Obviously, this is not the case: the sole value of p38MAPK is not enough to determine the resulting cellular fate.
Further studies to elucidate the mechanisms resulting in astrocytic fate of transplanted NSCs are necessary and ongoing in our laboratory.
If lin-12(n379) or lin-12(n676) activity is increased, some or all of the VPCs adopt the 2° fate, resulting in a "Multivulva" phenotype that is visible in the dissecting microscope [8], [18], [19] (Fig. 3A).
However, the mechanisms leading to the determination of cell fate resulting in either cell survival or death are still unclear.
In contrast, activation of Wnt/β-catenin signaling caused anterior endodermal cells to adopt a hindgut fate, resulting in a failure of liver formation (McLin et al., 2007).
In ceh-20 and unc-62 mutants this balance is lost and both daughters adopt the proliferative fate, resulting in a symmetrical division pattern.
Such events are known to cause changes in gene expression, which involve irregular signaling cues influencing cell fate resulting in further inflammation (Cui et al. 2005).
According to this model, the status of Wnt activity within the two daughter cells leads to selection of alternate terminal differentiation programs, resulting in cell fate diversity.
The asymmetric cell fate resulting from these divisions is likely determined by many factors, such as epigenetic changes and signaling, which we are only just beginning to identify.
However, a single change in intercellular signaling can route a large pool of sustentacular cells into acquiring a progenitor fate, resulting in the ectopic production of supernumerary hair cells.
