The genetic basis of variation in immune defense against Lysinibacillus fusiformis infection in Drosophila melanogaster.
The genetic basis of variation in immune defense against Lysinibacillus fusiformis infection in Drosophila melanogaster.
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DOI：
10.1371/journal.ppat.1010934
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发表时间：
2023-08
期刊：
影响因子：
6.7
通讯作者：
中科院分区：
文献类型：
--
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表型变异的遗传原因往往因所研究的群体而异，特别是如果群体是由相对较少的基因型建立的。类似地，相似性状之间表型变异的遗传原因（对不同异生素化合物或病原体的抗性）也可能完全不同或仅部分重叠。种群间同一性状变异的遗传原因差异表明，选择如何作用于这些性状取决于环境。另一方面，不同性状变异的遗传原因的相似性表明了多效性，这也会影响自然选择如何塑造性状的变异。我们在三个不同的人群中对天然果蝇病原体革兰氏阳性菌Lysinibacillus fusiformis的免疫防御进行了表征，发现感染后生存变异的遗传结构几乎没有重叠。然而，当将我们的结果与真菌病原体B的类似实验进行比较时，通过对两种病原菌的QTL分析，我们发现了一个令人信服的共有QTL峰。该峰含有果蝇免疫效应子的Bomanin簇。功能丧失突变体和RNAi敲除实验证实了这些基因中的一些在针对两种病原体的免疫防御中的作用。这表明自然选择可能作用于整个Bomanin基因簇（以及QTL下的连接区域）或特定病原体的特定肽。像大多数特征一样，个体对感染的反应方式在群体中的个体之间存在差异。其中一些变异是由宿主的遗传差异引起的。在过去的十年中，开发了两个突出的资源来评估果蝇（Drosophila melanogaster）复杂性状的遗传变异，并绘制相关的遗传变异图。我们最近描述了一种从果蝇中分离的梭形赖氨酸芽孢杆菌菌株，当果蝇通过脓毒性损伤感染时，该菌株具有中等毒性。我们绘制了抗性L的遗传变异。fusiformis使用这些映射资源。我们发现，不同的资源，不同的遗传变化与免疫防御。然而，我们也发现在同一种资源中，基因组的同一区域与对两种李斯特菌的抗性有关。梭形菌和真菌病原体。这些结果表明，不同的人群适应不同的相同的病原体，但两个不同的病原体共享一个单一的人口内的遗传变异的相似原因。
The genetic causes of phenotypic variation often differ depending on the population examined, particularly if the populations were founded by relatively small numbers of genotypes. Similarly, the genetic causes of phenotypic variation among similar traits (resistance to different xenobiotic compounds or pathogens) may also be completely different or only partially overlapping. Differences in genetic causes for variation in the same trait among populations suggests context dependence for how selection acts on those traits. Similarities in the genetic causes of variation for different traits, on the other hand, suggests pleiotropy which would also influence how natural selection shapes variation in a trait. We characterized immune defense against a natural Drosophila pathogen, the Gram-positive bacterium Lysinibacillus fusiformis, in three different populations and found almost no overlap in the genetic architecture of variation in survival post infection. However, when comparing our results to a similar experiment with the fungal pathogen, B. bassiana, we found a convincing shared QTL peak for both pathogens. This peak contains the Bomanin cluster of Drosophila immune effectors. Loss of function mutants and RNAi knockdown experiments confirms a role of some of these genes in immune defense against both pathogens. This suggests that natural selection may act on the entire cluster of Bomanin genes (and the linked region under the QTL) or specific peptides for specific pathogens. Like most traits, the way individuals respond to infection vary among individuals within a population. Some of this variation is caused by genetic differences in the host. Over the past decade, two prominent resources were developed to assess genetic variation for complex traits of the fruit fly, Drosophila melanogaster and map the genetic variants responsible. We recently described a strain of Lysinibacillus fusiformis bacteria that was isolated from fruit flies and is moderately virulent when flies are infected via septic injury. We mapped genetic variation in resistance L. fusiformis using these mapping resources. We find that among the resources, different genetic changes were associated with immune defense. However, we also found that within a resource, the same region of the genome was associated with resistance to both L. fusiformis and a fungal pathogen. These results suggest that different populations adapt differently to the same pathogens, but two distinct pathogens share similar causes of genetic variation within a single population.
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影响因子：
6.7
作者：
Binggeli O;Neyen C;Poidevin M;Lemaitre B
通讯作者：
Lemaitre B
DOI：
10.1007/978-1-4939-3572-7_13
发表时间：
2016-01-01
期刊：
DATA MINING TECHNIQUES FOR THE LIFE SCIENCES
影响因子：
--
作者：
Dobin, Alexander;Gingeras, Thomas R.
通讯作者：
Gingeras, Thomas R.
影响因子：
64.8
作者：
COVID-19 Host Genetics Initiative
通讯作者：
COVID-19 Host Genetics Initiative
果蝇先天免疫：酚氧化酶原的区域和功能专业化。
影响因子：
5.4
作者：
Dudzic JP;Kondo S;Ueda R;Bergman CM;Lemaitre B
通讯作者：
Lemaitre B
影响因子：
3.3
作者：
Cao C;Cogni R;Barbier V;Jiggins FM
通讯作者：
Jiggins FM