C. elegans heritably adapts to P. vranovensis infection via a mechanism that requires the cysteine synthases cysl-1 and cysl-2
C. elegans heritably adapts to P. vranovensis infection via a mechanism that requires the cysteine synthases cysl-1 and cysl-2
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DOI：
10.1101/675132
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发表时间：
2019-06
期刊：
影响因子：
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通讯作者：
N. Burton;C. Riccio;Alexandra Dallaire;Jonathan Price;Benjamin J. Jenkins;A. Koulman;E. Miska
中科院分区：
文献类型：
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作者：
N. Burton;C. Riccio;Alexandra Dallaire;Jonathan Price;Benjamin J. Jenkins;A. Koulman;E. Miska
父母接触病原体可以激发后代在不同生物体中的免疫力。这种遗传启动发生的机制在很大程度上是未知的。在这里，我们报告说，土壤细菌假单胞菌vranovensis是线虫线虫的天然病原体，父母的动物暴露于P. vranovensis促进后代抵抗感染。此外，我们证明了一个跨代增强后代的生存时，连续三代的动物暴露于P. vranovensis。通过研究动物遗传性地适应弗氏疟原虫感染的机制，我们发现，弗氏疟原虫的亲本感染导致后代中半胱氨酸脱氨酶CYSL-1和CYSL-2以及缺氧诱导因子RHY-1的调节因子的表达增加，并且这三个基因是适应弗氏疟原虫所必需的。据我们所知，这些观察结果代表了迄今为止在任何生物体中报道的对病原体感染的后代存活率的最大可遗传增加，并建立了动物适应感染的新的CYSL-1，CYSL-2和RHY-1依赖机制。
Parental exposure to pathogens can prime offspring immunity in diverse organisms. The mechanisms by which this heritable priming occurs are largely unknown. Here we report that the soil bacteria Pseudomonas vranovensis is a natural pathogen of the nematode Caenorhabditis elegans and that parental exposure of animals to P. vranovensis promotes offspring resistance to infection. Furthermore, we demonstrate a transgenerational enhancement of progeny survival when three consecutive generations of animals are exposed to P. vranovensis. By investigating the mechanisms by which animals heritably adapt to P. vranovensis infection, we found that parental infection by P. vranovensis results in increased expression of the cysteine synthases CYSL-1 and CYSL-2 and the regulator of hypoxia inducible factor RHY-1 in progeny and that these three genes are required for adaptation to P. vranovensis. To our knowledge, these observations represent the largest heritable increase in offspring survival in response to a pathogen infection reported in any organism to date and establish a new CYSL-1, CYSL-2, and RHY-1 dependent mechanism by which animals adapt to infection.