LIFE HISTORY SWITCH POINT PLASTICY IN RESPONSE TO POND DRYING ALYERS METAMORPH ALLOMETRY AND JUMPING PERFORMANCE

Animals with complex life cycles can cope with environmental uncertainty by altering life history switch points through developmental plasticity. Pond drying is an important factor which may alter life history switch points in aquatic organisms. Many amphibians can plastically respond to changes in pond drying by emerging earlier, but few studies have examined the post-metamorphic consequences for performance. To investigate the potential carry-over effects of plasticity to pond drying, we studied the túngara frog, Physalaemus pustulosus, a tropical anuran that breeds in highly ephemeral habitats. We conducted a field study with three different water depth treatments in 60 L mesocosms and measured time and size at metamorphosis, hind limb length and jumping performance. We also conducted a complimentary laboratory study that manipulated resources and water depth. In the field experiment, metamorphs from dry-down treatments emerged earlier, but at a similar size to constant volume treatments. In the laboratory experiment, metamorphs from the low depth and dry-down treatments emerged both earlier and smaller. In both studies, frogs from dry-down treatments had relatively shorter hind limbs, which negatively impacted their jumping performance. Reductions in resources delayed and reduced size at metamorphosis, but had no effect on jumping performance. We demonstrate that conditions experienced early in ontogeny can transcend the metamorphic boundary by erasing the relationship between hind limb length and jumping performance

Tadpole density changes the relationship of red-eyed treefrog morphology and jumping performance [poster]

As organisms develop, increased body size is often accompanied by shape changes that alter the morphology–performance relationship. Animals with different growth histories may also have different shapes at similar body sizes. To investigate how larval growth history affects the morphology–performance relationship, we raised red-eyed treefrog tadpoles (Agalychnis callidryas) at three densities (5, 25 and 50 tadpoles per 400 L tank) and measured jump distance during metamorphosis. We predicted that tadpoles grown at low density would metamorphose into larger frogs with relatively longer legs than those grown at higher densities. We also expected low density frogs to jump further – both absolutely, because of their larger body size and relative to their size if they had longer legs. Frogs from low density had longer snout-vent lengths (SVL) than those from medium and high densities and longer tibiafibula lengths and greater masses relative to their SVL. Jump distance was strongly correlated with tibiafibula length; however, there was a significant density*tibiafibula interaction. While longer tibiafibulas in high and medium density frogs were correlated with longer jump distances, there was no such correlation in the frogs from low density tanks. We interpret these results as a consequence of the greater relative mass of the frogs from low density tanks. The relatively long legs of these frogs may not fully compensate for their disproportionately higher mass. This study demonstrates that different larval densities can change not only red-eyed treefrog morphology, but also the morphology–performance relationship. It suggests a trade-off where low larval density can increase body size and presumably fat reserves, but the latter may decrease jumping performance

Consequences of life history switch point plasticity for juvenile morphology and locomotion in the Túngara frog

Many animals with complex life cycles can cope with environmental uncertainty by altering the timing of life history switch points through plasticity. Pond hydroperiod has important consequences for the fitness of aquatic organisms and many taxa alter the timing of life history switch points in response to habitat desiccation. For example, larval amphibians can metamorphose early to escape drying ponds. Such plasticity may induce variation in size and morphology of juveniles which can result in carry-over effects on jumping performance. To investigate the carry-over effects of metamorphic plasticity to pond drying, we studied the Túngara frog,Physalaemus pustulosus, a tropical anuran that breeds in highly ephemeral habitats. We conducted an outdoor field mesocosm experiment in which we manipulated water depth and desiccation and measured time and size at metamorphosis, tibiofibula length and jumping performance. We also conducted a complimentary laboratory experiment in which we manipulated resources, water depth and desiccation. In the field experiment, metamorphs from dry-down treatments emerged earlier, but at a similar size to metamorphs from constant depth treatments. In the laboratory experiment, metamorphs from the low depth and dry-down treatments emerged earlier and smaller. In both experiments, frogs from dry-down treatments had relatively shorter legs, which negatively impacted their absolute jumping performance. In contrast, reductions in resources delayed and reduced size at metamorphosis, but had no negative effect on jumping performance. To place these results in a broader context, we review past studies on carry-over effects of the larval environment on jumping performance. Reductions in mass and limb length generally resulted in lower jumping performance across juvenile anurans tested to date. Understanding the consequences of plasticity on size, morphology and performance can elucidate the linkages between life stages

Persistence of carry-over effects in the spotted salamander.

