Jack of all trades versus master of one: how generalist versus specialist strategies of transposable elements relate to their horizontal transfer between lineages.

Transposable elements (TEs) are obligate genomic parasites, relying on host germline cells to ensure their replication and passage to future generations. While some TEs exhibit high fidelity to their host genome, being passed from parent to offspring through vertical transmission for millions of years, others frequently invade new and distantly related hosts through horizontal transfer. In this review, I highlight how the complexity of interactions between TE and host required for transposition may be an important determinant of horizontal transfer: with TEs with more complex regulatory requirements being less able to invade new host genomes.

Protein-Protein Interactions Shape Genomic Autoimmunity in the Adaptively Evolving Rhino-Deadlock-Cutoff Complex.

The Piwi-interacting RNA (piRNA) pathway is a genomic defense system that controls the movement of transposable elements (TEs) through transcriptional and post-transcriptional silencing. Although TE defense is critical to ensuring germline genome integrity, it is equally critical that the piRNA pathway avoids autoimmunity in the form of silencing host genes. Ongoing cycles of selection for expanded control of invading TEs, followed by selection for increased specificity to reduce impacts on host genes, are proposed to explain the frequent signatures of adaptive evolution among piRNA pathway proteins.

Adaptive evolution among cytoplasmic piRNA proteins leads to decreased genomic auto-immunity.

In metazoan germlines, the piRNA pathway acts as a genomic immune system, employing small RNA-mediated silencing to defend host DNA from the harmful effects of transposable elements (TEs). Expression of genomic TEs is proposed to initiate self regulation by increasing the production of repressive piRNAs, thereby "adapting" piRNA-mediated control to the most active TE families. Surprisingly, however, piRNA pathway proteins, which execute piRNA biogenesis and enforce silencing of targeted sequences, evolve rapidly and adaptively in animals.

Taming the Turmoil Within: New Insights on the Containment of Transposable Elements.

Transposable elements (TEs) are mobile genetic parasites that can exponentially increase their genomic abundance through self-propagation. Classic theoretical papers highlighted the importance of two potentially escalating forces that oppose TE spread: regulated transposition and purifying selection. Here, we review new insights into mechanisms of TE regulation and purifying selection, which reveal the remarkable foresight of these theoretical models.

Rapid evolution of piRNA-mediated silencing of an invading transposable element was driven by abundant de novo mutations.

The regulation of transposable element (TE) activity by small RNAs is a ubiquitous feature of germlines. However, despite the obvious benefits to the host in terms of ensuring the production of viable gametes and maintaining the integrity of the genomes they carry, it remains controversial whether TE regulation evolves adaptively. We examined the emergence and evolutionary dynamics of repressor alleles after -elements invaded the genome in the mid-twentieth century.

Uninvited guests: how transposable elements take advantage of Drosophila germline stem cells, and how stem cells fight back.

Transposable elements (TEs) are mobile genetic parasites that spread through host genomes by replicating in germline cells. New TE copies that arise in the genomes of germline stem cells (GSCs) are of particular value, because they are potentially transmitted to multiple offspring through the plethora of gametes arising from the same progenitor GSC. However, the fidelity of GSC genomes is also of utmost importance to the host in ensuring the production of abundant and fit offspring.

QTL mapping of natural variation reveals that the developmental regulator bruno reduces tolerance to P-element transposition in the Drosophila female germline.

Transposable elements (TEs) are obligate genetic parasites that propagate in host genomes by replicating in germline nuclei, thereby ensuring transmission to offspring. This selfish replication not only produces deleterious mutations-in extreme cases, TE mobilization induces genotoxic stress that prohibits the production of viable gametes. Host genomes could reduce these fitness effects in two ways: resistance and tolerance.

The Evolution of Small-RNA-Mediated Silencing of an Invading Transposable Element.

