Adjustments in fatty acid composition is a mechanism that can explain resilience to marine heatwaves and future ocean conditions in the habitat‐forming seaweed Phyllospora comosa (Labillardière) C.Agardh

Marine heatwaves are extreme events that can have profound and lasting impacts on marine species. Field observations have shown seaweeds to be highly susceptible to marine heatwaves, but the physiological drivers of this susceptibility are poorly understood. Furthermore, the effects of marine heatwaves in conjunction with ocean warming and acidification are yet to be investigated. To address this knowledge gap, we conducted a laboratory culture experiment in which we tested the growth and physiological responses of Phyllospora comosa juveniles from the southern extent of its range (43–31°S) to marine heatwaves, ocean warming and acidification. We used a ‘collapsed factorial design’ in which marine heatwaves were superimposed on current (today's pH and temperature) and future (pH and temperature projected by 2100) ocean conditions. Responses were tested both during the heatwaves, and after a 7‐day recovery period. Heatwaves reduced net photosynthetic rates in both current and future conditions, while respiration rates were elevated under heatwaves in the current conditions only. Following the recovery period, there was little evidence of heatwaves having lasting negative effects on growth, photosynthesis or respiration. Exposure to heatwaves, future ocean conditions or both caused an increase in the degree of saturation of fatty acids. This adjustment may have counteracted negative effects of elevated temperatures by decreasing membrane fluidity, which increases at higher temperatures. Furthermore, P. comosa appeared to down‐regulate the energetically expensive carbon dioxide concentrating mechanism in the future conditions with a reduction in δ¹³C values detected in these treatments. Any saved energy arising from this down‐regulation was not invested in growth and was likely invested in the adjustment of fatty acid composition. This adjustment is a mechanism by which P. comosa and other seaweeds may tolerate the negative effects of ocean warming and marine heatwaves through benefits arising from ocean acidification.     

Spawning strategies in cypriniform fishes in a lowland river invaded by non-indigenous European barbel Barbus barbus

Spawning strategies of lowland river fishes include single spawning, where reproduction generally occurs in early spring to provide 0+ fish with an extended growth season through the summer, but with a high risk of stochastic mortality events occurring, such as early summer floods. This risk can be reduced by multiple or protracted spawning strategies, where 0+ fish are produced over an extended period, often into mid-summer, but with the trade-off being a shorter growth season. The spawning strategies of cypriniform fish were explored in the River Teme, a spate river in Western England, which has non-indigenous European barbel Barbus barbus present. Sampling 0+ fish in spring and summer and across three spawning periods, B. barbus, chub Squalius cephalus and minnow Phoxinus phoxinus always revealed multiple spawning events, with 0+ fish of < 20 mm present in samples collected from June to August. Fish below 20 mm in August remained relatively small by the end of their growth season (October). For dace Leuciscus leuciscus, only single spawning events were evident, but with 0+ dace always being relatively large. Therefore, multiple spawning appears to be a common strategy that provides resilience in 0+ fish against stochastic mortality events in lowland rivers.

     

Otolith microstructure reveals consequences for juvenile growth of fractional spawning in an invasive goldfish Carassius auratus (Linnaeus, 1758) population

The consequences of fractional spawning on the early‐life growth rates of invasive goldfish (Carassius auratus) from the Qinghai‐Tibet Plateau were studied using the otolith microstructure of samples collected in June 2011. The effect of the estimated hatching date on the subsequent growth of individual fish was determined by back‐calculating their number of growth days, daily growth rates and the onset of their second growth season. The number of growth days in the first growth season ranged from 93 to 186 days. Following hatching, daily growth rates increased rapidly to a maximum of 0.55 mm days^?1 before declining to 0.09 mm days^?1. The effect of the duration of the first growth season on individuals was significant (P < 0.01), with later spawned fish having faster growth rates. These later spawned fish were, however, still significantly smaller in body length at the end of the first growth season (37 ± 4 mm in late hatched fish vs 55 ± 9 mm in early hatched fish). However, the smaller, later hatched fish started growing earlier in their second growth season than all other fish (P < 0.01) and subsequently achieved larger growth increments (P < 0.01), suggesting that the larger, early‐hatched fish were investing more resources in gonadal growth than somatic growth in their second growth year. Thus, this invasive population revealed considerable plasticity in their early‐life growth rates that were associated with the hatching date, potentially having substantial effects on their development in their second year of life.     

Phosphorylation of SAF-A/hnRNP-U Serine 59 by Polo-Like Kinase 1 Is Required for Mitosis

Scaffold attachment factor A (SAF-A), also called heterogenous nuclear ribonuclear protein U (hnRNP-U), is phosphorylated on serine 59 by the DNA-dependent protein kinase (DNA-PK) in response to DNA damage. Since SAF-A, DNA-PK catalytic subunit (DNA-PKcs), and protein phosphatase 6 (PP6), which interacts with DNA-PKcs, have all been shown to have roles in mitosis, we asked whether DNA-PKcs phosphorylates SAF-A in mitosis. We show that SAF-A is phosphorylated on serine 59 in mitosis, that phosphorylation requires polo-like kinase 1 (PLK1) rather than DNA-PKcs, that SAF-A interacts with PLK1 in nocodazole-treated cells, and that serine 59 is dephosphorylated by protein phosphatase 2A (PP2A) in mitosis. Moreover, cells expressing SAF-A in which serine 59 is mutated to alanine have multiple characteristics of aberrant mitoses, including misaligned chromosomes, lagging chromosomes, polylobed nuclei, and delayed passage through mitosis. Our findings identify serine 59 of SAF-A as a new target of both PLK1 and PP2A in mitosis and reveal that both phosphorylation and dephosphorylation of SAF-A serine 59 by PLK1 and PP2A, respectively, are required for accurate and timely exit from mitosis.     

