Can spatial sorting associated with spawning migration explain evolution of body size and vertebral number in Anguilla eels?

Spatial sorting is a process that can contribute to microevolutionary change by assembling phenotypes through space, owing to nonrandom dispersal. Here we first build upon and develop the “neutral” version of the spatial sorting hypothesis by arguing that in systems that are not characterized by repeated range expansions, the evolutionary effects of variation in dispersal capacity and assortative mating might not be independent of but interact with natural selection. In addition to generating assortative mating, variation in dispersal capacity together with spatial and temporal variation in quality of spawning area is likely to influence both reproductive success and survival of spawning migrating individuals, and this will contribute to the evolution of dispersal‐enhancing traits. Next, we use a comparative approach to examine whether differences in spawning migration distance among 18 species of freshwater Anguilla eels have evolved in tandem with two dispersal‐favoring traits. In our analyses, we use information on spawning migration distance, body length, and vertebral number that was obtained from the literature, and a published whole mitochondrial DNA‐based phylogeny. Results from comparative analysis of independent contrasts showed that macroevolutionary shifts in body length throughout the phylogeny have been associated with concomitant shifts in spawning migration. Shifts in migration distance were not associated with shifts in number of vertebrae. These findings are consistent with the hypothesis that spatial sorting has contributed to the evolution of more elongated bodies in species with longer spawning migration distances, or resulted in evolution of longer migration distances in species with larger body size. This novel demonstration is important in that it expands the list of ecological settings and hierarchical levels of biological organization for which the spatial sorting hypothesis seems to have predictive power.     

Habitat deterioration promotes the evolution of direct development in metamorphosing species

Although metamorphosis is widespread in the animal kingdom, several species have evolved life-cycle modifications to avoid complete metamorphosis. Some species, for example, many salamanders and newts, have deleted the adult stage via a process called paedomorphosis. Others, for example, some frog species and marine invertebrates, no longer have a distinct larval stage and reach maturation via direct development. Here we study which ecological conditions can lead to the loss of metamorphosis via the evolution of direct development. To do so, we use size-structured consumer-resource models in conjunction with the adaptive-dynamics approach. In case the larval habitat deteriorates, individuals will produce larger offspring and in concert accelerate metamorphosis. Although this leads to the evolutionary transition from metamorphosis to direct development when the adult habitat is highly favorable, the population will go extinct in case the adult habitat does not provide sufficient food to escape metamorphosis. With a phylogenetic approach we furthermore show that among amphibians the transition of metamorphosis to direct development is indeed, in line with model predictions, conditional on and preceded by the evolution of larger egg sizes.     

Genome-wide CRISPR Screens Reveal Host Factors Critical for SARS-CoV-2 Infection

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Phosphoproteome Profiling of the Receptor Tyrosine Kinase MuSK Identifies Tyrosine Phosphorylation of Rab GTPases

Muscle-specific receptor tyrosine kinase (MuSK) agonist antibodies were developed 2 decades ago to explore the benefits of receptor activation at the neuromuscular junction. Unlike agrin, the endogenous agonist of MuSK, agonist antibodies function independently of its coreceptor low-density lipoprotein receptor–related protein 4 to delay the onset of muscle denervation in mouse models of ALS. Here, we performed dose–response and time-course experiments on myotubes to systematically compare site-specific phosphorylation downstream of each agonist. Remarkably, both agonists elicited similar intracellular responses at known and newly identified MuSK signaling components. Among these was inducible tyrosine phosphorylation of multiple Rab GTPases that was blocked by MuSK inhibition. Importantly, mutation of this site in Rab10 disrupts association with its effector proteins, molecule interacting with CasL 1/3. Together, these data provide in-depth characterization of MuSK signaling, describe two novel MuSK inhibitors, and expose phosphorylation of Rab GTPases downstream of receptor tyrosine kinase activation in myotubes.