Using bioinformatics tools to identify and map out specific components and regulatory interconnections, the study team found highly dynamic activities during CD8 + T cell responses: a distinct repertoire of super enhancers — groups of enhancers that interact with promoters to
drive gene transcription, new groups of enhancers that jump into activity only in the memory cell stage, and extensive re-wiring of regulatory circuits from one cell stage to another.
Not exact matches
In the paper, the researchers illustrate how it could influence proteins that activate the
transcription factors that transcribe major bone - related
genes to
drive bone formation — showing a link between metabolite usage and activation of
transcription factors.
The researchers also showed that histone propionylation can
drive transcription in the test tube (in vitro) suggesting it is a stimulatory mark capable of causing
genes to be expressed when it is present.
Activated E2F leading to
transcription of several target
genes including cyclin E in late G1 phase which form active complex with CDK2
drives progression from G1 to S phase [7].
This is believed to be true given the results of previous RNA - seq experiments (1, 4, 5) along with a belief that the odds are very low that Cas9 would have an off - target that lands in the promoter of another
gene, thereby
driving aberrant
transcription.
7) Van de Wetering, M., Cavallo, R., Dooijes, D., Van Beest, M., Van Es, J., Loureiro, J., Ypma, A., Hursh, D., Jones, T., Bejsovec, A., Peifer, M., Mortin, M., and Clevers, H. Armadillo co-activates
transcription driven by the product of the Drosophila segment polarity
gene dTCF.
Overall, this study highlights the close links between
transcription factor -
driven genome topology dynamics, chromatin state, and
gene expression and highlights a critical role for genome topology in enforcing transcriptional programs and cell fate.
While the small changes in lineage
transcription observed in our data set would be consistent with a stochastic model, the ES cell model described in Figure 9 would require both cross-repression and additional positive feedback loops to
drive these random changes in
gene expression down multiple distinct routes.
DNA regions bound at low occupancy by
transcription factors do not
drive patterned reporter
gene expression in Drosophila.
Our results reveal the regulatory mechanisms that interplay to
drive transcription factor occupancy, chromatin state, and
gene expression in complex mammalian cell states.