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

Nature genetics | Jun 29, 2008

http://www.ncbi.nlm.nih.gov/pubmed/18469815

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 RIS Download

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

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Associated grants

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

Mouse Genome Informatics (Data, Gene Annotation)

Comparative Toxicogenomics Database (Data, Disease Annotation)

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