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As such, chromatin organization plays a central role in establishing and maintaining cell state during development, with gene regulation and genome organization being mutually dependent effectors of cell identity.
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The lineage-specifying factors do not appear to have as fundamental effects on the epigenetic landscape as the pioneer factors, consistent with the requirement for the continued expression of these proteins to maintain cell state and the plasticity that is evident between lineages.
Consequently, a well-timed, fine-tuned and plastic regulation of translation is needed to adjust and maintain cell states under dynamically changing environments.
These models make it possible to systematically and efficiently identify the regulatory modules (tumor checkpoints) that are responsible for maintaining cells in a cancerous state as well as the individual proteins (master regulators) that comprise these modules.
Maintaining cells in the arrested state for long periods does not switch reversible arrest to cellular senescence.
It is not known if p130 is required for terminal cell cycle exit in the developing retina, for maintaining cells in the postmitotic state or both.
Developing systematic, network-based approaches to elucidate the regulatory logic that is responsible for maintaining cancer cell state.
Project 1 - Elucidating the regulatory logic that is responsible for maintaining cancer cell state, independent of specific initiating events and endogenous/exogenous perturbations.
This result is consistent with the mycelia maintaining resting cell state under the depletion of a compulsory nutrient element condition (Willrodt et al. 2016).
Importantly, these proteins are not themselves mutated, but are nevertheless essential for maintaining cells in their cancer-related state.
In earlier research Califano has used this approach to identify regulatory mechanisms that are necessary to maintain tumor cell state but not the state of related normal, noncancerous cells.
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