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Based on all the above, I think it can reasonably be argued that cell cognition and intercellular communication are central to all levels of life.
It could be argued that cell culture models are rough representations of physiological systems and that TNT-like structures are the sole result of stress conditions in this in vitro situation.
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It may be argued that cells that are blocked in differentiation have lost pluripotency.
It has been argued that cell cycle checkpoint arrest, although important for maintaining genomic stability post irradiation, makes a less significant contribution to survival.
Here, it is argued that cell type-specific instructions for 3D folding, e.g., enhancer-promoter pairing, compartments, etc., are encoded in local properties of chromatin and that no specific memory for higher order 3D folding is required.
For example, it has been argued that cell-free ethanol fermentation systems would replace microbe-based ethanol fermentation someday [39].
Furthermore, it has recently been argued that cell-to-cell heterogeneity is practically unavoidable and can come from a multitude of sources – from stochastic heterogeneity in oxidative DNA damage due to e.g. variations in metabolic loads to deterministic heterogeneity due to variations in cell size, cell density, stage in cell-cycle, etc. [ 31].
It could also be argued that evolved cell death genes include those genes that promote the death of one cell to sustain the survival of another cell by providing nutrients derived from the dead cell.
It can be argued that the cell division time asymmetry may be a result of stochastic morphological asymmetry.
At this stage, it could be argued that stem cell models have not yet provided novel mechanistic insights into AD.
It could be argued that host cell defences against viral infections that mutate their RNA genomes may account for the various under- and over-representations of specific dinucleotides.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com