Transposable elements (TEs) are genomic parasites that impose fitness costs on their hosts by producing deleterious mutations and disrupting gametogenesis. Host genomes avoid these costs by regulating TE activity, particularly in germline cells where new insertions are heritable and TEs are exceptionally active. However, the capacity of different TE-associated fitness costs to select for repression in the host, and the role of selection in the evolution of TE regulation more generally remain controversial.

p53 is required for female germline stem cell maintenance in P-element hybrid dysgenesis.

Hybrid dysgenesis is a sterility syndrome resulting from the mobilization of certain transposable elements in the Drosophila germline. Particularly extreme is the hybrid dysgenesis syndrome caused by P-element DNA transposons, in which dysgenic female ovaries often contain few or no germline cells. Those offspring that are produced from dysgenic germlines exhibit high rates of de novo mutation and recombination, implicating transposition-associated DNA damage as the cause of germline loss.

Retrotransposons: Stowaways in the Primordial Germline.

In order to succeed, retrotransposon transcripts must identify the subset of nuclei that will be transmitted to offspring. A new study reveals that the primordial germline is a hideout for retrotransposon transcripts, providing early access to future gametes.

Targeted identification of TE insertions in a genome through hemi-specific PCR.

Background: Transposable elements (TEs) are major components of eukaryotic genomes and drivers of genome evolution, producing intraspecific polymorphism and interspecific differences through mobilization and non-homologous recombination. TE insertion sites are often highly variable within species, creating a need for targeted genome re-sequencing (TGS) methods to identify TE insertion sites.

Methods: We present a hemi-specific PCR approach for TGS of -elements in genomes on the Illumina platform.

Paternal Induction of Hybrid Dysgenesis in Is Weakly Correlated with Both -Element and Element Dosage.

Transposable elements (TEs) are virtually ubiquitous components of genomes, yet they often impose significant fitness consequences on their hosts. In addition to producing specific deleterious mutations by insertional inactivation, TEs also impose general fitness costs by inducing DNA damage and participating in ectopic recombination. These latter fitness costs are often assumed to be dosage-dependent, with stronger effects occurring in the presence of higher TE copy numbers.

Reexamining the P-Element Invasion of Drosophila melanogaster Through the Lens of piRNA Silencing.

Transposable elements (TEs) are both important drivers of genome evolution and genetic parasites with potentially dramatic consequences for host fitness. The recent explosion of research on regulatory RNAs reveals that small RNA-mediated silencing is a conserved genetic mechanism through which hosts repress TE activity. The invasion of the Drosophila melanogaster genome by P elements, which happened on a historical timescale, represents an incomparable opportunity to understand how small RNA-mediated silencing of TEs evolves.

Analysis of piRNA-mediated silencing of active TEs in Drosophila melanogaster suggests limits on the evolution of host genome defense.

The Piwi-interacting RNA (piRNA) pathway defends animal genomes against the harmful consequences of transposable element (TE) infection by imposing small-RNA-mediated silencing. Because silencing is targeted by TE-derived piRNAs, piRNA production is posited to be central to the evolution of genome defense. We harnessed genomic data sets from Drosophila melanogaster, including genome-wide measures of piRNA, mRNA, and genomic abundance, along with estimates of age structure and risk of ectopic recombination, to address fundamental questions about the functional and evolutionary relationships between TE families and their regulatory piRNAs.

Drosophila interspecific hybrids phenocopy piRNA-pathway mutants.

The Piwi-interacting RNA (piRNA) pathway defends the germline of animals from the deleterious activity of selfish transposable elements (TEs) through small-RNA mediated silencing. Adaptation to novel invasive TEs is proposed to occur by incorporating their sequences into the piRNA pool that females produce and deposit into their eggs, which then propagates immunity against specific TEs to future generations. In support of this model, the F1 offspring of crosses between strains of the same Drosophila species sometimes suffer from germline derepression of paternally inherited TE families, caused by a failure of the maternal strain to produce the piRNAs necessary for their regulation.

