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In This Issue

during an infection and have been found to kill a broad range of pathogens, although the mechanistic details are unclear. Matthew Crawford et al. (pp. 17159–17164) screened a mutant library of the anthraxcausing bacterium Bacillus anthracis for genetic mutations that conveyed resistance to a chemokine called CXCL10. The authors identified three unique genomic loci whose disruption affected the anthrax microbe’s resistance. One loci was the well-conserved bacterial gene ftsX, which encodes a protein thought to help transport molecules across the cell membrane. Deletion of ftsX increased the bacteria’s resistance to CXCL10mediated death and also reduced the chemokine’s ability to localize to the B. anthracis cell membrane, where it is thought to act. The authors noted that part of the FtsX protein is similar to a region of the native CXCL10 receptor. According to the authors, this could indicate that CXCL10 directly binds to this part of FtsX to mediate antibacterial activity. The authors suggest that FtsX is crucial to the ability of a host chemokine to target and kill the anthrax pathogen, and suggest that the finding may aid in the design of more effective antimicrobial therapeutic strategies. — S.R. October 11, 2011 u vol. 108 u no. 41 u 16859–17236