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Title: Hybrid Dysgenesis in Drosophila simulans Associated with a Rapid Invasion of the P-Element}
Article:
Abstract:
In a classic example of the invasion of a species by a selfish genetic element, the P-element was horizontally transferred from a distantly related species into Drosophila melanogaster. Despite causing ‘hybrid dysgenesis’, a syndrome of abnormal phenotypes that include sterility, the P-element spread globally in the course of a few decades in D. melanogaster. Until recently, its sister species, including D. simulans, remained P-element free. Here, we find a hybrid dysgenesis-like phenotype in the offspring of crosses between D. simulans strains collected in different years; a survey of 181 strains shows that around 20% of strains induce hybrid dysgenesis. Using genomic and transcriptomic data, we show that this dysgenesis-inducing phenotype is associated with the invasion of the P-element. To characterize this invasion temporally and geographically, we survey 631 D. simulans strains collected on three continents and over 27 years for the presence of the P-element. We find that the D. simulans P-element invasion occurred rapidly and nearly simultaneously in the regions surveyed, with strains containing P-elements being rare in 2006 and common by 2014. Importantly, as evidenced by their resistance to the hybrid dysgenesis phenotype, strains collected from the latter phase of this invasion have adapted to suppress the worst effects of the P-element.
Introduction:
Discovered in the 1950’s by Barbara McClintock[1], transposable elements( TEs) are the ‘ultimate parasite’[2, 3]. They are genetically simple, with autonomous elements consisting of as little as one protein coding gene, but remarkably successful, comprising much of the bulk of large eukaryotic genomes[4, 5]. Those that persist do so by inserting copies of themselves into new genomic locations faster than they are eliminated. TEs can also be a source of beneficial mutations; particular TE insertions have been implicated in a number of adaptive phenotypes( reviewed in[6]), and some TE families now form essential components of genomes[7, 8]. But most TE insertions are probably deleterious, as insertions can damage genes and may impose other fitness costs on their host[9–11]. In fact, the mutagenic properties of transposons have been harnessed by molecular geneticists to disrupt thousands of Drosophila genes( e. g.,[12]). In the short-term, transposable elements are vertically transmitted, and so can only cause limited damage to their hosts without extinguishing themselves. In the long-term, however, they are also horizontally transmitted[13–15], and, initially, may cause substantial damage to their hosts[16, 17]. The best-studied example of a horizontally transferred element is that of the P-element, a DNA transposon. P-element was acquired by D. melanogaster by horizontal transfer from a distant relative, D. willistoni[18], and spread rapidly through the species, as evidenced by its absence from old laboratory stocks collected before the P-element was widespread[19–21]. In its native species, and in current D. melanogaster populations, the P-element is not associated with any gross defects[18, 22]. But when males from strains collected after the invasion( ‘P strains’) are crossed to females from old laboratory stocks( ‘M strains’), the F1 offspring suffer a number of abnormalities, including recombination in males, increased mutation rates, frequent sterility, and abnormally small( dysgenic) gonads[16, 19, 23–25]. These abnormalities, collectively called ‘hybrid dysgenesis’, appear to be due to DNA damage caused by actively transposing P-element in the germline[17, 22, 26, 27]. In the reciprocal direction, the F1 offspring, though genetically identical, are normal. The reason is that these offspring are protected by piRNAs( PIWI interacting RNAs, a type of small RNA) homologous to the P-element, which are sequestered in the egg cytoplasm of P-type females. As these protective piRNAs target the P-element mRNA for degradation[28], their presence reduces P-element activity and the resulting DNA damage that lead to hybrid dysgenesis. Since its initial discovery, P-element has been one of the most important tools in Drosophila genetics, providing the basis for genetic manipulations and mutagenesis( e. g.,[12, 29]). The P-element had been thought to be absent from D. melanogaster’s close relatives[30], but recent work has detected it in D. simulans, apparently horizontally acquired from D. melanogaster[31]. As the D. simulans elements recovered are identical in sequence to a type that segregates at low frequency in D. melanogaster, and do not include the most common D. melanogaster element, this acquisition is likely due to a single transfer event[31]. Here, we report a hybrid dysgenesis-like phenotype in crosses between strains from different D. simulans populations, and show this phenotype occurs in crosses between strains collected before and after a rapid invasion of the P-element.
