Interactive Influence of Turbidity and Light on Larval Bluegill (Lepomis macrochirus) Foraging

Abstract in English and French.In a series of in situ enclosure experiments with larval bluegill (lepomis macrochirus), we demonstrate that turbidity from suspended sediments reduces bluegill consumption of crustacean zooplankton, primarily cyclopoid copepods and cogepod nauplii. However, this reduction occurred only when light intensity in parts of enclosures fell below a threshold, estimated at <450 lx. Following recent studies demonstrating copepod die1 vertical migration in response to predators, it appears that copepods in our experiments used low-light strata as a refuge. Without this apparent refuge present, larval bluegill consumption increased with increasing turbidity, but prey were smaller on average. Thus, prey biomass consumed by larval bluegill did not differ with turbidity in high-light conditions. We postulate that the shift to smaller prey across taxa at higher turbidity, when light intensity exceeded 450 lx, derives from increased prey-background contrast. In low-light conditions, larval bluegill consumed larger, but fewer, zooplankton with increasing turbidity, resulting in lower prey biomass consumed. Thus, we demonstrate the field conditions causing negative turbidity effects on larval fish foraging success, and thus growth and recruitment.This research was supported in part by National Science Foundation grants BSR-8715730 and BSR-9107173 to R. A. Stein and Sigma Xi Grants-in-Aid-of-Research to J. G. Miner

Stocking Threadfin Shad: Consequences for Young-of-Year Fishes

Threadfin shad Dorosoma petenense are commonly introduced into reservoirs to supplement prey available to piscivorous fishes. To determine how early life stages of threadfin shad and their potential competitors and predators interact, we introduced this species into two Ohio lakes—Clark and Stonelick—and evaluated how its young of year influenced young-of-year bluegills Lepomis macrochirus and largemouth bass Micropterus salmoides. After adults were stocked in April, peak abundance of young-of-year threadfin shad occurred in August in both lakes. Bluegills generally spawned earlier than threadfin shad, which apparently reduced competition between young of these species. In Clark Lake, young-of-year threadfin shad did not reduce zooplankton populations, but in Stonelick Lake, peak abundance of young-of-year threadfin shad was followed by a precipitous decline in zooplankton. Data on cladoceran birth rates indicated this decline was due to increased predation by threadfin shad. Survival of bluegills to a size at which they move into the littoral zone also declined in Stonelick Lake, perhaps because of the virtual elimination of zooplankton. Limited survival of bluegills in turn contributed to reduced growth of young-of-year largemouth bass dependent on them as prey. Given that zooplankton declined in one but not the other lake, interactions among young-of-year fishes due to annually introduced threadfin shad will likely vary among systems and years. Nonetheless, introduced threadfin shad could, in some systems in some years, negatively affect growth and recruitment of the very species they were meant to enhance.This work was funded in part by National Science Foundation grants NSF BSR-8705518 to R. A. Stein and NSF BSR-8715730 to G. G. Mittelbach, and by Federal Aid in Fish Restoration Project F-57-R awarded to R. A. Stein and administered through the Ohio Division of Wildlife

Parietal epithelial cell differentiation to a podocyte fate in the aged mouse kidney

Healthy aging is typified by a progressive and absolute loss of podocytes over the lifespan of animals and humans. To test the hypothesis that a subset of glomerular parietal epithelial cell (PEC) progenitors transition to a podocyte fate with aging, dual reporte

Energetic Adaptations along a Broad Latitudinal Gradient: Implications for Widely Distributed Assemblages

Most community-based models in ecology assume that all individuals within a species respond similarly to environmental conditions and thereby exert identical effects as consumers or prey. Rather, individuals differ among systems, with important implications for population demographics and community interactions. For widely distributed assemblages made up of poikilotherms with high first-year mortality, species-specific differences in growth reaction norms as affected by both temperature and genotype will influence biotic interactions. For a broadly distributed fish assemblage, first-year growth does not vary with latitude for a planktivorous prey species, but declines with increasing latitude for a terminal piscivore. Size-based competitive interactions between these species are likely to be more intense at high latitudes, as they spend an extended time sharing resources during early life. Such patterns probably are pervasive and must be considered when seeking to understand species interactions. Improving our knowledge of how temperature and local adaptations affect size-based interactions should enhance our ability to manage and conserve widespread assemblages

Epithelial laminin α5 is necessary for distal epithelial cell maturation, VEGF production, and alveolization in the developing murine lung