Most organisms have complex life cycles. Early conditions can constrain phenotype and influence growth and survival later in life. Linkages between life stages are important for conservation and management

Cross-Life Stage Effects of Aquatic Larval Density and Terrestrial Moisture on Growth and Corticosterone in the Spotted Salamander

For organisms with complex life cycles, conditions experienced during early life stages may constrain later growth and survival. Conversely, compensatory mechanisms may attenuate negative effects from early life stages. We used the spotted salamander, Ambystoma maculatum, to test how aquatic larval density and terrestrial moisture influence juvenile growth, food intake, evaporative water loss and water reuptake rates, and corticosterone levels. We conducted an outdoor mesocosm experiment to manipulate larval density and transferred metamorphosed salamanders into low and high terrestrial moisture treatments in laboratory terrariums. After the larval stage, high-density salamanders were significantly smaller and had higher corticosterone release rates than those from low-density treatments. Salamanders in the low terrestrial moisture treatment consumed fewer roaches, had lower mass-specific growth rates, higher water reuptake, and higher corticosterone release rates than salamanders in high terrestrial moisture treatments. Across moisture treatments, smaller salamanders had higher mass-specific growth rates than larger salamanders. Our results suggest that salamanders can partially compensate for competition in the larval aquatic habitat with increased growth as juveniles, but this response is dependent on terrestrial habitat quality. Thus, the persistence of early life stage effects can be an important, yet context-dependent, component of amphibian life cycles

A collaborative analysis of land use and frog diversity across spatial scales

Amphibians are sensitive to changes in land use because they require both upland terrestrial habitat and aquatic wetland habitat to complete their life cycle. Our previous work demonstrates that land-use change including road density, development, and wetland area impact amphibian diversity. We build upon this previous work to examine the relative influences of these factors across different landscape scales. Incorporating scale within our model allows us to explore by which mechanism different factors impact amphibians (e.g. do roads increase roadkill in the immediate surrounding area or do they isolate populations at the larger scale?). North American amphibian monitoring program (NAAMP) compiles data from standardized roadside surveys of calling frogs and toads across the majority of the contiguous United States to examine the impacts of human activity on amphibian populations over time. In this study we used NAAMP call data from 18 eastern U.S. states and National Land Cover Data to address the following research questions 1) How is the impact of road length and landscape change mediated by distance from the habitat and 2) how do species differ in the relative influence of these effects over the landscape? We quantified landscape features (e.g., habitat types, wetland –forest connectivity, road density and arrangement) using a GIS program and calculated amphibian diversity estimates of each survey at six locations ranging from 300 meters (local scale, the core terrestrial habitat) to 10, 000 meters (associations should decline at this distance). This approached allows us to explore the relative influence of factors at the regional level to build a predictive model to answer our research questions. This project is supported by the National Science Foundation, Transforming Undergraduate Education in Science program coordinated by David Marsh and the National Center for Ecological Analysis and Synthesis.https://scholarscompass.vcu.edu/uresposters/1105/thumbnail.jp

Regional and scale-specific effects of land use on amphibian diversity [poster]