Discussion:
Here, we identified a hybrid dysgenesis-like system in D. simulans. Using next generation sequencing information and PCR, we find that the P-element, which has recently invaded D. simulans[31], is associated with the hybrid dysgenesis phenotype, and spread rapidly across Europe, Africa, and North America. In fact, compared to D. melanogaster, the spread of the P-element in D. simulans is surprisingly fast: In D. melanogaster, the first P-type fly was collected from the wild in 1954, and most wild strains were infected by 1974[20]. We find the first evidence of the P-element in D. simulans samples from 2006, with P-elements appearing in nearly all lines sampled since 2013, seven years later( apart from one sample from Ethiopia; Fig 3, Fig 4, S1 Table). There are a number of reasons the P-element invasion may have occurred more rapidly in D. simulans than in D. melanogaster. For one, D. simulans appears to enjoy lower rates of P-element induced gonadal dysgenesis than D. melanogaster; high rates of sterility are expected to hamper the spread of the P-element by reducing the fitness of its carriers. Direct comparisons between the species are problematic, as the severity of hybrid dysgenesis increases with copy number, which differs between the species([19, 24, 26, 31]; S2, S4 and S6 Figs). But in comparisons between artificially constructed D. melanogaster and D. simulans strains with comparable copy numbers, P-element does appear to be less active in D. simulans[32, 45, 55]. Another, simpler explanation for the difference in the speed of invasion is higher migration rates between D. simulans populations than for D. melanogaster as they experienced the P-element invasion. Such a scenario seems reasonable: Unlike D. melanogaster, D. simulans cannot over-winter in temperate regions, and instead reinvades the northern limits of its range annually. Sequence data correspondingly suggests a high rate of homogenization between D. simulans populations at nuclear loci[56–61]. Furthermore, for both species, migration might be largely human-aided, and the global movement of fruit has increased dramatically in the years since the spread of the P-element in D. melanogaster. That is, global imports and exports of fleshy fruits( measured in tons) grew about 4% per year from 1961–2013( the years tracked by the Food and Agriculture Organization of the United Nations Statistics Division). As a result, the average tonnage of fruit imports was 5-fold higher in the years measured during the spread of the P-element in D. simulans compared to D. melanogaster( for imports, 1961–1974: 12. 5 vs. 2006–2014: 61. 5 million tons/year; exports tracked imports closely). While these statistics capture only the movement of fruit between countries, the increase in movement seems likely to have boosted the global spread of the P-element in later years. The P-element in D. simulans adds to a handful of documented cases of the spread of a horizontally transmitted element through a Drosophila species[33, 62–65]. Several of the other cases include intracellular bacteria, which are capable of behaving selfishly, but in these cases also appear to be conferring a benefit to their hosts[64–67]. In contrast, the P-element appears to be spreading mainly via a selfish mechanism; though the occasional insertion may be beneficial[22, 68]. In response, both D. simulans and D. melanogaster have quickly evolved to suppress the dysgenesis phenotype by the end of the invasion( present study,[20, 38]), suggesting strong selection to ameliorate the the P-element’s worst effects, and underscoring the evolutionary challenge posed by selfish elements.
Some genes perform necessary organismal functions , others hijack the cellular machinery to replicate themselves , potentially harming the host in the process . These ‘selfish genes’ can spread through genomes and species; as a result , eukaryotic genomes are typically saddled with large amounts of parasitic DNA . Here , we chronicle the surprisingly rapid global spread of a selfish transposable element through a close relative of the genetic model , Drosophila melanogaster . We see that , as it spreads , the transposable element is associated with damaging effects , including sterility , but that the flies quickly adapt to the negative consequences of the transposable element .