Fundamental Niche Narrows through Larval Stages of a Filter-Feeding Marine Invertebrate.

AbstractOntogenetic niche theory predicts that resource use should change across complex life histories. To date, studies of ontogenetic shifts in food niches have mainly focused on a few systems (e.g., fish), with less attention on organisms with filter-feeding larval stages (e.g., marine invertebrates). Recent studies suggest that filter-feeding organisms can select specific particles, but our understanding of whether niche theory applies to this group is limited. We characterized the fundamental niche (i.e., feeding proficiency) by examining how niche breadth changes across the larval stages of the filter-feeding marine polychaete Galeolaria caespitosa. Using a no-choice experimental design, we measured feeding rates of trochophore, intermediate-stage, and metatrochophore larvae on the prey phytoplankton species Nannochloropsis oculata, Tisochrysis lutea, Dunaliella tertiolecta, and Rhodomonas salina, which vary 10-fold in size, from the smallest to the largest. We formally estimated Levins's niche breadth index to determine the relative proportions of each species in the diet of the three larval stages and also tested how feeding rates vary with algal species and stage. We found that early stages eat all four algal species in roughly equal proportions, but niche breadth narrows during ontogeny, such that metatrochophores are feeding specialists relative to early stages. We also found that feeding rates differed across phytoplankton species: the medium-sized cells (Tisochrysis and Dunaliella) were eaten most, and the smallest species (Nannochloropsis) was eaten the least. Our results demonstrate that ontogenetic niche theory describes changes in fundamental niche in filter feeders. An important next step is to test whether the realized niche (i.e., preference) changes during the larval phase as well.

Mapping the correlations and gaps in studies of complex life histories.

For species with complex life histories, phenotypic correlations between life-history stages constrain both ecological and evolutionary trajectories. Studies that seek to understand correlations across the life history differ greatly in their experimental approach: some follow individuals ("individual longitudinal"), while others follow cohorts ("cohort longitudinal"). Cohort longitudinal studies risk confounding results through Simpson's Paradox, where correlations observed at the cohort level do not match that of the individual level. Individual longitudinal studies are laborious in comparison, but provide a more reliable test of correlations across life-history stages. Our understanding of the prevalence, strength, and direction of phenotypic correlations depends on the approaches that we use, but the relative representation of different approaches remains unknown. Using marine invertebrates as a model group, we used a formal, systematic literature map to screen 17,000+ papers studying complex life histories, and characterized the study type (i.e., cohort longitudinal, individual longitudinal, or single stage), as well as other factors. For 3315 experiments from 1716 articles, 67% focused on a single stage, 31% were cohort longitudinal and just 1.7% used an individual longitudinal approach. While life-history stages have been studied extensively, we suggest that the field prioritize individual longitudinal studies to understand the phenotypic correlations among stages.

Effects of embryo energy, egg size, and larval food supply on the development of asteroid echinoderms.

Organisms have limited resources available to invest in reproduction, causing a trade-off between the number and size of offspring. One consequence of this trade-off is the evolution of disparate egg sizes and, by extension, developmental modes. In particular, echinoid echinoderms (sea urchins and sand dollars) have been widely used to experimentally manipulate how changes in egg size affect development. Here, we test the generality of the echinoid results by (a) using laser ablations of blastomeres to experimentally reduce embryo energy in the asteroid echinoderms (sea stars), Pisaster ochraceus and Asterias forbesi and (b) comparing naturally produced, variably sized eggs (1.7-fold volume difference between large and small eggs) in A. forbesi. In P. ochraceus and A. forbesi, there were no significant differences between juveniles from both experimentally reduced embryos and naturally produced eggs of variable size. However, in both embryo reduction and egg size variation experiments, simultaneous reductions in larval food had a significant and large effect on larval and juvenile development. These results indicate that (a) food levels are more important than embryo energy or egg size in determining larval and juvenile quality in sea stars and (b) the relative importance of embryo energy or egg size to fundamental life history parameters (time to and size at metamorphosis) does not appear to be consistent within echinoderms.

EML4-ALK V3 oncogenic fusion proteins promote microtubule stabilization and accelerated migration through NEK9 and NEK7.

EML4-ALK is an oncogenic fusion present in ∼5% of non-small cell lung cancers. However, alternative breakpoints in the EML4 gene lead to distinct variants of EML4-ALK with different patient outcomes. Here, we show that, in cell models, EML4-ALK variant 3 (V3), which is linked to accelerated metastatic spread, causes microtubule stabilization, formation of extended cytoplasmic protrusions and increased cell migration. EML4-ALK V3 also recruits the NEK9 and NEK7 kinases to microtubules via the N-terminal EML4 microtubule-binding region. Overexpression of wild-type EML4, as well as constitutive activation of NEK9, also perturbs cell morphology and accelerates migration in a microtubule-dependent manner that requires the downstream kinase NEK7 but does not require ALK activity. Strikingly, elevated NEK9 expression is associated with reduced progression-free survival in EML4-ALK patients. Hence, we propose that EML4-ALK V3 promotes microtubule stabilization through NEK9 and NEK7, leading to increased cell migration. This represents a novel actionable pathway that could drive metastatic disease progression in EML4-ALK lung cancer.