differentially expressed genes were observed in maternal compared to fetal placentomes of MIMT1Del/WT fetuses.
  • AST1, SCRN3, and PEG3 genes within the PEG3 domain showed altered expression and imprinting patterns in IUGR placentomes.
  • Loss of strict monoallelic expression of PEG3 in the maternal placenta may correlate with incomplete penetrance of the MIMT1 deletion.

Conclusions:

  • Dysregulation of the PEG3 domain is implicated in IUGR development.
  • Maternal placental tissues play a role in modulating the penetrance of paternally inherited IUGR mutations.