EXPERIMENTAL EVOLUTION SHOWS<i>DROSOPHILA MELANOGASTER</i>RESISTANCE TO A MICROSPORIDIAN PATHOGEN HAS FITNESS COSTS

Vijendravarma, Roshan K.; Kraaijeveld, Alex R.; Godfray, H. Charles J.

doi:10.1111/j.1558-5646.2008.00516.x

Cited by 63 publications

(53 citation statements)

References 106 publications

(155 reference statements)

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“…Despite ample knowledge of the genes triggered by parasite attacks against Drosophila, only a few key studies have analyzed how an outbred fly population may adapt to a given parasite (11)(12)(13)15). However, the genetic basis and the consequences of such adaptation for host susceptibility to other parasites have not been determined.…”

mentioning

confidence: 99%

Host adaptation to viruses relies on few genes with different cross-resistance properties

Martins

Faria

Nolte

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

125

208

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Significance Despite ample knowledge of the genetics and physiology of host responses to parasites, little is known about the genetic basis of host adaptation to parasites. Moreover, adaptation to one parasite is likely to impact the outcome of different infections. Yet these correlated responses, seminal to the understanding of host evolution in multiparasite environments, remain poorly studied. We determined the genetic and phenotypic changes underlying adaptation upon experimental evolution of a Drosophila melanogaster population under viral infection [ Drosophila C virus (DCV)]. After 20 generations, selected flies showed increased survival upon infection with DCV and two other viruses. Using whole-genome sequencing and through RNAi, we identified and functionally validated three genes underlying the adaptive process and revealed their differential roles in the correlated responses observed.

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mentioning

confidence: 99%

Host adaptation to viruses relies on few genes with different cross-resistance properties

Martins

Faria

Nolte

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

125

208

View full text Add to dashboard Cite

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“…Thus, insects and plants, for example, which depend on more generalized defences (Burdon & Thrall 1999;Kraaijeveld & Godfray 1999;Hultmark 2003;Vijendravarma et al 2009), should form secondary sympatry more readily and thus diversify more rapidly. Certainly, these groups exhibit very high diversity.…”

Section: Discussionmentioning

confidence: 99%

Host–pathogen coevolution, secondary sympatry and species diversification

Ricklefs

2010

Phil. Trans. R. Soc. B

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The build-up of species locally within a region by allopatric speciation depends on geographically separated (allopatric) sister populations becoming reproductively incompatible followed by secondary sympatry. Among birds, this has happened frequently in remote archipelagos, spectacular cases including the Darwin's finches (Geospizinae) and Hawaiian honeycreepers (Drepanidinae), but similar examples are lacking in archipelagos nearer to continental landmasses. Of the required steps in the speciation cycle, achievement of secondary sympatry appears to be limiting in near archipelagos and, by extension, in continental regions. Here, I suggest that secondary sympatry might be prevented by apparent competition mediated through pathogens that are locally coevolved with one population of host and are pathogenic in sister populations. The absence of numerous pathogens in remote archipelagos might, therefore, allow sister populations to achieve secondary sympatry more readily and thereby accelerate diversification. By similar reasoning, species should accumulate relatively slowly within continental regions. In this essay, I explore the assumptions and some implications of this model for species diversification.

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“…First, high energetic and life-history tradeoffs in the ability to fend off disease could lead to a mixed strategy, whereby some individuals might opt for a low-cost but risky strategy of maintaining weak immune defenses while others invest more heavily in defense. There is some evidence that heightened immune function carries a cost for honey bees (Evans and Pettis, 2005), and such costs of an induced response are widely supported in fruit flies (Vijendravarma et al, 2009) and aphids (Gwynn et al, 2005), among other insects. Second, variation across individuals in how well they respond to a specific pathogen strain could reflect a general fact of host-parasite coevolution, namely the unceasing evolutionary arms race between hosts and their parasites and pathogens.…”

Section: Breeding For Resistant or Tolerant Honey Beesmentioning

confidence: 99%