Multitrophic enemy escape of invasive Phragmites australis and its introduced herbivores in North America

© 2015, Springer International Publishing Switzerland. One explanation for why invasive species are successful is that they escape natural enemies from their native range or experience lower attack from natural enemies in the introduced range relative to native species (i.e., the enemy-release hypothesis). However, little is known about how invasive plants interact with co-introduced herbivores or natural enemies of the introduced herbivores. We focus on Phragmites australis, a wetland grass native to Europe (EU) and North America (NA). Within the past 100–150 years, invasive European genotypes of P. australis and several species of specialist Lipara gall flies have spread within NA. On both continents we surveyed P. australis patches for Lipara infestation (proportion of stems infested) and Lipara mortality from natural enemies. Our objectives were to assess evidence for enemy-release in the invaded (NA) versus native (EU) range and whether Lipara infestation or mortality differed between invasive and native P. australis genotypes in NA. Enemy-release varied regionally; Lipara were absent throughout most of NA, supporting enemy-release of Phragmites. However, where Lipara were present, the proportion of invasive P. australis stems infested with Lipara was higher in the introduced (11 %) than native range (\u3c1 \u3e%). This difference may be explained by the absence of Lipara parasitoids in our NA survey, strongly supporting enemy-release of Lipara. In NA, native P. australis genotypes exhibited higher Lipara infestation (32 %) than invasive genotypes (11 %), largely driven by L. rufitarsis. We attribute genotypic differences in infestation to a combination of Lipara exhibiting 34 % greater performance (gall diameter) and suffering four times less vertebrate predation on native than invasive genotypes. Our study suggests that complex interactions can result from the co-introduction of plants and their herbivores, and that a multitrophic perspective is required for investigating how biotic interactions influence invasion success

Doyle_etal_SystBiol_SuppInfo

Doyle_etal_SystBiol_SuppInf

Ancestral polymorphisms explain the role of chromosomal inversions in speciation

<div><p>Understanding the role of chromosomal inversions in speciation is a fundamental problem in evolutionary genetics. Here, we perform a comprehensive reconstruction of the evolutionary histories of the chromosomal inversions in <i>Drosophila persimilis</i> and <i>D</i>. <i>pseudoobscura</i>. We provide a solution to the puzzling origins of the selfish <i>Sex-Ratio</i> arrangement in <i>D</i>. <i>persimilis</i> and uncover surprising patterns of phylogenetic discordance on this chromosome. These patterns show that, contrary to widely held views, all fixed chromosomal inversions between <i>D</i>. <i>persimilis</i> and <i>D</i>. <i>pseudoobscura</i> were already present in their ancestral population long before the species split. Our results suggest that patterns of higher genomic divergence and an association of reproductive isolation genes with chromosomal inversions may be a direct consequence of incomplete lineage sorting of ancestral polymorphisms. These findings force a reconsideration of the role of chromosomal inversions in speciation, not as protectors of existing hybrid incompatibilities, but as fertile grounds for their formation.</p></div

Smooth Muscle Differentiation Is Essential for Airway Size, Tracheal Cartilage Segmentation, but Dispensable for Epithelial Branching

Airway smooth muscle is best known for its role as an airway constrictor in diseases such as asthma. However, its function in lung development is debated. A prevalent model, supported by in&nbsp;vitro data, posits that airway smooth muscle promotes lung branching through peristalsis and pushing intraluminal fluid to branching tips. Here, we test this model in&nbsp;vivo by inactivating Myocardin, which prevented airway smooth muscle differentiation. We found that Myocardin mutants show normal branching, despite the absence of peristalsis. In contrast, tracheal cartilage, vasculature, and neural innervation patterns were all disrupted. Furthermore, airway diameter is reduced in the mutant, counter to the expectation that the absence of smooth muscle constriction would lead to a more relaxed and thereby wider airway. These findings together demonstrate that during development, while airway smooth muscle is dispensable for epithelial branching, it is integral for building the tracheal architecture and promoting airway growth

The distribution of divergence estimated across genomic regions.

<p>Divergence was estimated in 10 kb windows as the Relative Node Depth (RND; <i>d</i>_<i>xy</i> normalized to the outgroup) across the genome. The boxplots show the distribution of RND for each comparison in all collinear regions, and across the <i>XR</i>, <i>XL</i> and <i>2</i>^<i>nd</i> chromosome inversions. The horizontal lines depicted in the three fixed inversions indicate the mean RND estimated in the regions flanking the inversion breakpoints (±250 kb) for <i>D</i>. <i>pseudoobscura</i>-<i>D</i>. <i>persimilis</i> ST (solid) and <i>D</i>. <i>pseudoobscura</i>-<i>D</i>. <i>persimilis</i> SR (dashed).</p

Discordance may be produced by introgression or incomplete lineage sorting of the <i>XR</i> arrangements.

<p>Under model <i>(A)</i>, the <i>D</i>. <i>persimilis ST</i> inversion segregates in the ancestral population of the species. Later divergence between <i>D</i>. <i>persimilis SR</i> and <i>D</i>. <i>pseudoobscura</i> chromosomes and recombination restriction between the two <i>D</i>. <i>persimilis</i> chromosomes leads to phylogenetic discordance at the inversion breakpoints. <i>(B)</i> An introgression model again predicts discordance if the <i>D</i>. <i>persimilis SR</i> chromosome introgressed from <i>D</i>. <i>pseudoobscura</i> after species divergence. Recombination between the introgressed chromosome <i>and D</i>. <i>persimilis ST</i> will gradually homogenize the two chromosomes excluding the inversion breakpoints.</p

Inversions accelerate the formation of hybrid incompatibilities.

<p><i>(A)</i> Polymorphic inversions arise in the ancestor of the two species. <i>(B)</i> Restricted recombination between the inversions leads to accumulating divergence (red, blue) distinct from collinear regions of the genome (grey). <i>(C)</i> Incomplete sorting of the inversions between two isolated populations generates immediate divergence between the two populations. <i>(D)</i> Preexisting divergence increases the chance of hybrid incompatibilities forming in the inverted regions as compared to the collinear regions.</p

Incomplete lineage sorting of the inversions of <i>D</i>. <i>persimilis</i> and <i>D</i>. <i>pseudoobscura</i>.

<p>The fixed inversions on the <i>XL</i> and <i>2nd</i> chromosomes, as well as the polymorphic inversions on <i>XR</i> and the Pikes Peak (<i>3</i>^<i>PP</i>) inversion arose before species divergence. Incomplete lineage sorting produced the observed inversion patterns in the species present today.</p