Still I am convinced that, in addition to personal drives, fate plays a major role in the development of a scientific career, a bit like in natural evolution.
The molecular mechanism of activin action in this tissue provides a likely explanation for its fate-controlling effect, as it targets for rapid degradation the transcription factor Ascl1, which is known to drive neuronal fate choice (in this tissue and in others [ 5, 40- 42]).
Global gene expression profiling of hESC differentiation thus enables a systems-based analysis of the biological processes, networks, and genes that drive hESC fate decisions.
Alternatively, the differences might not be played out in differential responses to environmental cues, but might reflect intrinsic differences that drive cell fate decisions, and/or cell cycle decisions, relatively independent of the environment.
Taken together, global gene expression profiling of hESC differentiation enables a systems-based analysis of the biological processes, networks, and genes that drive hESC fate decisions, and studies such as this will serve as the foundation for future clinical applications of stem cell therapies.
MMR sensitisation may arise through futile cycling of DNA damage or indirectly by generating signals that drive cell fate pathways [ 18].
Similarly, dominant-negative Yap or Taz disrupts RPE genesis whereas, conversely, overexpression of either Yap or Taz can drive RPE fate from optic cup progenitor cells.
These in turn are capable of activating inflammatory transcription factors such as NF-κB and proinflammatory gene expression programs that drive cellular fate towards CNS dys-homeostasis, compromised neuronal function and, ultimately, apoptosis and brain cell death [ 2, 3, 38- 48].
Large-scale transcriptome profiling allows new questions to be asked about the roles of transcription factors in development and the cascades of genes that they influence to drive cell fate and differentiation.
