January 6, 2011 § Leave a comment
You’re probably familiar with the idea that gradients of signaling molecules determine cell fate in early animal embryos. Now, a recent paper from the Laub lab (Chen et al. 2010. Spatial gradient of protein phosphorylation underlies replicative asymmetry in a bacterium, PNAS doi:10.1073/pnas.1015397108) has discovered gradients of active signaling molecules within a single bacterial cell. The existence of this gradient had been missed until now because the signaling protein itself, CtrA, is evenly distributed across the dividing cell. But, Chen et al. find, the active phosphorylated form of the protein, CtrA-P, is not. You’ll have to read a little further to find out why not.
First, the model system. Caulobacter crescentus is unusual among the familiar bacterial model organisms, in that it divides asymmetrically; it’s used as a model system for studying cell differentiation. There are two forms, called “stalked” and “swarmer”: the stalked form is able to copy its DNA and divide, producing one stalked daughter and one swarmer daughter; later, the swarmer daughter may differentiate and become stalked, and then have daughters of its own. The protein that stops swarmers from undergoing replication is CtrA, a transcription factor that, when activated by phosphorylation, binds to the bacterial replication origin and prevents the initiation of DNA synthesis. So, in theory, one way you could give stalked and swarmer cells different fates is to wait until the cell divides into two (cytokinesis), then selectively dephosphorylate CtrA-P in stalked cells. By making CtrA-P levels high in swarmer cells and low in stalked cells, you would block division in swarmers but not in stalked cells. « Read the rest of this entry »