prdm1a and olig4 act downstream of Notch signaling to regulate cell fate at the neural plate border.

The zinc finger domain transcription factor prdm1a plays an integral role in the development of the neural plate border cell fates, including neural crest cells and Rohon-Beard (RB) sensory neurons. However, the mechanisms underlying prdm1a function in cell fate specification is unknown. Here, we test more directly how prdm1a functions in this cell fate decision. Rather than affecting cell death or proliferation at the neural plate border, prdm1a acts explicitly on cell fate specification by counteracting olig4 expression in the neighboring interneuron domain. olig4 expression is expanded in prdm1a mutants and olig4 knockdown can rescue the reduced or abrogated neural crest and RB neuron phenotype in prdm1a mutants, suggesting a permissive role for prdm1a in neural plate border-derived cell fates. In addition, prdm1a expression is upregulated in the absence of Notch function, and inhibiting Notch signaling fails to rescue prdm1a mutants. This suggests that prdm1a functions downstream of Notch in the regulation of cell fate at the neural plate border and that Notch regulates the total number of progenitor cells at the neural plate border.

A uniaxial bioMEMS device for imaging single cell response during quantitative force-displacement measurements.

A microfabricated device has been developed for imaging of a single, adherent cell while quantifying force under an applied displacement. The device works in a fashion similar to that of a displacement-controlled uniaxial tensile machine. The device was calibrated using a tipless atomic force microscope (AFM) cantilever and shows excellent agreement with the calculated spring constant. A step input was applied to a single, adherent fibroblast cell and the viscoelastic response was characterized with a mechanical model. The adherent fibroblast was imaged by use of epifluorescence and phase contrast techniques.