Different timings of dicer deletion affect neurogenesis and gliogenesis in the developing mouse central nervous system
Copyright policy )Different timings of dicer deletion affect neurogenesis and gliogenesis in the developing mouse central nervous system
AbstractMicroRNAs, processed by the RNAase III enzyme Dicer, are ∼22 nucleotide endogenous noncoding small RNAs. The function of Dicer in the mouse central nervous system (CNS) development is not well understood. Here, we show that specifically deleting Dicer expression in the CNS and in the cerebral cortex using two Cre lines results in reduced progenitor numbers, abnormal neuronal differentiation, and thinner cortical wall. Incomplete Dicer deletion during early embryonic stages contributes to normal development of early‐born neurons in the cortex and motor neurons in the spinal cord. However, at late embryonic stages when Dicer is completely ablated in the CNS, the migration of late‐born neurons in the cortex and oligodendrocyte precursor expansion and differentiation in the spinal cord are greatly affected. Our studies of different timings of Dicer deletion demonstrate the importance of the Dicer‐mediated microRNA pathway in regulating distinct phases of neurogenesis and gliogenesis during the CNS development. Developmental Dynamics 238:2800–2812, 2009. © 2009 Wiley‐Liss, Inc.
- Cornell University United States
Central Nervous System, Mice, Knockout, Neurons, Ribonuclease III, Genotype, Neurogenesis, Mice, Transgenic, Embryo, Mammalian, DEAD-box RNA Helicases, Mice, Inbred C57BL, Mice, MicroRNAs, Oligodendroglia, Cell Movement, Endoribonucleases, Animals, Gene Deletion
Central Nervous System, Mice, Knockout, Neurons, Ribonuclease III, Genotype, Neurogenesis, Mice, Transgenic, Embryo, Mammalian, DEAD-box RNA Helicases, Mice, Inbred C57BL, Mice, MicroRNAs, Oligodendroglia, Cell Movement, Endoribonucleases, Animals, Gene Deletion
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