I wish I did. The hints in the literature are spread far and wide among older papers, often misinterpreted as something else. A lot of it is unpublished data from my graduate work.
First, penicillin does bind to enzymes that cross link cell wall. It's getting from there to dead cells that's the problem. First, if you knock out a set of proteins called autolysins, cultures exposed to penicillin plateau in population, but the population does not decrease. That is, there is a suicide response. Second, changing the external turgor pressure, such as by adding PEG to the medium, doesn't change the rate of death. Third, if you watch a culture under a microscope when you add penicillin, all the cells in the culture stop growing long before they die. So the unbalanced growth model can't work. I have a vague memory that the kinetics don't work out either, but it's been too many years.
More interestingly, other antibiotics, such as rifampicin and chloramphenicol, which don't target anything related to cell wall, cause bacteria to stop growing when they are added to the medium. That implies that there are active mechanisms involved, not some random fact about cell wall synthesis that happens to stop when something is inhibited. Rifampicin is supposed to inhibit protein production (and does mess up ribosome activity), but there was an interesting paper that showed that a few mRNAs were translated as normal in the presence of rifampicin, even though most were messed up. And how would inhibiting protein synthesis lead to cells exploding (which they do) by a direct, physical mechanism?
I've thought about going back and writing a review article on all this stuff, but biology is a long ways in my past at this point.
First, penicillin does bind to enzymes that cross link cell wall. It's getting from there to dead cells that's the problem. First, if you knock out a set of proteins called autolysins, cultures exposed to penicillin plateau in population, but the population does not decrease. That is, there is a suicide response. Second, changing the external turgor pressure, such as by adding PEG to the medium, doesn't change the rate of death. Third, if you watch a culture under a microscope when you add penicillin, all the cells in the culture stop growing long before they die. So the unbalanced growth model can't work. I have a vague memory that the kinetics don't work out either, but it's been too many years.
More interestingly, other antibiotics, such as rifampicin and chloramphenicol, which don't target anything related to cell wall, cause bacteria to stop growing when they are added to the medium. That implies that there are active mechanisms involved, not some random fact about cell wall synthesis that happens to stop when something is inhibited. Rifampicin is supposed to inhibit protein production (and does mess up ribosome activity), but there was an interesting paper that showed that a few mRNAs were translated as normal in the presence of rifampicin, even though most were messed up. And how would inhibiting protein synthesis lead to cells exploding (which they do) by a direct, physical mechanism?
I've thought about going back and writing a review article on all this stuff, but biology is a long ways in my past at this point.