AbstractLaminin α5 is prominent in the basement membrane of alveolar walls, airways, and pleura in developing and adult lung. Targeted deletion of laminin α5 in mice causes developmental defects in multiple organs, but embryonic lethality has precluded examination of the latter stages of lung development. To identify roles for laminin α5 in lung development, we have generated an inducible lung epithelial cell-specific Lama5 null (SP-CLama5fl/−) mouse through use of the Cre/loxP system, the human surfactant protein C promoter, and the reverse tetracycline transactivator. SP-CLama5fl/− embryos exposed to doxycycline from E6.5 died a few hours after birth. Compared to control littermates, SP-CLama5fl/− lungs had dilated, enlarged distal airspaces, but basement membrane ultrastructure was preserved. Distal epithelial cell differentiation was perturbed, with a marked reduction of alveolar type II cells and a virtual absence of type I cells. Cell proliferation was reduced and apoptosis was increased. Capillary density was diminished, and this was associated with a decrease in total lung VEGF production. Overall, these findings indicate that epithelial laminin α5, independent of its structural function, is necessary for murine lung development, and suggest a role for laminin α5 in signaling pathways that promote alveolar epithelial cell differentiation and VEGF expression

Fatty acid transport protein 4 (FATP4) prevents light-induced degeneration of cone and rod photoreceptors by inhibiting RPE65 isomerase

Although rhodopsin is essential for sensing light for vision, it also mediates light-induced apoptosis of photoreceptors in mouse. RPE65, which catalyzes isomerization of all-trans retinyl fatty acid esters to 11-cis-retinol (11cROL) in the visual cycle, controls the rhodopsin regeneration rate and photoreceptor susceptibility to light-induced degeneration. Mutations in RPE65 have been linked to blindness in affected children. Despite such importance, the mechanism that regulates RPE65 function remains unclear. Through unbiased expression screening of a bovine retinal pigment epithelium (RPE) cDNA library, we have identified elongation of very long-chain fatty acids-like 1 (ELOVL1) and fatty acid transport protein 4 (FATP4), which each have very long-chain fatty acid acyl-CoA synthetase (VLCFA-ACS) activity, as negative regulators of RPE65. We found that the VLCFA derivative lignoceroyl (C24:0)-CoA inhibited synthesis of 11cROL, whereas palmitoyl (C16:0)-CoA promoted synthesis of 11cROL. We further found that competition of FATP4 with RPE65 for the substrate of RPE65 was also involved in the mechanisms by which FATP4 inhibits synthesis of 11cROL. FATP4 was predominantly expressed in RPE, and the FATP4-deficient RPE showed significantly higher isomerase activity. Consistent with these results, the regeneration rate of 11-cis-retinaldehyde and the recovery rate for rod light sensitivity were faster in FATP4-deficient mice than wild-type mice. Moreover, FATP4-deficient mice displayed increased accumulation of the cytotoxic all-trans retinaldehyde and hypersusceptibility to light-induced photoreceptor degeneration. Our findings demonstrate that ELOVL1, FATP4, and their products comprise the regulatory elements of RPE65 and play important roles in protecting photoreceptors from degeneration induced by light damage

Notch-Deficient Skin Induces a Lethal Systemic B-Lymphoproliferative Disorder by Secreting TSLP, a Sentinel for Epidermal Integrity

Epidermal keratinocytes form a highly organized stratified epithelium and sustain a competent barrier function together with dermal and hematopoietic cells. The Notch signaling pathway is a critical regulator of epidermal integrity. Here, we show that keratinocyte-specific deletion of total Notch signaling triggered a severe systemic B-lymphoproliferative disorder, causing death. RBP-j is the DNA binding partner of Notch, but both RBP-j–dependent and independent Notch signaling were necessary for proper epidermal differentiation and lipid deposition. Loss of both pathways caused a persistent defect in skin differentiation/barrier formation. In response, high levels of thymic stromal lymphopoietin (TSLP) were released into systemic circulation by Notch-deficient keratinocytes that failed to differentiate, starting in utero. Exposure to high TSLP levels during neonatal hematopoiesis resulted in drastic expansion of peripheral pre- and immature B-lymphocytes, causing B-lymphoproliferative disorder associated with major organ infiltration and subsequent death, a previously unappreciated systemic effect of TSLP. These observations demonstrate that local skin perturbations can drive a lethal systemic disease and have important implications for a wide range of humoral and autoimmune diseases with skin manifestations