scholarly journals NFκB Signaling Directs Neuronal Fate Decision

10.5772/53503 ◽  
2013 ◽  
Author(s):  
Yonggang Zhang ◽  
Wenhui Hu
Keyword(s):  
Neuronal Fate ◽  
Fate Decision

scholarly journals Baicalin Regulates Neuronal Fate Decision in Neural Stem/Progenitor Cells and Stimulates Hippocampal Neurogenesis in Adult Rats

2013 ◽  
Vol 19 (3) ◽  
pp. 154-162 ◽  
Author(s):  
Peng-Wei Zhuang ◽  
Guang-Zhi Cui ◽  
Yan-Jun Zhang ◽  
Mi-Xia Zhang ◽  
Hong Guo ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Hippocampal Neurogenesis ◽  
Adult Rats ◽  
Neuronal Fate ◽  
Neural Stem Progenitor Cells ◽  
Fate Decision

scholarly journals miRNA suppression of a Notch repressor directs non-neuronal fate in Drosophila mechanosensory organs

2017 ◽  
Vol 217 (2) ◽  
pp. 571-583 ◽  
Author(s):  
Joshua Kavaler ◽  
Hong Duan ◽  
Rajaguru Aradhya ◽  
Luis F. de Navas ◽  
Brian Joseph ◽  
...  
Keyword(s):  
Notch Signaling ◽  
Cell Fate ◽  
Large Scale ◽  
Notch Pathway ◽  
Neuronal Cell ◽  
Loss Of Function ◽  
Cell Specification ◽  
Neuronal Fate ◽  
Fate Decision ◽  
Peripheral Sensory

Although there is abundant evidence that individual microRNA (miRNA) loci repress large cohorts of targets, large-scale knockout studies suggest that most miRNAs are phenotypically dispensable. Here, we identify a rare case of developmental cell specification that is highly dependent on miRNA control of an individual target. We observe that binary cell fate choice in the Drosophila melanogaster peripheral sensory organ lineage is controlled by the non-neuronally expressed mir-279/996 cluster, with a majority of notum sensory organs exhibiting transformation of sheath cells into ectopic neurons. The mir-279/996 defect phenocopies Notch loss of function during the sheath–neuron cell fate decision, suggesting the miRNAs facilitate Notch signaling. Consistent with this, mir-279/996 knockouts are strongly enhanced by Notch heterozygosity, and activated nuclear Notch is impaired in the miRNA mutant. Although Hairless (H) is the canonical nuclear Notch pathway inhibitor, and H heterozygotes exhibit bristle cell fate phenotypes reflecting gain-of-Notch signaling, H/+ does not rescue mir-279/996 mutants. Instead, we identify Insensible (Insb), another neural nuclear Notch pathway inhibitor, as a critical direct miR-279/996 target. Insb is posttranscriptionally restricted to neurons by these miRNAs, and its heterozygosity strongly suppresses ectopic peripheral nervous system neurons in mir-279/996 mutants. Thus, proper assembly of multicellular mechanosensory organs requires a double-negative circuit involving miRNA-mediated suppression of a Notch repressor to assign non-neuronal cell fate.

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