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Related Experiment Videos

Metallothionein-null mice express altered genes during development.

T Kimura1, I Oguro, J Kohroki

  • 1Department of Toxicology, Graduate School of Pharmaceutical Sciences, Osaka University, 1-6, Yamada-oka, Suita, Osaka, 565-0871, Japan.

Biochemical and Biophysical Research Communications
|February 7, 2001
PubMed
Summary

The absence of metallothionein (MT) in neonatal mice alters gene expression, affecting key genes like contrapsin, transketolase, and vanin-3. This study reveals in vivo effects of MT deficiency on hepatic RNA profiles.

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Area of Science:

  • Molecular Biology
  • Genetics
  • Biochemistry

Background:

  • Metallothionein (MT) is known to modulate transcriptional activity in vitro.
  • The role of MT in regulating gene expression in vivo remains less understood.
  • Hepatic MT levels are notably high during neonatal development.

Purpose of the Study:

  • To investigate the in vivo effects of metallothionein absence on gene expression.
  • To compare hepatic RNA profiles between wild-type and MT-null neonatal mice.
  • To identify specific genes whose expression is altered due to MT deficiency.

Main Methods:

  • Utilized improved differential display to compare hepatic RNA profiles.
  • Analyzed neonatal wild-type and MT-null mouse models.

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  • Sequenced and identified differentially expressed cDNA fragments.

    • Main Results:

    • Identified five differentially expressed cDNA fragments in MT-null mice compared to wild-type.
    • Two fragments were related to MT-I and mutant MT-I.
    • Contrapsin was down-regulated, while transketolase and vanin-3 were up-regulated in neonatal MT-null mice.

    Conclusions:

    • The absence of metallothionein significantly impacts hepatic gene expression in neonatal mice.
    • Specific genes, including contrapsin, transketolase, and vanin-3, show altered expression levels in MT-deficient neonates.
    • Further research is needed to ascertain if these changes are primary or secondary effects of MT deficiency.