Abstract:
In the dimorphic bacterial model, Caulobacter crescentus stalked and flagellated
pole-specific localisation and activation of proteins leads to cell-fate determination and
asymmetry during the cell cycle. For example, the initiation of the cell-fate determining
signalling cascade begins with the stalked-pole specific localisation of the polar morphogen, SpmX, which in turn recruits and activates a set of proteins including the cell-fate determining kinase DivJ. The SpmX-mediated signalling negatively regulates the activity of the master cell cycle regulator, CtrA - through DivJ, and the σ 54-dependen transcriptional activator, TacA, through another polarised component SpmY. Deletion of spmX and/or spmY results in cell cycle and developmental defects shown to be caused by hyperactive TacA. However, the mechanism by which SpmX-SpmY regulates the activity of TacA still remains unclear. Herein, findings from a combination of genetic and biochemical experiments, have helped us gain preliminary insights into the possible signalling mechanism that SpmY might use to curb the activity of TacA is reported.
