Cell polarity/motility in bacteria: closer to eukaryotes than expected?

The Gram-negative bacterium Myxococcus xanthus glides on solid surfaces and periodically reverses the direction of movement. Work published in this issue of The EMBO Journal (Leonardy et al, 2010) reports on the small GTPase MglA that ensures the correct polarity of the motility engines through its GTP/GDP cycle in conjunction with its cognate GAP, MglB. MglA has also been shown to interact with the actin-like protein MreB in eukaryoticlike motility complexes. Altogether, the data suggest that compelling similarities exist between the mechanisms of motility and establishment of cell polarity in M. xanthus and eukaryotes. M. xanthus moves through the synergistic activity of two genetically, functionally and structurally different motility engines (Hodgkin and Kaiser, 1979). The first motility system, Social (S) motility, functions through the extension and retraction of polar Type IV Pili (Sun et al, 2000), whereas the second motility system, Adventurous (A) motility, is powered by distributed motors that assemble at the leading cell pole. These motors behave similarly to the eukaryotic focal adhesion complexes observed in apicomplexan parasites (Mignot et al, 2007). M. xanthus cells periodically reverse the direction of their movement by switching the polarity of the A and S engines at a frequency that is modulated by the Frz chemosensory system (Zusman et al, 2007) (Figure 1). Recently, evidence indicates the fact that similar mechanisms are shared by M. xanthus and eukaryotic cells regarding the way in which motility functions and cell polarity are established. In particular, the featured paper from the Sogaard–Andersen laboratory describes the importance of a small GTPase, MglA and its GTP/GDP cycle in the regulation of cell polarity in M. xanthus (Leonardy et al, 2010). The GTPases of the Ras superfamily perform a broad range of functions in eukaryotic cells including transport, signal transduction and cell migration (Charest and Firtel, 2007). The gene encoding MglA was first reported by Hodgkin and Kaiser (1979) and annotated as mutual gliding A (mglA) mutant, because its deletion caused defects in both A and S motility (Hodgkin and Kaiser, 1979). Some years later, Hartzell (1997) showed that MglA belongs to the Ras superfamily of small eukaryotic GTPases. In fact, the expression of the yeast Ras family protein SAR1 in mglA cells that were unable to sporulate rescued sporulation (Hartzell, 1997). Mauriello