Copper transport and bacterial pathogenesis in rice.

The successful pathogen targets host defenses at multiple points; indeed, the number of targets and the breadth of strategies for disarming these defenses are quite amazing. To target host defenses, the pathogen secretes effector proteins, which act to suppress defenses and to manipulate host metabolism to favor pathogen growth and transmission (reviewed in Hogenhout et al., 2009). To protect the host (along with other strategies), its defense system may recognize effectors, either directly or as a consequence of their action, and initiate various defense mechanisms (reviewed in Dodds and Rathjen, 2010). Host protection is a difficult assignment; lacking an adaptive immune system, plants have to protect against an astounding breadth of effectors from bacterial, fungal, nematode, and oomycete pathogens, using only the recognition factors in their genomes. Many effectors directly target host defenses by altering phosphorylation, protein degradation, or RNA interference, but a class of transcription activator–like (TAL) effectors from the bacterial pathogen Xanthomonas directly activates transcription of host genes. These host targets facilitate pathogen infection, and their mechanisms are of great interest in the study of plant protection. Indeed, alteration of these targets to be unresponsive to the TAL effector can produce resistant alleles. For example, the rice xa13 allele confers resistance to transcriptional activation by aXanthomonas oryzae pv oryzae (Xoo) TAL effector from strain PXO99; this results in recessive resistance that is specific to strain PXO99. Thus, genetics shows that Xa13 facilitates Xoo infection, but how? A new study by Yuan et al. (pages 3164–3176) examines the mechanism of action of the Xa13 host factor. The authors find that Xa13 is a plasma membrane protein that interacts with two copper transporter proteins (COPT1 and 5). Expression of the three proteins together complemented a yeast mutant deficient in copper transport, indicating that they act in cooperation to transport copper (see figure). Transcription of Xa13, COPT1, and COPT5 increases under copper deficiency and is repressed under copper excess, further supporting their role in copper transport. Also, overexpression of Xa13, COPT1, or COPT5 increased the copper contents of roots and shoots but decreased the copper content of xylem sap. This observation proved telling, as Xoo spreads through the xylem. Indeed, the authors found that copper inhibits the growth of Xoo strain PXO99 but does not affect the growth of other Xoo strains. Moreover, they could recapitulate the resistance by growing Xoo in extracted xylem sap: sap from sensitive Xa13 plants allowed growth of Xoo PXO99, but adding copper to the same concentration as in xa13 plants reduced the growth of the pathogen. Thus, it seems that this coppersensitive Xoo strain exploits the host’s copper transport mechanisms to clear its path of toxic amounts of copper.