Evidence for female-biased juvenile dispersal in corophiid amphipods from a New Zealand estuary

This study examined the distribution and dispersal of corophiid amphipods (Paracorophium spp.) in a temperate New Zealand estuary. Individuals in the sediment (resident population) and those caught in bed-load (local-scale movement) and suspended-load (larger-scale movement) were counted, measured, and sexed, during two tidal cycles at 4-6 week intervals spanning 13 months. Gravid females and juveniles were present in the resident population on all sample dates suggesting near continuous reproduction. Juveniles (< 2.2 mm body length) accounted for 49.8% of individuals in the sediment, compared to 65.4% of those caught in the bed-load and suspended-load traps. For the majority of sample dates, there was a net export of juveniles from the estuary. The total number of juveniles captured in suspended-load traps was significantly greater during the ebb tide relative to the flood tide (n = 541 versus 256), whereas no significant differences were found for adults. Similarly, numbers in the bed-load traps were significantly greater for juveniles during the ebb versus the flood tide (n = 900 versus 484), and also for adult females (n = 180 versus 86). Juvenile sex ratios were female biased in the sediment (9.8:1) and in suspended-load traps (7.6:1) and both were significantly more female-biased than that recorded for juveniles caught in bed-load traps (5.8:1). By contrast, there was a significantly lower proportion of adult females to adult males found in bed-load traps (1.7:1) and in suspended-load traps (0.98:1) compared to the resident population in the sediment (3.6:1). The mean size of juvenile females caught on a flood tide was significantly larger compared to those on the ebb tide, yet juvenile males were not significantly different, suggesting that smaller females were not returning on the flood tide. We suggest that female-biased juvenile dispersal for estuarine Paracorophium spp. lowers the risk of inbreeding and reduces competition. This may have evolved in response to a polygamous breeding system with little or no social organisation where a female produces more female offspring to maximise her inclusive fitness.     

Effects of biotic disturbances on forest carbon cycling in the United States and Canada

Forest insects and pathogens are major disturbance agents that have affected millions of hectares in North America in recent decades, implying significant impacts to the carbon (C) cycle. Here, we review and synthesize published studies of the effects of biotic disturbances on forest C cycling in the United States and Canada. Primary productivity in stands was reduced, sometimes considerably, immediately following insect or pathogen attack. After repeated growth reductions caused by some insects or pathogens or a single infestation by some bark beetle species, tree mortality occurred, altering productivity and decomposition. In the years following disturbance, primary productivity in some cases increased rapidly as a result of enhanced growth by surviving vegetation, and in other cases increased slowly because of lower forest regrowth. In the decades following tree mortality, decomposition increased as a result of the large amount of dead organic matter. Net ecosystem productivity decreased immediately following attack, with some studies reporting a switch to a C source to the atmosphere, and increased afterward as the forest regrew and dead organic matter decomposed. Large variability in C cycle responses arose from several factors, including type of insect or pathogen, time since disturbance, number of trees affected, and capacity of remaining vegetation to increase growth rates following outbreak. We identified significant knowledge gaps, including limited understanding of carbon cycle impacts among different biotic disturbance types (particularly pathogens), their impacts at landscape and regional scales, and limited capacity to predict disturbance events and their consequences for carbon cycling. We conclude that biotic disturbances can have major impacts on forest C stocks and fluxes and can be large enough to affect regional C cycling. However, additional research is needed to reduce the uncertainties associated with quantifying biotic disturbance effects on the North American C budget.     

Variations of the candidate SEZ6L2 gene on Chromosome 16p11.2 in patients with autism spectrum disorders and in human populations

Background

Autism spectrum disorders (ASD) are a group of severe childhood neurodevelopmental disorders with still unknown etiology. One of the most frequently reported associations is the presence of recurrent de novo or inherited microdeletions and microduplications on chromosome 16p11.2. The analysis of rare variations of 8 candidate genes among the 27 genes located in this region suggested SEZ6L2 as a compelling candidate.

