Two interrelated models have been presented which describe: 1) the regulation of surface growth of Streptococcus faecalis by chromosome replication; and 2) a shape-determining mechanism which directs the assembly of envelope precursors into new cell surface. The first model provides that during a round of chromosome synthesis a signal is produced which results in the formation of a growth zone. This site, once formed, enlarges the cell surface until a second signal, produced during the terminal stages of chromosome replication, inhibits enlargement and promotes septation. The second model is concerned with the construction and function of the growth zone once it has been formed. This model suggests that surface growth proceeds by a regulated flow of cell wall precursors into a growth zone essentially along two channels. One channel would assemble a bilayered cross wall (possibly by the addition of precursors to the leading edge of the cross wall), while a second channel of precursors would convert this cross wall into two layers of peripheral wall. Under the influence of the chromosome termination signal, the flow of precursors along this second channel would be progressively reduced in the latter portion of the cycle. This reduction coupled with the continued flow of precursors into cross wall synthesis could result in cell division. Methods have been devised which can compare the geometry of the envelope with the macromolecular content and autolytic activity of cells. In attempting to test many aspects of the above models, these methods will be applied to steady-state, synchronous, and unbalanced populations where specific inhibition of DNA, RNA, protein, or wall biosynthesis has been induced.
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