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Altered brain microRNA biogenesis contributes to phenotypic deficits in a 22q11-deletion mouse model.

Individuals with 22q11.2 microdeletions show behavioral and cognitive deficits and are at high risk of developing schizophrenia. We analyzed an engineered mouse strain carrying a chromosomal deficiency spanning a segment syntenic to the human 22q11.2 locus. We uncovered a previously unknown alteration in the biogenesis of microRNAs (miRNAs) and identified a subset of brain miRNAs affected by the microdeletion. We provide evidence that the abnormal miRNA biogenesis emerges because of haploinsufficiency of the Dgcr8 gene, which encodes an RNA-binding moiety of the 'microprocessor' complex and contributes to the behavioral and neuronal deficits associated with the 22q11.2 microdeletion.

Pubmed ID: 18469815

Authors

  • Stark KL
  • Xu B
  • Bagchi A
  • Lai WS
  • Liu H
  • Hsu R
  • Wan X
  • Pavlidis P
  • Mills AA
  • Karayiorgou M
  • Gogos JA

Journal

Nature genetics

Publication Data

June 29, 2008

Associated Grants

  • Agency: NIMH NIH HHS, Id: MH067068
  • Agency: NIMH NIH HHS, Id: MH077235
  • Agency: NIGMS NIH HHS, Id: R01 GM076990

Mesh Terms

  • Animals
  • Behavior, Animal
  • Brain
  • Chromosome Deletion
  • Chromosomes, Human, Pair 22
  • Cognition Disorders
  • Disease Models, Animal
  • Female
  • Gene Expression Profiling
  • Habituation, Psychophysiologic
  • Heterozygote
  • Humans
  • Learning Disorders
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • MicroRNAs
  • Oligonucleotide Array Sequence Analysis
  • Phenotype
  • Proteins
  • RNA-Binding Proteins
  • Sensation Disorders
  • Spine