Heterospecific courtship,minority effects and niche separation between cryptic butterfly species

Species interacting in varied ecological conditions often evolve in different directions in different local populations. The butterflies of the cryptic Leptidea complex are sympatrically distributed in different combinations across their Eurasian range. Interestingly, the same species is a habitat generalist in some regions and a habitat specialist in others, where a sibling species has the habitat generalist role. Previous studies suggest that this geographically variable niche divergence is generated by local processes in different contact zones. By varying the absolute and relative densities of Leptidea sinapis and Leptidea juvernica in large outdoor cages, we show that female mating success is unaffected by conspecific density, but strongly negatively affected by the density of the other species. Whereas 80% of the females mated when a conspecific couple was alone in a cage, less than 10% mated when the single couple shared the cage with five pairs of the other species. The heterospecific courtships can thus affect the population fitness, and for the species in the local minority, the suitability of a habitat is likely to depend on the presence or absence of the locally interacting species. If the local relative abundance of the different species depends on the colonization order, priority effects might determine the ecological roles of interacting species in this system.     

Extreme divergence in floral scent among woodland star species (Lithophragma spp.) pollinated by floral parasites

Backgrounds and Aims

A current challenge in coevolutionary biology is to understand how suites of traits vary as coevolving lineages diverge. Floral scent is often a complex, variable trait that attracts a suite of generalized pollinators, but may be highly specific in plants specialized on attracting coevolved pollinating floral parasites. In this study, floral scent variation was investigated in four species of woodland stars (Lithophragma spp.) that share the same major pollinator (the moth Greya politella, a floral parasite). Three specific hypotheses were tested: (1) sharing the same specific major pollinator favours conservation of floral scent among close relatives; (2) selection favours ‘private channels’ of rare compounds particularly aimed at the specialist pollinator; or (3) selection from rare, less-specialized co-pollinators mitigates the conservation of floral scent and occurrence of private channels.

Methods

Dynamic headspace sampling and solid-phase microextraction were applied to greenhouse-grown plants from a common garden as well as to field samples from natural populations in a series of experiments aiming to disentangle the genetic and environmental basis of floral scent variation.

Key Results

Striking floral scent divergence was discovered among species. Only one of 69 compounds was shared among all four species. Scent variation was largely genetically based, because it was consistent across field and greenhouse treatments, and was not affected by visits from the pollinating floral parasite.

Conclusions

The strong divergence in floral scents among Lithophragma species contrasts with the pattern of conserved floral scent composition found in other plant genera involved in mutualisms with pollinating floral parasites. Unlike some of these other obligate pollination mutualisms, Lithophragma plants in some populations are occasionally visited by generalist pollinators from other insect taxa. This additional complexity may contribute to the diversification in floral scent found among the Lithophragma species pollinated by Greya moths.     

Autocrine stimulation of osteoblast activity by Wnt5a in response to TNF-α in human mesenchymal stem cells

Although anti-tumor necrosis factor (TNF)-α treatments efficiently block inflammation in ankylosing spondylitis (AS), they are inefficient to prevent excessive bone formation. In AS, ossification seems more prone to develop in sites where inflammation has resolved following anti-TNF therapy, suggesting that TNF-α indirectly stimulates ossification. In this context, our objectives were to determine and compare the involvement of Wnt proteins, which are potent growth factors of bone formation, in the effects of TNF-α on osteoblast function. In human mesenchymal stem cells (MSCs), TNF-α significantly increased the levels of Wnt10b and Wnt5a. Associated with this effect, TNF-α stimulated tissue-non specific alkaline phosphatase (TNAP) and mineralization. This effect was mimicked by activation of the canonical β-catenin pathway with either anti-Dkk1 antibodies, lithium chloride (LiCl) or SB216763. TNF-α reduced, and activation of β-catenin had little effect on expression of osteocalcin, a late marker of osteoblast differentiation. Surprisingly, TNF-α failed to stabilize β-catenin and Dkk1 did not inhibit TNF-α effects. In fact, Dkk1 expression was also enhanced in response to TNF-α, perhaps explaining why canonical signaling by Wnt10b was not activated by TNF-α. However, we found that Wnt5a also stimulated TNAP in MSCs cultured in osteogenic conditions, and increased the levels of inflammatory markers such as COX-2. Interestingly, treatment with anti-Wnt5a antibodies reduced endogenous TNAP expression and activity. Collectively, these data suggest that increased levels of Dkk1 may blunt the autocrine effects of Wnt10b, but not that of Wnt5a, acting through non-canonical signaling. Thus, Wnt5a may be potentially involved in the effects of inflammation on bone formation.     

Macroparasites at peripheral sites of infection are major and dynamic modifiers of systemic antimicrobial pattern recognition responses

Immune defences and the maintenance of immunological homeostasis in the face of pathogenic and commensal microbial exposures are channelled by innate antimicrobial pattern recognition receptors (PRRs) such as toll‐like receptors (TLRs). Whilst PRR‐mediated response programmes are the result of long‐term host‐pathogen or host–commensal co‐evolutionary dynamics involving microbes, an additional possibility is that macroparasitic co‐infections may be a significant modifier of such interactions. We demonstrate experimentally that macroparasites (the model gastrointestinal nematode, Heligmosomoides) at peripheral sites of infection cause substantial alteration of the expression and function of TLRs at a systemic level (in cultured splenocytes), predominantly up‐regulating TLR2, TLR4 and TLR9‐mediated cytokine responses at times of high standing worm burdens. We consistently observed such effects in BALB/c and C57BL/6 mice under single‐pulse and trickle exposures to Heligmosomoides larvae and in SWR and CBA mice under single‐pulse exposures. A complementary long‐term survey of TLR2‐mediated tumour necrosis factor‐alpha responses in wild wood mice (Apodemus sylvaticus) was consistent with substantial effects of macroparasites under some environmental conditions. A general pattern, though, was for the associations of macroparasites with TLR function to be temporally dynamic and context‐dependent: varying with different conditions of infection exposure in the field and laboratory and with host genetic strain in the laboratory. These results are compelling evidence that macroparasites are a major and dynamic modifier of systemic innate antimicrobial responsiveness in naturally occurring mammals and thus likely to be an important influence on the interaction between microbial exposures and the immune system.     

