Coordination of cell proliferation and cell fate determination by C. elegans CES-1 Snail

2013 ◽  
Author(s):  
Bo. Yan
Development ◽  
2000 ◽  
Vol 127 (24) ◽  
pp. 5277-5284 ◽  
Author(s):  
T. von Zelewsky ◽  
F. Palladino ◽  
K. Brunschwig ◽  
H. Tobler ◽  
A. Hajnal ◽  
...  

The Mi-2 protein is the central component of the recently isolated NuRD nucleosome remodelling and histone deacetylase complex. Although the NuRD complex has been the subject of extensive biochemical analyses, little is known about its biological function. Here we show that the two C. elegans Mi-2 homologues, LET-418 and CHD-3, play essential roles during development. The two proteins possess both shared and unique functions during vulval cell fate determination, including antagonism of the Ras signalling pathway required for vulval cell fate induction and the proper execution of the 2 degrees cell fate of vulval precursor cells, a process under the control of LIN-12 Notch signalling.


PLoS Genetics ◽  
2013 ◽  
Vol 9 (10) ◽  
pp. e1003884 ◽  
Author(s):  
Bo Yan ◽  
Nadin Memar ◽  
Julia Gallinger ◽  
Barbara Conradt

2006 ◽  
Vol 298 (2) ◽  
pp. 485-497 ◽  
Author(s):  
Timothy Walston ◽  
Chaobo Guo ◽  
Rui Proenca ◽  
Mingfu Wu ◽  
Michael Herman ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Lu Liu ◽  
Zhengjun Peng ◽  
Zezhen Xu ◽  
Xi Wei

Introduction. Dental pulp cells (DPCs) are promising cell source for dental tissue regeneration. Recently, small molecules which optimize microenvironment or activate the reprogramming network provide a new way to enhance the pluripotency. Two promising bioflavonoids luteolin and apigenin were reported to enhance reprogramming efficiency in mouse embryonic fibroblast (MEF). However, their effect and underlying mechanism in cell fate determination of human DPCs remain unclear.Methods. To elucidate the effect of luteolin and apigenin on the cell fate determination of DPCs, we explored the cell proliferation, cell cycle, senescence, apoptosis, expression of pluripotency markers Oct-4, Sox2, and c-Myc, and multilineage differentiation capability of DPCs with luteolin or apigenin treatment.Results. We demonstrated that luteolin and apigenin inhibited cell proliferation, arrested DPCs in G2/M and S phase, and upregulated PI value and apoptosis. Moreover, luteolin and apigenin increased telomerase activity, maintained DPCs in a presenescent state, and activated the expression of Oct-4, Sox2, and c-Myc at a dose- and time-dependent pattern in DPCs even at late passages, albeit repressed lineage-specific differentiation.Conclusions. Addition of luteolin and apigenin in the culture medium might provide an effective way to maintain DPCs in an undifferentiated stage and inhibit lineage-specific differentiation.


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