it is now clear that they also have the ability to promote apoptosis and inhibit

Limb specific deletion of Dicer results in decrease in limb size in correlation with an increase supplier Bicalutamide in cell death while deletion of Dicer in lung epithelium results in branching defects with concurrent increase in cell death. During skeletal muscle development, the loss of Dicer leads to an increase in cell death producing muscle hypoplasia as well as abnormal myofiber morphology. In the CNS, deletion of Dicer results in region specific defects. In the cortex and hippocampus, Dicer is needed for cell survival and dendritic branching. In the neocortex, the loss of Dicer results in neurogenic progenitor cell death but not neuroepithelial progenitors. These studies suggest that Dicer may be required for cell survival during the switch from uncommitted to committed neuronal progenitors. In addition to its early role in cell survival, Dicer is also required for post mitotic Purkinje cell survival following terminal differentiation. However, Skin infection Dicer is not required for survival of all differentiated cells. Dicer ablation in post mitotic dopaminoceptive neurons show that Dicer is required for maintenance of cell size but not cell survival. Here, we investigate the role of Dicer during development of NC derived tissues by deleting Dicer in NC using Wnt1 Cre. Our results show that loss of Dicer in NCCs results in developmental defects in all NC derived tissues. Dicer loss does not prevent colonization of target tissues or initial differentiation of NCCs, however, as differentiation progresses cells are lost through apoptosis. In the head, where NC differentiate to form number of lineages including bone, deletion of supplier PR-957 Dicer leads to the loss of facial and cranial vault structures. In the trunk, NC form the peripheral nervous systems. Deletion of Dicer does not effect initial formation of the sympathetic, sensory or enteric nervous systems, but as the nervous systems begin to terminally differentiate, neurons undergo apoptotic cell death. The NC lineage contributes to several structures of the head including bones, smooth muscle, glia and connective tissue. To investigate the roles of Dicer during cranial NC development, we deleted the Dicer gene in NC by crossing conditional allele of Dicer with the Wnt1 Cre deleter mouse line. Genotype analysis of neonates showed that all genetic backgrounds survived to birth at the expected Mendelian ratio. Mice with the genotypes Dicerfx, Dicerfxfx, and Dicerfx, Wnt1 Cre mice did not have morphological defects and were used as the control embryos. All Dicerfxfx, Wnt1 Cre neonates have severe craniofacial malformations and extended forelimbs. Aanalysis of mutant embryos did not show skeletal abnormalities outside the head, suggesting that the extended forelimb phenotype in mutant embryos is due to neurological defects.