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

Puccinia triticina reproduces asexually in France and thus individual genotype is the unit of selection. A strong link has been observed between genotype identities (as assessed by microsatellite markers) and pathotypes (pools of individuals with the same combination of qualitative virulence factors). Here, we tested whether differences in quantitative traits of aggressiveness could be detected within those clonal lineages by comparing isolates of identical pathotype and microsatellite profile. Pairs of isolates belonging to different pathotypes were compared for their latent period, lesion size and spore production capacity on adult plants under greenhouse conditions, with a high number of replicates. Isolates of the same pathotype showed remarkably similar values for the measured traits, except in three situations: differences were obtained within two pathotypes for latent period and within one pathotype for sporulation capacity. One of these differences was tested again and confirmed. This indicates that the average aggressiveness level of a leaf rust pathotype may increase without any change in its virulence factors or microsatellite profile

Quantitative resistance can lead to evolutionary changes in traits not targeted by the resistance QTLs.

This paper addresses the general concern in plant pathology that the introduction of quantitative resistance in the landscape can lead to increased pathogenicity. Hereto, we study the hypothetical case of a quantitative trait loci (QTL) acting on pathogen spore production per unit lesion area. To regain its original fitness, the pathogen can break the QTL, restoring its spore production capacity leading to an increased spore production per lesion. Or alternatively, it can increase its lesion size, also leading to an increased spore production per lesion. A data analysis shows that spore production per lesion (affected by the resistance QTL) and lesion size (not targeted by the QTL) are positively correlated traits, suggesting that a change in magnitude of a trait not targeted by the QTL (lesion size) might indirectly affect the targeted trait (spore production per lesion). Secondly, we model the effect of pathogen adaptation towards increased lesion size and analyse its consequences for spore production per lesion. The model calculations show that when the pathogen is unable to overcome the resistance associated QTL, it may compensate for its reduced fitness by indirect selection for increased pathogenicity on both the resistant and susceptible cultivar, but whereby the QTLs remain effective.Rothamsted Research receives support from the Biotechnology and Biological Sciences Research Council (BBSRC) of the United Kingdom. F v d Berg was funded by an INRA-BBSRC funded project entitled ‘Epidemiological and evolutionary models for invasion and persistence of disease’. CAG gratefully acknowledges support of a BBSRC Professional Fellowship

Genome-wide signatures of selection in Colletotrichum kahawae reveal candidate genes potentially involved in pathogenicity and aggressiveness

Original ResearchPlants and their pathogens are engaged in continuous evolutionary battles, with pathogens evolving to circumvent plant defense mechanisms and plants responding through enhanced protection to prevent or mitigate damage induced by pathogen attack. Managed ecosystems are composed of genetically identical populations of crop plants with few changes from year to year. These environments are highly conducive to the emergence and dissemination of pathogens and they exert selective pressure for both qualitative virulence factors responsible for fungal pathogenicity, and quantitative traits linked to pathogen fitness, such as aggressiveness. In this study, we used a comparative genome-wide approach to investigate the genomic basis underlying the pathogenicity and aggressiveness of the fungal coffee pathogen Colletotrichum kahawae infecting green coffee berries. The pathogenicity was investigated by comparing genomic variation between C. kahawae and its non-pathogenic sibling species, while the aggressiveness was studied by a genome-wide association approach with groups of isolates with different phenotypic profiles. High genetic differentiation was observed between C. kahawae and the most closely related species with 5,560 diagnostic SNPs identified, in which a significant enrichment of non-synonymous mutations was detected. Functional annotation of these non-synonymous mutations revealed a significant enrichment mainly in two gene ontology categories, “oxidation– reduction process” and “integral component of membrane.” Finally, the annotation of several genes potentially under-selection revealed that C. kahawae’s pathogenicity may be a complex biological process, in which important biological functions, such as, detoxification and transport, regulation of host and pathogen gene expression, and signaling are involved. On the other hand, the genome-wide association analyses for aggressiveness were able to identify 10 SNPs and 15 SNPs of small effect in single and multi-association analysis, respectively, from which 7 were common, giving in total 18 SNPs potentially associated. The annotation of these genomic regions allowed the identification of four candidate genes encoding F-box domain-containing, nitrosoguanidine resistance, Fungal specific transcription factor domain-containing and C6 transcription factor that could be associated with aggressiveness. This study shed light, for the first time, on the genetic mechanisms of C. kahawae host specializationOriginalinfo:eu-repo/semantics/publishedVersio

