Abstract:
:22q11.2 microdeletions result in specific cognitive deficits and schizophrenia. Analysis of Df(16)A(+/-) mice, which model this microdeletion, revealed abnormalities in the formation of neuronal dendrites and spines, as well as altered brain microRNAs. Here, we show a drastic reduction of miR-185, which resides within the 22q11.2 locus, to levels more than expected by a hemizygous deletion, and we demonstrate that this reduction alters dendritic and spine development. miR-185 represses, through an evolutionarily conserved target site, a previously unknown inhibitor of these processes that resides in the Golgi apparatus and shows higher prenatal brain expression. Sustained derepression of this inhibitor after birth represents the most robust transcriptional disturbance in the brains of Df(16)A(+/-) mice and results in structural alterations in the hippocampus. Reduction of miR-185 also has milder age- and region-specific effects on the expression of some Golgi-related genes. Our findings illuminate the contribution of microRNAs in psychiatric disorders and cognitive dysfunction.
journal_name
Celljournal_title
Cellauthors
Xu B,Hsu PK,Stark KL,Karayiorgou M,Gogos JAdoi
10.1016/j.cell.2012.11.052subject
Has Abstractpub_date
2013-01-17 00:00:00pages
262-75issue
1-2eissn
0092-8674issn
1097-4172pii
S0092-8674(12)01440-7journal_volume
152pub_type
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