Quantitative disease resistance in wild Silene vulgaris to its endemic pathogen Microbotryum silenes-inflatae.
Quantitative disease resistance in wild Silene vulgaris to its endemic pathogen Microbotryum silenes-inflatae.
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DOI：
10.1002/ece3.10797
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发表时间：
2023-12
影响因子：
2.6
通讯作者：
Bruns, Emily L.
中科院分区：
文献类型：
--
作者：
Hood, Michael E.;Nelson, Sydney;Cho, Jae-Hoon;Launi, Michelle;Antonovics, Janis;Bruns, Emily L.
抗病能力的进化是植物-病原菌系统的预期特征，但这一性状的遗传学最常产生的表型变异是定性的还是定量的，这是我们对自然种群理解的一个重大差距。这两种形式的抗性变异通常与潜在基因座数量的差异、宿主-病原菌共同进化的特殊性以及预防或减缓感染过程的不同机制有关。花药黑穗病是一种常见的野生物种病害模型，感染对其适应性有严重影响，先前的研究表明，在几个寄主物种中存在抗性变异。然而，由于将个体宿主暴露在这种病原体下的结果是二元的(健康的或患病的)，以前已经在家庭一级测量了抵抗力，即患病的兄弟姐妹的比例。这使得不确定家系间的差异是反映了分离的离散表型的对比比率，还是反映了个体之间的连续特征变异。通过无性繁殖的方法在寄主Silene ual garis上复制植株，以量化个体对特有的花药黑穗病病原菌Microbotryum silenes-ifatae的侵染率。田间采集的家系间抗病性差异显著，不同基因型间的抗病性存在单峰连续变异。利用等位抗性四分位数内的基因型间杂交，根据亲本抗性值预测后代感染率。虽然抗性基因在这个系统中仍有潜在的主要作用，因为在先前的研究中有这种质量抗性的建议，但在这里，对地方性花药黑穗病病原菌的定量抗病表明了普通链球菌属。自然种群的变异和该性状的较强遗传力，再加上花药黑粉病的严重适合性后果，表明这些寄主种群的抗性对疾病诱导的选择具有很强的反应能力。传染病是野生动物生物学中无处不在的组成部分，但在我们对自然种群的理解中，个体之间的抗病能力如何变化是一个巨大的差距。利用一种对野生植物物种具有严重适合度后果的疾病，我们揭示了对表现出高度遗传性的连续表型变异的抗性，表明寄主种群对疾病诱导的选择具有高度的反应能力。
The evolution of disease resistances is an expected feature of plant–pathogen systems, but whether the genetics of this trait most often produces qualitative or quantitative phenotypic variation is a significant gap in our understanding of natural populations. These two forms of resistance variation are often associated with differences in number of underlying loci, the specificities of host–pathogen coevolution, as well as contrasting mechanisms of preventing or slowing the infection process. Anther‐smut disease is a commonly studied model for disease of wild species, where infection has severe fitness impacts, and prior studies have suggested resistance variation in several host species. However, because the outcome of exposing the individual host to this pathogen is binary (healthy or diseased), resistance has been previously measured at the family level, as the proportion of siblings that become diseased. This leaves uncertain whether among‐family variation reflects contrasting ratios of segregating discrete phenotypes or continuous trait variation among individuals. In the host Silene vulgaris, plants were replicated by vegetative propagation in order to quantify the infection rates of the individual genotype with the endemic anther‐smut pathogen, Microbotryum silenes‐inflatae. The variance among field‐collected families for disease resistance was significant, while there was unimodal continuous variation in resistance among genotypes. Using crosses between genotypes within ranked resistance quartiles, the offspring infection rate was predicted by the parental resistance values. While the potential remains in this system for resistance genes having major effects, as there were suggestions of such qualitative resistance in a prior study, here the quantitative disease resistance to the endemic anther‐smut pathogen is indicated for S. vulgaris. The variation in natural populations and strong heritability of the trait, combined with severe fitness consequences of anther‐smut disease, suggests that resistance in these host populations is highly capable of responding to disease‐induced selection. Infectious disease is a ubiquitous component of wildlife biology, but how disease resistance varies among individuals is a significant gap in our understanding of natural populations. Using a disease with severe fitness consequences for a wild plants species, we reveal resistance to display continuous phenotypic variation with a high degree of heritability, indicating that the host populations are highly capable of responding to disease‐induced selection.
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影响因子：
2.1
作者：
通讯作者：
--
DOI：
10.1086/715013
发表时间：
2021-08
期刊：
The American naturalist
影响因子：
--
作者：
Lerner N;Luizzi V;Antonovics J;Bruns E;Hood ME
通讯作者：
Hood ME
DOI：
10.1126/science.1171663
发表时间：
2009-05-08
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Burdon JJ;Thrall PH
通讯作者：
Thrall PH
影响因子：
3.4
作者：
Wilfert L;Schmid-Hempel P
通讯作者：
Schmid-Hempel P
影响因子：
5.5
作者：
ALEXANDER, HM;ANTONOVICS, J;KELLY, AW
通讯作者：
KELLY, AW