Geographically variable biotic interactions and implications for species ranges

The challenge Understanding how biotic interactions affect species' geographical ranges, biodiversity patterns and ecological responses to environmental change is one of the most pressing challenges in macroecology. Extensive efforts are underway to detect signals of biotic interactions in macroecological data. However, efforts are limited by bias in the taxa and spatial scale for which occurrence data are available and by difficulty in ascribing causality to co-occurrence patterns. Moreover, we are not necessarily looking in the right places; analyses are largely ad hoc, depending on availability of data, rather than focusing on regions, taxa, ecosystems or interaction types where biotic interactions might affect species' geographical ranges most strongly. Unpicking biotic interactions We suggest that macroecology would benefit from the recognition that abiotic conditions alter two key components of biotic interaction strength: frequency and intensity. We outline how and why variation in biotic interaction strength occurs, explore the implications for species' geographical ranges and discuss the challenges inherent in quantifying these effects. In addition, we explore the role of behavioural flexibility in mediating biotic interactions potentially to mitigate impacts of environmental change. New data We argue that macroecology should take advantage of "independent" data on the strength of biotic interactions measured by other disciplines, in order to capture a far wider array of taxa, locations and interaction types than are typically studied in macroecology. Data on biotic interactions are readily available from community, disease, microbial and parasite ecology, evolution, palaeontology, invasion biology and agriculture, but most are yet to be exploited within macroecology. Integrating biotic interaction strength data into macroecology Harmonization of data across interdisciplinary sources, taxa and interaction types could be achieved by breaking down interactions into elements that contribute to frequency and intensity. This would allow quantitative biotic interaction data to be incorporated directly into models of species distributions and macroecological patterns

Periodic Host Absence Can Select for Higher or Lower Parasite Transmission Rates

This paper explores the effect of discontinuous periodic host absence on the evolution of pathogen transmission rates by using Ro maximisation techniques. The physiological consequence of an increased transmission rate can be either an increased virulence, i.e. there is a transmission-virulence trade-off or ii) a reduced between season survival, i.e. there is a transmission-survival trade-off. The results reveal that the type of trade-off determines the direction of selection, with relatively longer periods of host absence selecting for higher transmission rates in the presence of a trade-off between transmission and virulence but lower transmission rates in the presence of a trade-of between transmission and between season survival. The fact that for the transmission-virulence trade-off both trade-off parameters operate during host presence whereas for the transmission-survival trade-off one operates during host presence (transmission) and the other (survival) during the period of host absence is the main cause for this difference in selection direction. Moreover, the period of host absence seems to be the key determinant of the pathogens transmission rate. Comparing plant patho-systems with contrasting biological features suggests that airborne plant pathogen respond differently to longer periods of host absence than soil-borne plant pathogens

Agressivité de Puccinia triticina (agent de la rouille brune du blé) et adaptation à l'hôte

La capacité d'évolution des agents pathogènes pour les traits quantitatifs doit être caractérisée afin d'utiliser durablement les résistances quantitatives des plantes. Basée sur la rouille brune du blé (Puccinia triticina - Triticum aestivum), ma thèse aborde trois questions: (i) Les populations pathogènes peuvent elles s'adapter quantitativement aux variétés, et quels sont les traits de vie impliqués?; (ii) L'évolution du niveau d'agressivité des pathotypes est-elle soumise à des contraintes?; et (iii) Les populations pathogènes peuvent-elles avoir un haut niveau d'agressivité sur toutes les variétés?. Des expériences en serre sur plantes adultes montrent que P. triticina est capable de s'adapter pour les caractères quantitatifs, possiblement par sélection d'individus plus agressifs au sein des pathotypes. La plupart des traits du cycle asexué sont concernés: latence, sporulation, taille et durée de vie des lésions. On montre l'existence de contraintes d'évolution entre certains traits, mais les pathotypes semblent pouvoir adopter des stratégies contrastées selon leur capacité de croissance ou d'exploitation de la ressource hôte. Un des pathotypes étudiés est très agressif et il semble avoir un ratio optimal entre sa transmission et son effet délétère sur son hôte (réduction de photosynthèse). De plus, nos résultats indiquent qu'il pourrait conserver un fort niveau d'agressivité sur de nombreuses variétés. Cependant, bien que très agressif, ce pathotype n'est pas capable d'infecter de nombreuses variétés. Combiner les résistances qualitatives et quantitatives dans les variétés est un moyen envisageable de gestion du niveau d'agressivité des populations de P. triticina.Pathogen capacity to adapt to their hosts for quantitative traits has to be characterized to use quantitative resistances in a durable way. Based on wheat leaf rust (Puccinia triticina - Triticum aestivum), my thesis investigated three questions: (i) Are pathotypes able to adapt to their hosts for quantitative traits, and which of these traits are involved? (ii) Do evolutionary trade-offs exist between P. triticina life history traits? (iii) Can pathotypes have a high level of aggressiveness on several host genotypes?. Greenhouse experiments on adult plants showed that P. triticina can adapt, possibly through the selection of more aggressive individuals within the pathotypes. Several traits of the multiplication cycle were involved (latency, sporulation, lesion size and life span), and investigating the correlations between them revealed trade-offs. Nonetheless, despite these global trends, the pathotypes may adopt different strategies, relying either on growth or on host resource exploitation capacity. One of the pathotypes studied was particularly aggressive and seemed to present an optimal ratio between transmission and deleterious effect on the host, as measured by the decrease in photosynthesis. Our data suggest that pathotypes are able to keep their aggressiveness profile on several host genetic backgrounds, but that their aggressiveness level is linked to the number of cultivars they can infect, due to compatibility relationships. In particular, the highly aggressive pathotype remains restricted to a few cultivars. Thus, combining qualitative and quantitative resistances in the cultivars can be a means to manage the aggressiveness level of P. triticina populations.ORSAY-PARIS 11-BU Sciences (914712101) / SudocSudocFranceF