Methodology/Principal Findings

We further explored the role of SEZ6L2 variations by screening its coding part in a group of 452 individuals, including 170 patients with ASD and 282 individuals from different ethnic backgrounds of the Human Genome Diversity Panel (HGDP), complementing the previously reported screening. We detected 7 previously unidentified non-synonymous variations of SEZ6L2 in ASD patients. We also identified 6 non-synonymous variations present only in HGDP. When we merged our results with the previously published, no enrichment of non-synonymous variation in SEZ6L2 was observed in the ASD group compared with controls.

Conclusions/Significance

Our results provide an extensive ascertainment of the genetic variability of SEZ6L2 in human populations and do not support a major role for SEZ6L2 sequence variations in the susceptibility to ASD.     

Signaling through integrin LFA-1 leads to filamentous actin polymerization and remodeling,resulting in enhanced T cell adhesion

The integrins can activate signaling pathways, but the final downstream outcome of these pathways is often unclear. This study analyzes the consequences of signaling events initiated by the interaction of the leukocyte integrin LFA-1 with its ligand, dimeric ICAM-1. We show that the active form of LFA-1 regulates its own function on primary human T cells by directing the remodeling of the F-actin cytoskeleton to strengthen T cell adhesion to ICAM-1. Confocal microscopy revealed that both F-actin bundling and overall levels of F-actin are increased in the ICAM-1-adhering T cells. This increase in F-actin levels and change in F-actin distribution was quantitated for large numbers of T cells using the technique of laser scanning cytometry and was found to be significant. The study went on to show that clustering of conformationally altered LFA-1 is essential for the changes in F-actin, and a model is proposed in which clustered, high-avidity T cell LFA-1, interacting with multivalent ICAM-1, causes LFA-1 signaling, which results in F-actin polymerization and higher-order F-actin bundling. The findings demonstrate that LFA-1 acts not only as an adhesion receptor but also as a signaling receptor by actively initiating the F-actin reorganization that is essential for many T cell-dependent processes.     

Effect of soil potassium availability on soybean aphid (Hemiptera: Aphididae) population dynamics and soybean yield

Studies were conducted to examine the effect of potassium (K) on soybean aphid, Aphis glycines Matsumura, population growth. A laboratory feeding assay examined the effect of K-deficient foliage on life table parameters of soybean aphids, and field experiments were designed to determine the effect of three soil K treatment levels on aphid populations and their impact on soybean yields. The feeding assay found that life table parameters differed between aphids feeding on the K-deficient and nondeficient soybean leaves. Soybean aphids in the K-deficient treatment exhibited significantly greater intrinsic rate of increase (r(m)), finite rate of increase (lambda), and net reproductive rate (Ro) relative to aphids feeding on nondeficient leaves. No significant difference was observed in mean generation time (T) between the two treatments. However, the field experiment repeated over 2 yr showed no effect of K on soybean aphid populations. Soybean aphid populations were high in unsprayed plots and feeding resulted in significant yield losses in 2002 at all three K treatment levels: when averaged across 2001 and 2002, unsprayed treatments yielded 22, 18, and 19.5% less than the sprayed plots in the low, medium, and high K treatments, respectively. No significant interaction was observed between aphid abundance and K level on soybean yields in either year. This study therefore suggests that although aphids can perform better on K-deficient plants, aphid abundance in the field may be dependent on additional factors, such as dispersal, that may affect final densities within plots.     

Tetrahydrobiopterin-dependent inhibition of superoxide generation from neuronal nitric oxide synthase.

The binding of calcium/calmodulin stimulates electron transfer between the reductase and oxygenase domains of neuronal nitric oxide synthase (nNOS). Here, we demonstrate using electron spin resonance spin-trapping with 5-diethoxyphosphoryl-5-methyl-1-pyrroline N-oxide that pterin-free nNOS generates superoxide from the reductase and the oxygenase domain by a calcium/calmodulin-dependent mechanism. Tetrahydrobiopterin (BH(4)) diminishes the formation of superoxide by a mechanism that does not cause inhibition of NADPH consumption. In contrast, BH(4) analogs 7,8-dihydrobiopterin and sepiapterin do not affect superoxide yields. L-Arginine alone inhibits the generation of superoxide by nNOS but not by C331A-nNOS mutant that has a low affinity for L-arginine. A greater decrease in superoxide yields is observed when nNOS is preincubated with L-arginine. This effect is in accordance with the slow binding rates of L-arginine to NOS in the absence of BH(4). L-Arginine alone or in combination with BH(4) decreases the rates of NADPH consumption. The effect of L-arginine on superoxide yields, however, was less dramatic than that caused by BH(4) as much higher concentrations of L-arginine are necessary to attain the same inhibition. In combination, L-arginine and BH(4) inhibit the formation of superoxide generation and stimulate the formation of L-citrulline. We conclude that, in contrast to L-arginine, BH(4) does not inhibit the generation of superoxide by controlling electron transfer through the enzyme but by stimulating the formation of the heme-peroxo species.     

