Reuter Max, Lehmann Laurent, Guillaume Frédéric
Research Department for Genetics, Evolution and Environment, Faculty of Life Sciences, University College London, Wolfson House, 4 Stephenson Way, London, NW1 2HE, UK.
BMC Evol Biol. 2008 May 6;8:134. doi: 10.1186/1471-2148-8-134.
Maternally transmitted symbionts have evolved a variety of ways to promote their spread through host populations. One strategy is to hamper the reproduction of uninfected females by a mechanism called cytoplasmic incompatibility (CI). CI occurs in crosses between infected males and uninfected females and leads to partial to near-complete infertility. CI-infections are under positive frequency-dependent selection and require genetic drift to overcome the range of low frequencies where they are counter-selected. Given the importance of drift, population sub-division would be expected to facilitate the spread of CI. Nevertheless, a previous model concluded that variance in infection between competing groups of breeding individuals impedes the spread of CI.
In this paper we derive a model on the spread of CI-infections in populations composed of demes linked by restricted migration. Our model shows that population sub-division facilitates the invasion of CI. While host philopatry (low migration) favours the spread of infection, deme size has a non-monotonous effect, with CI-invasion being most likely at intermediate deme size. Individual-based simulations confirm these predictions and show that high levels of local drift speed up invasion but prevent high levels of prevalence across the entire population. Additional simulations with sex-specific migration rates further show that low migration rates of both sexes are required to facilitate the spread of CI.
Our analyses show that population structure facilitates the invasion of CI-infections. Since some level of sub-division is likely to occur in most natural populations, our results help to explain the high incidence of CI-infections across species of arthropods. Furthermore, our work has important implications for the use of CI-systems in order to genetically modify natural populations of disease vectors.
母系传播的共生体已经进化出多种方式来促进它们在宿主种群中的传播。一种策略是通过一种称为细胞质不相容性(CI)的机制来阻碍未感染雌性的繁殖。CI发生在感染雄性与未感染雌性的杂交中,并导致部分至几乎完全不育。CI感染处于正频率依赖选择之下,并且需要遗传漂变来克服它们被反向选择的低频范围。鉴于漂变的重要性,种群细分预计会促进CI的传播。然而,先前的一个模型得出结论,繁殖个体竞争群体之间感染的差异会阻碍CI的传播。
在本文中,我们推导了一个关于CI感染在由有限迁移连接的种群中传播的模型。我们的模型表明,种群细分促进了CI的入侵。虽然宿主留居性(低迁移)有利于感染的传播,但种群大小具有非单调效应,CI入侵最有可能发生在中等种群大小。基于个体的模拟证实了这些预测,并表明高水平的局部漂变加速了入侵,但阻止了整个种群的高感染率。具有性别特异性迁移率的额外模拟进一步表明,两性的低迁移率都需要促进CI的传播。
我们的分析表明,种群结构促进了CI感染的入侵。由于在大多数自然种群中可能会发生某种程度的细分,我们的结果有助于解释节肢动物物种中CI感染的高发生率。此外,我们的工作对于使用CI系统来对病媒的自然种群进行基因改造具有重要意义。