Variation and Selection of Quantitative Traits in Plant Pathogens

Abstract

The first section presents the quantitative traits of pathogenicity that are most commonly measured by plant pathologists, how the expression of those traits is influenced by environmental factors, and why the traits must be taken into account for understanding pathogen evolution in agricultural systems. Particular attention is given to the shared genetic control of these traits by the host and the pathogen. Next, the review discusses how quantitative traits account for epidemic development and how they can be related to pathogen fitness. The main constraints that influence the evolution of quantitative traits in pathogen populations are detailed. Finally, possible directions for research on the management of pathogen virulence (as defined by evolutionists) and host quantitative resistance are presented. The review evaluates how the theoretical corpus developed by epidemiologists and evolutionists may apply to plant pathogens in the context of agriculture. The review also analyzes theoretical papers and compares the modeling hypotheses to the biological characteristics of plant pathogens.

Variation in aggressiveness is detected among Puccinia triticina isolates of the same pathotype and clonal lineage in the adult plant stage

“…The genetic support of quantitative traits of aggressiveness in plant pathogens is not known but QTL analyses of host resistance (e.g., Ballini et al 2008) and pathogen aggressiveness (Cumagun et al 2004;Lind et al 2007) corroborate the idea that quantitative traits of pathogenicity are under the shared control of the pathogen, the host and their interaction (see Lannou 2012 for a review). The genetic determinism of the quantitative traits is complex and still barely understood from the plant side and even less information is available from the pathogen side.…”

“…Pathotypes were sometimes compared for quantitative traits on the basis of a single isolate per pathotype (Katsuya and Green 1967). Quantitative variation in pathogenicity among individuals can be the consequence of a change from avirulence to virulence (Vera Cruz et al 2000), or related to the number of qualitative virulence factors (Thrall and Burdon 2003) but it is likely that aggressiveness variations also occur independently of qualitative virulence (Villaréal and Lannou 2000;Pilet et al 2005;Lannou 2012). From the available literature, this is however not easy to establish for pathogens with clonal population structures.…”

“…In an obligate fungal pathogen (Podosphaera plantaginis) of Plantago lanceola, genotype-by-temperature interactions were measured for spore infectivity and spore production (Laine 2008). Quantitative measurements of aggressiveness may be influenced by the environment sensu lato (Lannou 2012), including climatic parameters (Eyal and Peterson 1967;Tomerlin et al 1983), host physiological state (Milus and Line 1980;Tomerlin et al 1983) and pathogen maintenance (Jeffrey et al 1962;Mundt et al 2002).…”

Can Pl Resistance Gene in Sunflower Line D4 be Used to Differentiate the Pathogenicity in Four Plasmopara halstedii (Sunflower Downy Mildew) Races 304, 314, 704 and 714?

“…We still have little data on the evolution of life-history traits of plant pathogens and especially on the potential trade-off between fitness components that could limit their evolutionary potential (Lannou, 2012). However, a recent study has demonstrated that trade-offs do exist in plant pathogens, as found between latency period and spore production capacity in wheat brown rust (Pariaud et al, 2012).…”

Short Rotations in Forest Plantations Accelerate Virulence Evolution in Root-Rot Pathogenic Fungi

“…Among biological traits assumed to be under strong evolutionary pressure, the virulence of pathogens, generally defined as the quantitative ability of a pathogen to induce host mortality [11,12], is the focus of considerable attention from evolutionary ecologists [12] and plant pathologists [13]. Despite still imprecise experimental characterizations, mainly based on proxies, and a complex theory including the transmission-virulence trade-off hypothesis [14], the evolution at this trait is thought to be tightly related to the spread of diseases [11,15,16].…”