Effector Genes ofXanthamonas axonopodispv.vesicatoriaPromote Transmission and Enhance Other Fitness Traits in the Field

Abstract

Establishing durable disease resistance in agricultural crops, where much of the plant defense is provided through effector-R gene interactions, is complicated by the ability of pathogens to overcome R gene resistance by losing the corresponding effector gene. Many proposed methods to maintain disease resistance in the field depend on the idea that effector gene loss results in a fitness cost to the pathogen. In this article we test for fitness costs of effector gene function loss. We created directed knockouts of up to four effector genes from the bacterial plant pathogen Xanthomonas axonopodis pv. vesicatoria (Xav) and examined the effect of the loss of a functional gene product on several important fitness parameters in the field. These traits included transmission, lesion development, and epiphytic survival. We found that the products of all four effector genes had significant and often additive effects on fitness traits. Additional greenhouse tests revealed costs of effector gene loss on in planta growth and further showed that the effects on lesion development were separable from the effects on growth. Observable fitness effects of the three plasmid-borne effector genes were dependent upon the loss of functional avrBs2, indicating that complex functional interactions exist among effector genes with Xav.

Microbial life in the phyllosphere

“…3). However, it should be kept in mind that the type-III secretion system (T3SS) of phytopathogenic bacteria is also crucial to attain a maximal epiphytic population size 9,55 . In this context it is interesting to note that the importance of specific effectors for the development of aggregates on leaf surfaces was recently demonstrated for Pseudomonas syringae B728a and was shown to be mediated by a subpopulation of the epiphytic population and be host-dependent 56 [au:…”

The quasi-universality of nestedness in the structure of quantitative plant-parasite interactions

“…The positive correlation between parasite infectivity and host range breadth contrasts with qualitative host-parasite interactions and especially the GFG model, where the expansion of the host range of parasites is associated with a cost in fitness during infection of the previous hosts. Such so-called "virulence costs" have been experimentally measured in many plant-parasite systems, including viruses (Jenner et al, 2002;Desbiez et al, 2003;Janzac et al, 2010;Poulicard et al, 2010;Fraile et al, 2011;Ishibashi et al, 2012;Khatabi et al, 2013), fungi (Bahri et al, 2009;Huang et al, 2010;Caffier et al, 2010;Bruns et al, 2014), oomycetes (Montarry et al, 2010), bacteria (Vera Cruz et al, 2000Leach et al, 2001;Wichmann & Bergelson, 2004) or nematodes (Castagnone-Sereno et al, 2007), and could explain why universal pathogenicity is not fixed in pathogen populations . For quantitative plant resistance, few studies have estimated the occurrence of pathogenicity costs.…”

Host mixtures for plant disease control: Benefits from pathogen selection and immune priming

“…The idea of a cost as a counterpart of the ability of breaking a resistance gene originated as a theoretical hypothesis to explain the often‐observed maintenance of polymorphism in pathogen populations, in both agricultural and wild ecosystems (Brown, 2015; Gandon et al, 2002; Sasaki, 2000; Tellier & Brown, 2007b; Vanderplank, 1968). Since then, such a cost has been demonstrated and measured in a number of parasites, including bacteria (Cruz et al, 2000; Wichmann & Bergelson, 2004), fungi (Bahri et al, 2009; Bousset et al, 2018; Bruns et al, 2014; Caffier et al, 2010; Carson, 1998; Huang et al, 2010; Thrall & Burdon, 2003), viruses (Fraile et al, 2010; Ishibashi et al, 2012; Janzac et al, 2010; Jenner et al, 2002; Khatabi et al, 2013; Poulicard et al, 2010), nematodes (Castagnone‐Sereno et al, 2007), and oomycetes (Montarry et al, 2010).…”