Labavitch Lab

Cell wall metabolism and plant-pathogen interactions.
  The two most important contributors to losses of harvested fruits are uncontrolled softening (as discussed above) and spoilage caused by infection with pathogens.  Generally unripe fruits are relatively resistant to pathogen infection; however, when they ripen their pathogen susceptibility increases dramatically.  We have studied this ripening-related susceptibility increase by focusing on the interaction of the gray mold pathogen (Botrytis cinerea) and tomato fruit. Early work in our lab identified a fruit protein that inhibits the PG enzymes produced by pathogens as they digest fruit cell walls and infect fruit tissues.  These PG-inhibiting proteins (PGIPs) are present in many fruits, including tomatoes and pears.  Our expression of the pear fruit PGIP in tomato fruits enhanced fruit resistance to B. cinerea (Powell et al., 2000).  This was the first demonstration that PGIPs contribute to a plant's defenses against pathogens.  Tests of the B. cinerea susceptibility of the -PG-Exp tomatoes discussed above (Cantu et al., 2008a), revealed them to be very resistant to the gray mold even at the red ripe stage.  This provided a very useful understanding of the relationship of fruit ripening to increased pathogen susceptibility: at least for B. cinerea, even though the pathogen has a substantial arsenal of CWDPs encoded in its genome, it needs help from the fruit's wall metabolizing enzymes to establish infections. 

(Left) Tomato fruits that do not express PG and Exp during ripening are much less susceptible to Botrytis cinerea, the gray mold. The development of the pathogen was measured daily for 3 days after inoculation.
(Right) The decreased fruit susceptibility is statistically significant, but you do not need statistics to be convinced of the greatly reduced pathogen susceptibility.

In fact, many pathogens use PG and other CWDPs in their development of infection sites on plant hosts (Cantu et al., 2008b).  We also are studying Pierce's Disease (PD) of grapevines.  The disease is caused by a bacterium (Xylella fastidiosa, Xf) that is introduced into the grapevine's water-conducting vessels by an insect vector (the glassy-winged sharpshooter).  The Xf population eventually spreads throughout the vine, this expansion occurring via the xylem system.  PD-infected vines die soon after a systemic pathogen population has been established.  A collaborative study involving colleagues in the UCD Plant Pathology Department (Roper et al., 2007) showed that the systemic spread of Xf in grapevines depends on its production of PG, the enzyme digesting pectin polysaccharides in vessel pit membranes and permitting the vessel-to-vessel movement of the pathogen.  Other collaborative work (Aguero et al., 2005) showed that pear PGIP-expressing grapevines are less susceptible to PD than untransformed vines.  We then demonstrated that the pear PGIP inhibits Xf's PG (Greve et al., unpublished).  This was the first demonstration that a PGIP can inhibit the PG of a bacterial pathogen and explains why expression of the pear PGIP in grapevines reduces their susceptibility to PD.  We are currently developing a PD-management strategy that will involve the engineering of PGIP-expressing grapevine rootstocks.  We know that the PGIP will be moved in the xylem across the graft union and into non-transgenic scions, perhaps providing protection against PD.

Roper et al. (2007) describes the making of a strain of the Pierceís Disease-causing bacterium Xylella fastidiosa that is unable to make PG. Grapevines were inoculated with the X. fastidiosa that makes PG, the strain that does not, and with water (control). When examined 18 weeks after inoculation, the vines inoculated with PG-producing X. fastidiosa were dead (left), controls were disease-free (right) and vines inoculated with the X. fastidiosa that canít produce PG those were also healthy. X. fastidiosaís PG is required for Pierceís Disease development.


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