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Related Experiment Videos

An enhancer deletion affects both H19 and Igf2 expression

P A Leighton1, J R Saam, R S Ingram

  • 1Howard Hughes Medical Institute, Princeton University, New Jersey 08544, USA.

Genes & Development
|September 1, 1995
PubMed
Summary
This summary is machine-generated.

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This study shows that H19 and Insulin-like growth factor 2 (Igf2) share common regulatory elements for imprinting. Deleting these elements affects gene expression and prenatal growth in mice.

Area of Science:

  • Genetics
  • Developmental Biology
  • Genomic Imprinting

Background:

  • Mouse Chromosome 7 harbors four imprinted genes: Mash-2, H19, Insulin-2 (Ins-2), and Insulin-like growth factor 2 (Igf2).
  • H19 and Igf2 exhibit coordinated expression patterns, suggesting shared regulatory mechanisms.

Purpose of the Study:

  • To investigate the hypothesis that H19 and Igf2 imprinting are mechanistically linked via common regulatory elements.
  • To determine the role of specific endoderm enhancers located 3' of H19 in regulating Igf2 and H19 expression.

Main Methods:

  • Generation of a targeted deletion of two endoderm-specific enhancers using homologous recombination in embryonic stem cells.
  • Analysis of H19 and Igf2 gene expression in mice inheriting the enhancer deletion from either parent.

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Main Results:

  • Maternal inheritance of the deletion resulted in loss of H19 expression in endodermal tissues (liver, gut, kidney, lung).
  • Paternal inheritance of the deletion caused a similar loss of Igf2 expression in the same tissues.
  • Mice with paternal deletion exhibited reduced size (80% of normal), indicating Igf2's role in prenatal growth, and a minor decrease in Ins-2 RNA.

Conclusions:

  • H19 and Igf2 share common endoderm enhancers, utilized differentially based on parental origin.
  • The deletion impacts prenatal growth, confirming the systemic role of Insulin-like Growth Factor II (IGFII).
  • Mash-2 expression in the placenta remained unaffected by the enhancer deletion.