Background/Question/Methods Habitat loss and degradation influence amphibian distributions and are important drivers of population declines. Our previous research demonstrated that road disturbance, development and wetland area consistently influence amphibian richness across regions of the U.S. Here, we examined the relative importance of these factors in different regions and at multiple spatial scales. Understanding the scales at which habitat disturbance may be affecting amphibian distributions is important for conservation planning. Specifically, we asked: 1) Over what spatial scales do distinct landscape features affect amphibian richness? and 2) Do road types (non-rural and rural) have similar effects on amphibian richness? This is the second year of a collaborative, nationwide project involving 11 U.S. colleges integrated within undergraduate biology curricula. We summarized North American Amphibian Monitoring Program data in 13 Eastern and Central U.S states and used geographic information systems to extract landscape data for 471 survey locations. We developed models to quantify the influence of landscape variables on amphibian species richness and site occupancy across five concentric buffers ranging from 300m to 10,000m. Results/Conclusions Across spatial scales, development, road density and agriculture were the best predictors of amphibian richness and site occupancy by individual species. Across regions, we found that scale did not exert a large influence on how landscape features influenced amphibian richness as effects were largely comparable across buffers. However, development and percent impervious surface had stronger influence on richness at smaller spatial scales. Richness was lower at survey locations with higher densities of non-rural and rural roads, and non-rural road density had a larger negative effect at smaller scales. Within regions, landscape features driving patterns of species richness varied. The scales at which these factors were associated with richness were highly variable within regions, suggesting the scale effects may be region specific. Our project demonstrates that networks of undergraduate students can collaborate to compile and analyze large ecological data sets, while engaging students in authentic and inquiry-based learning in landscape-scale ecology

Implication of Melanopsin and Trigeminal Neural Pathways in Blue Light Photosensitivity in vivo

Photophobia may arise from various causes and frequently accompanies numerous ocular diseases. In modern highly illuminated world, complaints about greater photosensitivity to blue light increasingly appear. However, the pathophysiology of photophobia is still debated. In the present work, we investigated in vivo the role of various neural pathways potentially implicated in blue-light aversion. Moreover, we studied the light-induced neuroinflammatory processes on the ocular surface and in the trigeminal pathways. Adult male C57BL/6J mice were exposed either to blue (400–500 nm) or to yellow (530–710 nm) LED light (3 h, 6 mW/cm2). Photosensitivity was measured as the time spent in dark or illuminated parts of the cage. Pharmacological treatments were applied: topical instillation of atropine, pilocarpine or oxybuprocaine, intravitreal injection of lidocaine, norepinephrine or “blocker” of the visual photoreceptor transmission, and intraperitoneal injection of a melanopsin antagonist. Clinical evaluations (ocular surface state, corneal mechanical sensitivity and tear quantity) were performed directly after exposure to light and after 3 days of recovery in standard light conditions. Trigeminal ganglia (TGs), brainstems and retinas were dissected out and conditioned for analyses. Mice demonstrated strong aversion to blue but not to yellow light. The only drug that significantly decreased the blue-light aversion was the intraperitoneally injected melanopsin antagonist. After blue-light exposure, dry-eye-related inflammatory signs were observed, notably after 3 days of recovery. In the retina, we observed the increased immunoreactivity for GFAP, ATF3, and Iba1; these data were corroborated by RT-qPCR. Moreover, retinal visual and non-visual photopigments distribution was altered. In the trigeminal pathway, we detected the increased mRNA expression of cFOS and ATF3 as well as alterations in cytokines’ levels. Thus, the wavelength-dependent light aversion was mainly mediated by melanopsin-containing cells, most likely in the retina. Other potential pathways of light reception were also discussed. The phototoxic message was transmitted to the trigeminal system, inducing both inflammation at the ocular surface and stress in the retina. Further investigations of retina-TG connections are needed

Exome sequencing identifies novel AD-associated genes

The genetic component of Alzheimer’s disease (AD) has been mainly assessed using Genome Wide Association Studies (GWAS), which do not capture the risk contributed by rare variants. Here, we compared the gene-based burden of rare damaging variants in exome sequencing data from 32,558 individuals —16,036 AD cases and 16,522 controls— in a two-stage analysis. Next to known genes TREM2, SORL1 and ABCA7, we observed a significant association of rare, predicted damaging variants in ATP8B4 and ABCA1 with AD risk, and a suggestive signal in ADAM10. Next to these genes, the rare variant burden in RIN3, CLU, ZCWPW1 and ACE highlighted these genes as potential driver genes in AD-GWAS loci. Rare damaging variants in these genes, and in particular loss-of-function variants, have a large effect on AD-risk, and they are enriched in early onset AD cases. The newly identified AD-associated genes provide additional evidence for a major role for APP-processing, Aβ-aggregation, lipid metabolism and microglial function in AD

New insights into the genetic etiology of Alzheimer's disease and related dementias

Characterization of the genetic landscape of Alzheimer's disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/'proxy' AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE ε4 allele