Meant to thank you for pointing this paper out a while back, but I've been distracted lately.
I'd always been a bit frustrated with the "slightly salty lipid-enclosed bag of enzymes" approach that many go with for simplicity, but I think things are starting to turn around on this point. People are appreciating the role of membrane organization and sequestration, and of macromolecular crowding, and so on.
The physical nature of the cellular cytoplasm also depends on the time scales one is observing with, which has been known for a while:
As it seems I'm the only person that specializes in glycobiology, one way that cells can modify the physical properties of their cytoskeleton through metabolism is through the all important O-glcnac modification (at least in mammalian cells), which has been known for a while:
Talin, vaniculin, synapsins, and many proteins involved with regulation of tubulin and actin are modified by O-glcnac.
You could write an entire text book on the O-glcnac modification and its importance to all of life, but long story short: the O-glcnac modification is one of the end products of glycolysis. In otherwords, both the O-glcnac modification as well as the massive amount of proteins that are O-glcnac modified (such as the many proteins involved in cytoskeletal organization and regulation) are absolutely linked to the metabolic states of cells.
You constantly read about the abnormal metabolic states in cancer with subsquently abberrant signaling cascades, how stem cells differentiate based on their metabolic states, and in this case, how the cytoplasm's physical properties are a function of metabolism. Well, one way to explain all of these observations is that glycolytic metabolism is inherently linked to the master control mechanism of the O-glcnac modification which differentially responds to environmental cues/stress.
It would be interesting to see if the bacteria they use is capable of the O-glcnac modification.
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