Dexamethasone has pro-apoptotic effects on non-activated fresh peripheral blood mononuclear cells

Apoptosis is a physiological method of cell death commonly referred to as programmed cell death. However, non-apoptotic programmed cell death, such as autophagy and programmed necrosis, has been characterized by morphological criteria. In view of the human therapeutic use of DEX, and considering that no difference in the number and/or affinity of glucocorticoid receptors in activated and non-activated lymphocytes has been reported, we decided to evaluate the effect of DEX on fresh peripheral blood mononuclear cells (PBMC). Transmission electron microscopy showed that DEX can significantly induce apoptosis in non-activated PBMC. It was also observed by transmission electron microscopy that, independently of DEX treatment, PBMC also died by a process marked by extreme vacuolization and increase in cellular volume; these cells were erroneously classified as viable by flow cytometry using the 7-AAD assay. It is concluded that the DEX pro-apoptotic effect is not restricted to activated PBMC and, therefore, DEX-induced apoptosis could play either homeostatic (activated PBMC) or immunosuppressive (non-activated PBMC) roles.     

Endogenous reductions in N-methyl-d-aspartate receptor activity inhibit nitric oxide production in the anoxic freshwater turtle cortex

Increased nitric oxide (NO) production from hypoxic mammalian neurons increases cerebral blood flow (CBF) but also glutamatergic excitotoxicity and DNA fragmentation. Anoxia-tolerant freshwater turtles have evolved NO-independent mechanisms to increase CBF; however, the mechanism(s) of NO regulation are not understood. In turtle cortex, anoxia or NMDAR blockade depressed NO production by 27+/-3% and 41+/-5%, respectively. NMDAR antagonists also reduced the subsequent anoxic decrease in NO by 74+/-6%, suggesting the majority of the anoxic decrease is due to endogenous suppression of NMDAR activity. Prevention of NO-mediated damage during the transition to and from anoxia may be incidental to natural reductions of NMDAR activity in the anoxic turtle cortex.     

Isovolumetric and isobaric rabbit tracheal contraction in vitro

Isovolumetric and isobaric tracheal smooth muscle (TSM) contraction were studied in vitro in a preparation of the whole rabbit trachea. Eight tracheae from New Zealand White rabbits were excised and mounted at a fixed length in an organ bath. Electrical field stimulation (EFS) was performed in isovolumetric and isobaric conditions at varying transmural pressures (TMP). Supramaximal stimulation with methacholine was done at 0 TMP. Active change in pressure (delta P) with EFS showed a peak at 3.1 +/- 1.06 cmH2O TMP during inflation and at 4.1 +/- 1.18 cmH2O TMP during deflation (mean +/- SE). Active delta P decreased at higher or lower TMP. Active change in volume with EFS showed a peak at 3.2 +/- 1.26 cmH2O TMP during inflation and at 1.8 +/- 0.98 cmH2O TMP during deflation. A decrease in response was also observed at higher and lower TMP. From these data, we concluded that TSM is at optimal length (Lmax) at TMP of 2-3 cmH2O. Maximal TSM shortening with supramaximal stimulation with methacholine was 32% Lmax. This figure is considerably smaller than the 80% shortening found in unloaded strips of TSM. We conclude that rabbit TSM length is close to Lmax at TMP similar to those found at functional residual capacity and that the loads that the muscle has to overcome probably contribute to the limited shortening observed in situ.