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Related Experiment Videos

The gene encoding proline dehydrogenase modulates sensorimotor gating in mice.

J A Gogos1, M Santha, Z Takacs

  • 1The Rockefeller University, New York, New York 10021, USA.

Nature Genetics
|April 7, 1999
PubMed
Summary

Genetic deletions on chromosome 22q11 are linked to psychiatric disorders. We identified the PRODH gene in this region, and its mouse counterpart

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Area of Science:

  • Neurogenetics
  • Psychiatric Genetics
  • Molecular Biology

Background:

  • Hemizygous deletions in chromosome 22q11 are associated with psychiatric and behavioral phenotypes.
  • Sensorimotor gating deficits are observed in neuropsychiatric disorders.

Purpose of the Study:

  • To isolate and characterize the human PRODH gene, a homolog of Drosophila melanogaster sluggish-A (slgA).
  • To investigate the role of PRODH in psychiatric and behavioral phenotypes, particularly those linked to 22q11 deletions.

Main Methods:

  • Isolation and characterization of human and mouse PRODH genes.
  • Identification of a mutation in the mouse Prodh gene in the Pro/Re hyperprolinaemic mouse strain.
  • Assessment of sensorimotor gating and neurochemical alterations in mutant mice.

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Main Results:

  • PRODH, encoding proline dehydrogenase, is localized to chromosome 22q11.
  • Mice with a Prodh mutation exhibit sensorimotor gating deficits and brain neurochemical changes.
  • Proline may modulate synaptic transmission in the mammalian brain.

Conclusions:

  • The PRODH gene is a strong candidate for involvement in 22q11-associated psychiatric and behavioral phenotypes.
  • Dysregulation of proline metabolism may contribute to neuropsychiatric disorders.