Influence of Moisture, Temperature, Leaf Maturity, and Host Genotype on Infection of Elms byStegophora ulmea

1984 ◽  
Vol 74 (11) ◽  
pp. 1296 ◽  
Author(s):  
G. H. McGranahan
Keyword(s):  
Biomics ◽  
2020 ◽  
Vol 12 (3) ◽  
pp. 343-351
Author(s):  
S.V. Veselova ◽  
G.F. Burkhanova ◽  
S.D. Rumyantsev ◽  
T.V. Nuzhnaya

Stagonospora nodorum Berk. is the causal agent of Septoria nodorum blotch (SNB) of wheat (Triticum aestivum L.). It synthesizes host-specific necrotrophic effectors (NEs), which facilitate infection process and ensure virulence of pathogen on host plant with a dominant susceptibility gene. The interaction of virulence genes products of the NEs pathogen (SnTox) with susceptibility genes products of the host plant (Snn) in the S. nodorum - wheat pathosystem is carried out in inverted gene-for-gene system and causes the development of disease. In this study, we tested three main NEs SnToxA, SnTox1, SnTox3, which have already been identified in S. nodorum at the gene level. The NEs role in the development of SNB has already been proven; however, the overall host response to SNB does not always strictly follow the inverted gene-for-gene system, as multiple SnTox-Snn interactions can be additive or epistatic. In this regard, the aim of the work was to identify the NE genes in three S. nodorum isolates and to study effect of NEs genes transcriptional activity on the isolate virulence. We have shown that all three NEs SnToxA, SnTox3 and SnTox1 played an important role in the development of the disease in compatible interactions. Effectors SnTox3 and SnTox1 exhibited epistatic interaction that was removed by a triple compatible interaction (SnTox3-Snn3, SnToxA-Tsn1 and SnTox1-Snn1). This effect was shown by us for the first time. The mechanisms of epistatic and additive interactions, as well as the virulence of the isolate were associated with the regulation of the NEs genes transcriptional activity. The avirulent isolate Sn4VD lacked transcription of all three NEs genes, and the virulent isolate Sn9MH was characterized by a high level of mRNA accumulation of all three NEs genes during infection on susceptible cultivar. We also showed that SnTox expression depended both on the host genotype in SnToxA and SnTox3 and on the number of compatible interactions exhibiting additive or epistatic interactions in SnTox1 and SnTox3. Finally, the virulence of the S. nodorum isolate depended on the qualitative and quantitative composition of NEs.


Author(s):  
Erwin G. Zoetendal ◽  
Antoon D. L. Akkermans ◽  
Wilma M. Akkermans-van Vliet ◽  
J. Arjan G. M. De Visser ◽  
Willem M. De Vos

2021 ◽  
Author(s):  
Melanie R. Smee ◽  
Sally A. Raines ◽  
Julia Ferrari

AbstractMicrobial symbionts often alter the phenotype of their host. Benefits and costs to hosts depend on many factors, including host genotype, symbiont species and genotype, and environmental conditions. Here, we present a study demonstrating genotype-by-genotype (G×G) interactions between multiple species of endosymbionts harboured by an insect, and the first to quantify the relative importance of G×G interactions compared with species interactions in such systems. In the most extensive study to date, we microinjected all possible combinations of five Hamiltonella defensa and five Fukatsuia symbiotica (X-type; PAXS) isolates into the pea aphid, Acyrthosiphon pisum. We applied several ecological challenges: a parasitoid wasp, a fungal pathogen, heat shock, and performance on different host plants. Surprisingly, genetic identity and genotype × genotype interactions explained far more of the phenotypic variation (on average 22% and 31% respectively) than species identity or species interactions (on average 12% and 0.4%, respectively). We determined the costs and benefits associated with co-infection, and how these compared to corresponding single infections. All phenotypes were highly reliant on individual isolates or interactions between isolates of the co-infecting partners. Our findings highlight the importance of exploring the eco-evolutionary consequences of these highly specific interactions in communities of co-inherited species.


2010 ◽  
Vol 19 (8) ◽  
pp. 1705-1720 ◽  
Author(s):  
D. J. BARSHIS ◽  
J. H. STILLMAN ◽  
R. D. GATES ◽  
R. J. TOONEN ◽  
L. W. SMITH ◽  
...  

2014 ◽  
Vol 101 (5) ◽  
pp. 417-426 ◽  
Author(s):  
Petr Procházka ◽  
Hana Konvičková-Patzenhauerová ◽  
Milica Požgayová ◽  
Alfréd Trnka ◽  
Václav Jelínek ◽  
...  
Keyword(s):  

Oecologia ◽  
2017 ◽  
Vol 184 (1) ◽  
pp. 59-73 ◽  
Author(s):  
Raymond V. Barbehenn ◽  
Madhav Kapila ◽  
Sara Kileen ◽  
Caleb P. Nusbaum
Keyword(s):  

Parasitology ◽  
2007 ◽  
Vol 135 (3) ◽  
pp. 303-308 ◽  
Author(s):  
T. J. LITTLE ◽  
W. CHADWICK ◽  
K. WATT

SUMMARYUnderstanding genetic relationships amongst the life-history traits of parasites is crucial for testing hypotheses on the evolution of virulence. This study therefore examined variation between parasite isolates (the bacterium Pasteuria ramosa) from the crustacean Daphnia magna. From a single wild-caught infected host we obtained 2 P. ramosa isolates that differed substantially in the mortality they caused. Surprisingly, the isolate causing higher early mortality was, on average, less successful at establishing infections and had a slower growth rate within hosts. The observation that within-host replication rate was negatively correlated with mortality could violate a central assumption of the trade-off hypothesis for the evolution of virulence, but we discuss a number of caveats which caution against premature rejection of the trade-off hypothesis. We sought to test if the characteristics of these parasite isolates were constant across host genotypes in a second experiment that included 2 Daphnia host clones. The relative growth rates of the two parasite isolates did indeed depend on the host genotype (although the rank order did not change). We suggest that testing evolutionary hypotheses for virulence may require substantial sampling of both host and parasite genetic variation, and discuss how selection for virulence may change with the epidemiological state of natural populations and how this can promote genetic variation for virulence.


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