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Adaptation to novel ecological niches is known to be rapid. However, how ecological divergence translates into reproductive isolation remains a consequential question in speciation research. It is still unclear how coupling of ecological divergence loci and reproductive isolation loci occurs at the genomic level, ultimately enabling the formation of persistent species. Here, we investigate the genomic underpinning colonization of a new niche and formation of two host races inTephritis conurapeacock flies that persist in sympatry. To uncover the genomic differences underlying host plant adaptation, we take advantage of two independent sympatric zones, where host plant specialists using the thistle speciesCirsium heterophyllumandC. oleraceumco-occur, and address what regions of the genome that diverge between the host races in a parallel fashion. Using Population Branch Statistics, dxy and BayPass we identify 2996 and 3107 outlier regions associated with host use among western and eastern Baltic populations, respectively, with 82% overlap. The majority of outliers are located within putative inversions, adding to the growing body of evidence that structural changes to the genome are important for adaptations to persist in face of gene flow. Potentially, the high contents of repetitive elements could have given rise to the inversions, but this remains to be tested. The outlier regions were enriched for genes involved in e.g. metabolism and morphogenesis, potentially due to the selection for processing different metabolites, and changes in size and ovipositor length respectively. In conclusion, this study suggests that structural changes in the genome, and divergence in independent ecological functions may facilitate the formation of persistent host races in face of gene flow.

Dendrite morphogenesis is essential for neural circuit formation, yet the molecular mechanisms underlying complex dendrite branching remain elusive. Previous studies on the highly branchedC. elegansPVD sensory neuron identified a membrane co-receptor complex that links extracellular signals to intracellular actin remodeling machinery, promoting high-order dendrite branching. In this complex, the claudin-like transmembrane protein HPO-30 recruits the WAVE regulatory complex (WRC) to dendrite branching sites, stimulating the Arp2/3 complex to polymerize actin. We report here our biochemical and structural analysis of this interaction, revealing that the intracellular domain (ICD) of HPO-30 is intrinsically disordered and employs two distinct mechanisms to regulate the actin cytoskeleton. First, HPO-30 ICD binding to the WRC requires dimerization and involves the entire ICD sequence, rather than a short linear peptide motif. This interaction enhances WRC activation by the GTPase Rac1. Second, HPO-30 ICD directly binds to the sides and barbed end of actin filaments. Binding to the barbed end requires ICD dimerization and inhibits both actin polymerization and depolymerization, resembling the actin capping protein CapZ. These dual functions provide an intriguing model of how membrane proteins can integrate distinct mechanisms to fine-tune local actin dynamics.

The actin filament nucleator Arp2/3 complex is activated at cortical sites inS. pombeto assemble branched actin networks that drive endocytosis. Arp2/3 complex activators Wsp1 and Dip1 are required for proper actin assembly at endocytic sites, but how they coordinately control Arp2/3-mediated actin assembly is unknown. Alone, Dip1 activates Arp2/3 complex without preexisting actin filaments to nucleate “seed” filaments that activate Wsp1-bound Arp2/3 complex, thereby initiating branched actin network assembly. In contrast, because Wsp1 requires pre-existing filaments to activate, it has been assumed to function exclusively in propagating actin networks by stimulating branching from pre-existing filaments. Here we show that Wsp1 is important not only for propagation, but also for initiation of endocytic actin networks. Using single molecule TIRF microscopy we show that Wsp1 synergizes with Dip1 to co-activate Arp2/3 complex. Synergistic coactivation does not require pre-existing actin filaments, explaining how Wsp1 contributes to actin network initiation in cells.

Species richness varies considerably among the tree of life which can only be explained by heterogeneous rates of diversification (speciation and extinction). Previous approaches use phylogenetic trees to estimate branch-specific diversification rates. However, all previous approaches disregard diversification-rate shifts on extinct lineages although 99% of species that ever existed are now extinct. Here we describe a lineage-specific birth-death-shift process where lineages, both extant and extinct, may have heterogeneous rates of diversification. To facilitate probability computation we discretize the base distribution on speciation and extinction rates intokrate categories. The fixed number of rate categories allows us to extend the theory of state-dependent speciation and extinction models (e.g.,BiSSE and MuSSE) to compute the probability of an observed phylogeny given the set of speciation and extinction rates. To estimate branch-specific diversification rates, we develop two independent and theoretically equivalent approaches: numerical integration with stochastic character mapping and data-augmentation with reversible-jump Markov chain Monte Carlo sampling. We validate the implementation of the two approaches in RevBayes using simulated data and an empirical example study of primates. In the empirical example, we show that estimates of the number of diversification-rate shifts are, unsurprisingly, very sensitive to the choice of prior distribution. Instead, branch-specific diversification rate estimates are less sensitive to the assumed prior distribution on the number of diversification-rate shifts and consistently infer an increased rate of diversification for Old World Monkeys. Additionally, we observe that as few as 10 diversification-rate categories are sufficient to approximate a continuous base distribution on diversification rates. In conclusion, our implementation of the lineage-specific birth-death-shift model in RevBayes provides biologists with a method to estimate branch-specific diversification rates under a mathematically consistent model.