The principles that govern transcription factor network functions in stem cells

Abstract

Tissue-specific transcription factors primarily act to define the phenotype of the cell. The power of a single transcription factor to alter cell fate is often minimal, as seen in gain-of-function analyses, but when multiple transcription factors cooperate synergistically it potentiates their ability to induce changes in cell fate. By contrast, transcription factor function is often dispensable in the maintenance of cell phenotype, as is evident in loss-of-function assays. Why does this phenomenon, commonly known as redundancy, occur? Here, I discuss the role that transcription factor networks play in collaboratively regulating stem cell fate and differentiation by providing multiple explanations for their functional redundancy.