Sex-specific costs of resistance to the fungal pathogen Ustilago violacea (Microbotryum violaceum) in Silene alba
Sex-specific costs of resistance to the fungal pathogen Ustilago violacea (Microbotryum violaceum) in Silene alba
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DOI：
10.2307/2410650
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发表时间：
1996-06-01
期刊：
影响因子：
3.3
通讯作者：
Antonovics, J
中科院分区：
文献类型：
--
作者：
Biere, A;Antonovics, J
抗性的代价经常被用来解释自然植物群体中对真菌病原体的抗性多态性的维持。为了调查这些成本，从单一寄主种群中收集了27个白硅酮的半兄弟姐妹家族，在存在和不存在花药黑穗病真菌紫黑穗病菌（Ustilago violacea）的实验种群中生长，紫黑穗病菌是一种通过昆虫传播的致宿主绝育病原体，既是该疾病的传粉媒介，也是该疾病的媒介。1个丢失的家族在接种抗性方面存在显著差异，表明在宿主群体中一旦遇到疾病（“生化”抗性），阻碍真菌生长的机制存在遗传变异。此外。寄主家庭在没有疾病的情况下，开花和开花的时间显著不同。通径分析显示，雄性寄主家族的晚开花对高田间抗性有直接贡献（P < 0.01），这可能是由于寄主与携带高孢子负荷的媒介之间的接触率降低（避免）。或“物候”抗性)。低花产量对田间抗性的贡献接近显著（P < 0.10）。生物化学抗性和物候抗性之间存在显著的正相关，表明延迟开花可能是生物化学抗性的多效效应，或者控制这些性状的基因处于连锁不平衡状态。通径分析表明，雄性寄主的生化抗性对田间抗性既有直接贡献（P < 0.01），也有间接正向贡献（P < 0.05）。抗药成本是性别特异性的。高田间抗性的雄性寄主家庭在健康人群中繁殖成功率显著降低（P < 0.01），表明田间抗性的适应性成本（P < 0.01），而雌性寄主没有检测到适应性成本。通径分析显示，田间抗性的生化成分对雄性寄主的适应度成本没有直接贡献，而其通过物候的间接影响仅为极显著（P < 0.10）。这一发现表明，适合度成本主要由田间抗性的物候成分决定。因为宿主人群没有已知的疾病史。尚不清楚适应度成本是否对抗性多态性的维持负责，或者多态性是否由于与病原体感染无关的原因而存在。寄主家族与病原菌菌株之间的相互作用对接种成功的影响不显著。因此，没有证据表明生化抗性的间接代价，即对替代菌株的抗性降低。病原菌最初呈斑块分布的实验种群的感染率低于病原菌均匀分布的实验种群，这表明除了抗性的适应度成本外，有效的病原菌压力以及易感和抗性个体的相对成功可能取决于病原菌的空间种群结构。
Costs of resistance are often invoked to explain the maintenance of polymorphisms for resistance to fungal pathogens in natural plant populations. To investigate such costs, 27 half-sib families of Silene alba, collected from a single host population, were grown in experiment populations in the presence and absence of the anther-smut fungus Ustilago violacea, a host-sterilizing pathogen transmitted by insects that are both pollinators and vectors of the disease. I lost families differed significantly in resistance to inoculation, indicating the presence of genetic variation for mechanisms that impede fungal growth once the disease is encountered (''biochemical'' resistance) within the host population. in addition. host families differed significantly in onset of flowering and in flower production in the absence of the disease. Path analysis revealed that late onset of flowering In male host families made a direct contribution to high field resistance (P < 0.01), probably due to a reduced rate of contact between hosts and vectors carrying high spore loads (avoidance. or ''phenological'' resistance). The contribution of low flower production to field resistance only approached significance (P < 0.10). There was a significantly positive genetic association between biochemical and phenological resistance, suggesting that delayed flowering is either a pleiotropic effect of biochemical resistance, or that genes governing these traits art in linkage disequilibrium. Path analysis revealed that biochemical resistance made both a direct contribution to field resistance (P < 0.01) and a positive indirect contribution via its association with phenology and flower production (P < 0.05) in male hosts. Costs of resistance were sex specific. Male host families with high field resistance had significantly lower reproductive success in healthy populations, indicating a fitness cost of field resistance (P < 0.01), whereas no costs were detected for female hosts. Path analysis revealed thar the biochemical component of field resistance made: no direct contribution to the observed fitness cost in male hosts, whereas its indirect effect through phenology was only marginally significant (P < 0.10). This finding indicates that fitness costs were mainly due to the phenological component of field resistance. Because the host population had no known history of disease. it is not clear whether the fitness costs are responsible for maintenance of the resistance polymorphism or whether the polymorphism is present for reasons unrelated to pathogen infection. interactions between host families and pathogen strains with respect to inoculation success were not significant. Hence, there was no evidence for indirect costs of biochemical resistance, that is, reduced resistance to alternative strains. infection rates in experimental populations with an initially patchy distribution of the pathogen were lower than in populations with a uniform pathogen distribution, suggesting that the effective pathogen pressure and hence the relative success of susceptible and resistant individuals may, in addition to fitness costs of resistance, depend on the spatial population structure of the pathogen.