VEGF binding to NRP1 is essential for VEGF stimulation of endothelial cell migration, complex formation between NRP1 and VEGFR2, and signaling via FAK Tyr407 phosphorylation

In endothelial cells, neuropilin-1 (NRP1) binds vascular endothelial growth factor (VEGF)-A and is thought to act as a coreceptor for kinase insert domain-containing receptor (KDR) by associating with KDR and enhancing VEGF signaling. Here we report mutations in the NRP1 b1 domain (Y297A and D320A), which result in complete loss of VEGF binding. Overexpression of Y297A and D320A NRP1 in human umbilical vein endothelial cells reduced high-affinity VEGF binding and migration toward a VEGF gradient, and markedly inhibited VEGF-induced angiogenesis in a coculture cell model. The Y297A NRP1 mutant also disrupted complexation between NRP1 and KDR and decreased VEGF-dependent phosphorylation of focal adhesion kinase at Tyr407, but had little effect on other signaling pathways. Y297A NRP1, however, heterodimerized with wild-type NRP1 and NRP2 indicating that nonbinding NRP1 mutants can act in a dominant-negative manner through formation of NRP1 dimers with reduced binding affinity for VEGF. These findings indicate that VEGF binding to NRP1 has specific effects on endothelial cell signaling and is important for endothelial cell migration and angiogenesis mediated via complex formation between NRP1 and KDR and increased signaling to focal adhesions. Identification of key residues essential for VEGF binding and biological functions provides the basis for a rational design of antagonists of VEGF binding to NRP1.     

Exercise training reverses impaired skeletal muscle metabolism induced by artificial selection for low aerobic capacity

We have used a novel model of genetically imparted endurance exercise capacity and metabolic health to study the genetic and environmental contributions to skeletal muscle glucose and lipid metabolism. We hypothesized that metabolic abnormalities associated with low intrinsic running capacity would be ameliorated by exercise training. Selective breeding for 22 generations resulted in rat models with a fivefold difference in intrinsic aerobic capacity. Low (LCR)- and high (HCR)-capacity runners remained sedentary (SED) or underwent 6 wk of exercise training (EXT). Insulin-stimulated glucose transport, insulin signal transduction, and rates of palmitate oxidation were lower in LCR SED vs. HCR SED (P < 0.05). Decreases in glucose and lipid metabolism were associated with decreased β?-adrenergic receptor (β?-AR), and reduced expression of Nur77 target proteins that are critical regulators of muscle glucose and lipid metabolism [uncoupling protein-3 (UCP3), fatty acid transporter (FAT)/CD36; P < 0.01 and P < 0.05, respectively]. EXT reversed the impairments to glucose and lipid metabolism observed in the skeletal muscle of LCR, while increasing the expression of β?-AR, Nur77, GLUT4, UCP3, and FAT/CD36 (P < 0.05) in this tissue. However, no metabolic improvements were observed following exercise training in HCR. Our results demonstrate that metabolic impairments resulting from genetic factors (low intrinsic aerobic capacity) can be overcome by an environmental intervention (exercise training). Furthermore, we identify Nur77 as a potential mechanism for improved skeletal muscle metabolism in response to EXT.     

Drought alters carbon fluxes in alpine snowbed ecosystems through contrasting impacts on graminoids and forbs

? Climate change is predicted to increase the frequency of drought events in alpine ecosystems with the potential to affect carbon turnover. ? We removed intact turfs from a Nardus stricta alpine snowbed community and subjected half of them to two drought events of 8 d duration under controlled conditions. Leachate dissolved organic carbon (DOC) was measured throughout the 6 wk study period, and a (13)CO(2) pulse enabled quantification of fluxes of recent assimilate into shoots, roots and leachate and ecosystem CO(2) exchange. ? The amount of DOC in leachate from droughted cores was 62% less than in controls. Drought reduced graminoid biomass, increased forb biomass, had no effect on bryophytes, and led to an overall decrease in total above-ground biomass compared with controls. Net CO(2) exchange, gross photosynthesis and the amount of (13)CO(2) fixed were all significantly less in droughted turfs. These turfs also retained proportionally more (13)C in shoots, allocated less (13)C to roots, and the amount of dissolved organic (13)C recovered in leachate was 57% less than in controls. ? Our data show that drought events can have significant impacts on ecosystem carbon fluxes, and that the principal mechanism behind this is probably changes in the relative abundance of forbs and grasses.