I found Goodsell's images of the crowded intracellular environment in E. coli, useful visualisations in developing a model of a living cellular process, namely,

I found Goodsell's images of the crowded intracellular environment in E. coli, useful visualisations in developing a model of a living cellular process, namely, transcription control. Transcription is the first step in gene expression: in E. coli, RNA polymerase transcribes a complementary copy of a gene, namely, messenger RNA, for further processing to protein. The transcription process is controlled by proteins that either compete with RNA polymerase for the start site of transcription (turn off the gene) or bind adjacently and promote transcription (turn on the gene). The difficulty I had in constructing a mathematical model of transcription control was that I wanted to include nonspecific binding, where RNA polymerase binds with low affinity to random stretches of DNA. While such binding occurs with low affinity, the sheer length of the DNA meant that a significant proportion of the RNA polymerase was bound in that form. Fortunately, I became aware of the work of people like Allen Minton (NIH) and Tom Record (U Madison-Wisconsin) who studied molecular crowding. To borrow a sentence from Wikipedia, "[H]igh concentrations of macromolecules reduce the volume of solvent available for other molecules in the solution, which has the result of increasing their effective concentrations." https://en.wikipedia.org/wiki/Macromolecular_crowding https://en.wikipedia.org/wiki/Macromolecular_crowding I found (I hope correctly) that Tom Record's quantification of crowding, as affecting a 100-fold increase in concentration, "exactly" compensated for the reduction due to nonspecific binding. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5425810/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5425810/