Postmating transcriptional changes in reproductive tracts of con- and heterospecifically mated Drosophila mojavensis females.

In internally fertilizing organisms, mating involves a series of highly coordinated molecular interactions between the sexes that occur within the female reproductive tract. In species where females mate multiply, traits involved in postcopulatory interactions are expected to evolve rapidly, potentially leading to postmating-prezygotic (PMPZ) reproductive isolation between diverging populations. Here, we investigate the postmating transcriptional response of the lower reproductive tract of Drosophila mojavensis females following copulation with either conspecific or heterospecific (Drosophila arizonae) males at three time points postmating.

Diversity-enhancing selection acts on a female reproductive protease family in four subspecies of Drosophila mojavensis.

Protein components of the Drosophila male ejaculate are critical modulators of reproductive success, several of which are known to evolve rapidly. Recent evidence of adaptive evolution in female reproductive tract proteins suggests this pattern may reflect sexual selection at the molecular level. Here we explore the evolutionary dynamics of a five-paralog gene family of female reproductive proteases within geographically isolated subspecies of Drosophila mojavensis.

Protease gene duplication and proteolytic activity in Drosophila female reproductive tracts.

Secreted proteases play integral roles in sexual reproduction in a broad range of taxa. In the genetic model Drosophila melanogaster, these molecules are thought to process peptides and activate enzymes inside female reproductive tracts, mediating critical postmating responses. A recent study of female reproductive tract proteins in the cactophilic fruit fly Drosophila arizonae, identified pervasive, lineage-specific gene duplication amongst secreted proteases.

Proteomic analysis of Drosophila mojavensis male accessory glands suggests novel classes of seminal fluid proteins.

Fruit-flies of the genus Drosophila are characterized by overwhelming variation in fertilization traits such as copulatory plug formation, sperm storage organ use, and nutritional ejaculatory donation. Despite extensive research on the genetic model Drosophila melanogaster, little is known about the molecular underpinnings of these interspecific differences. This study employs a proteomic approach to pin-point candidate seminal fluid proteins in Drosophila mojavensis, a cactophilic fruit-fly that exhibits divergent reproductive biology when compared to D.

Duplication, selection and gene conversion in a Drosophila mojavensis female reproductive protein family.

Protein components of the Drosophila male ejaculate, several of which evolve rapidly, are critical modulators of reproductive success. Recent studies of female reproductive tract proteins indicate they also are extremely divergent between species, suggesting that reproductive molecules may coevolve between the sexes. Our current understanding of intersexual coevolution, however, is severely limited by the paucity of genetic and evolutionary studies on the female molecules involved.

Reproductive tract interactions contribute to isolation in Drosophila.

The process of speciation requires the development of isolating mechanisms that act as barriers to gene flow between incipient species. Such mechanisms can occur at three different levels: precopulatory or behavioral isolation, postcopulatory-prezygotic isolation occurring in the female reproductive tract, or postzygotic isolation resulting in hybrid sterility or inviability. Only by extensively studying all three types of barriers in young species pairs can we begin to understand the evolution of early reproductive incompatibilities, which may be important to the speciation process.

Gene duplication and adaptive evolution of digestive proteases in Drosophila arizonae female reproductive tracts.

It frequently has been postulated that intersexual coevolution between the male ejaculate and the female reproductive tract is a driving force in the rapid evolution of reproductive proteins. The dearth of research on female tracts, however, presents a major obstacle to empirical tests of this hypothesis. Here, we employ a comparative EST approach to identify 241 candidate female reproductive proteins in Drosophila arizonae, a repleta group species in which physiological ejaculate-female coevolution has been documented.

Sperm fate and function in reproductive isolation in Drosophila.

Central to the study of speciation is the identification of the isolating mechanisms that reduce gene flow. Of special interest are those isolating mechanisms that are the earliest to arise. Sperm fate and function play a major role in two distinct types of reproductive isolation in the genus Drosophila.