Increased Rate of Arterial Stiffening with Obesity in Adolescents: A Five-Year Follow-Up Study

Background

We prospectively and longitudinally determined the effects of childhood obesity on arterial stiffening and vascular wall changes. Changes in arterial stiffness measured as pulse wave velocity (PWV) and vascular morphology of the radial (RA) and dorsal pedal arteries (DPA) were examined in obese adolescents compared to lean subjects in a 5-year follow-up study.

Methodology/Principal Findings

A total of 28 obese subjects and 14 lean controls participated in both baseline (14 years old) and follow-up studies. PWV was measured by tonometer (SphygmoCor®) and recorded at RA and carotid artery, respectively. Intima thickness (IT), intima-media thickness (IMT) and RA and DPA diameters were measured using high-resolution ultrasound (Vevo 770™). Over the course of 5 years, PWV increased by 25% in the obese subjects as compared to 3% in the controls (p = 0.01). Diastolic blood pressure (DBP) increased by 23% in the obese subjects as opposed to 6% in controls (p = 0.009). BMI increased similarly in both groups, as did the IT and IMT. The change in PWV was strongly associated to the baseline BMI z -score (r = 0.51, p<0.001), as was the change in DBP (r = 0.50, p = 0.001).

Conclusions/Significance

During the transition from early to late adolescence, there was a general increase in arterial stiffness, which was aggravated by childhood obesity. The increase in arterial stiffness and DBP after 5 years was closely correlated to the baseline BMI z -score, indicating that childhood obesity has an adverse impact on vascular adaptation.     

Serum tau fragments as predictors of death or poor neurological outcome after out-of-hospital cardiac arrest

Background: Anoxic brain injury is the primary cause of death after resuscitation from out-of-hospital cardiac arrest (OHCA) and prognostication is challenging. The aim of this study was to evaluate the potential of two fragments of tau as serum biomarkers for neurological outcome.

Methods: Single-center sub-study of 171 patients included in the Target Temperature Management (TTM) Trial randomly assigned to TTM at 33?°C or TTM at 36?°C for 24?h after OHCA. Fragments (tau-A and tau-C) of the neuronal protein tau were measured in serum 24, 48 and 72?h after OHCA. The primary endpoint was neurological outcome.

Results: Median (quartile 1 – quartile 3) tau-A (ng/ml) values were 58 (43–71) versus 51 (43–67), 72 (57–84) versus 71 (59–82) and 76 (61–92) versus 75 (64–89) for good versus unfavourable outcome at 24, 48 and 72?h, respectively (p_group = 0.95). Median tau C (ng/ml) values were 38 (29–50) versus 36 (29–49), 49 (38–58) versus 48 (33–59) and 48 (39–59) versus 48 (36–62) (p_group = 0.95). Tau-A and tau-C did not predict neurological outcome (area under the receiver-operating curve at 48?h; tau-A: 0.51 and tau-C: 0.51).

Conclusions: Serum levels of tau fragments were unable to predict neurological outcome after OHCA.     

Diapause decision in the small tortoiseshell butterfly,Aglais urticae

Insects in temperate areas spend the inhospitable winter conditions in a resting stage known as diapause. In species that diapause in the larval or pupal stage, the decision whether to diapause or develop directly is customarily taken during the late instars, with long days (i.e., long light phases) and high temperatures promoting direct development. Among butterflies that overwinter as adults, data are rare and variable, but imply that the larval daylength conditions can affect the pathway decision. We studied the small tortoiseshell, Aglais urticae L. (Lepidoptera: Nymphalidae, Nymphalini), which is partially bivoltine from Central Scandinavia and southwards, and tested whether the pathway decision is taken in the larval or adult stage. We reared larvae under long‐day (L22:D2) or short‐day (L12:D12) photoperiods, and recorded the pathway taken by the eclosing adults by scoring their propensity to mate and produce eggs. We also tested whether the larval photoperiod influenced adult ability to diapause by assessing adult survival. The results clearly indicate that (1) there is no detectable effect of larval photoperiod treatment on the pathway decision taken by adults whether to enter diapause or to develop directly, (2) some individuals are obligately univoltine and insensitive to photoperiod during adulthood, whereas (3) other individuals can facultatively enter diapause or direct development, depending on the photoperiod experienced after adult eclosion.     

Beta(2)-adrenergic receptor agonists increase intracellular free Ca(2+) concentration cycling in ventricular cardiomyocytes through p38 and p42/44 MAPK-mediated cytosolic phospholipase A(2) activation

We have recently reported that arachidonic acid mediates beta(2)-adrenergic receptor (AR) stimulation of [Ca(2+)](i) cycling and cell contraction in embryonic chick ventricular cardiomyocytes (Pavoine, C., Magne, S., Sauvadet, A., and Pecker, F. (1999) J. Biol. Chem. 274, 628-637). In the present work, we demonstrate that beta(2)-AR agonists trigger arachidonic acid release via translocation and activation of cytosolic phospholipase A(2) (cPLA(2)) and increase caffeine-releasable Ca(2+) pools from Fura-2-loaded cells. We also show that beta(2)-AR agonists trigger a rapid and dose-dependent phosphorylation of both p38 and p42/44 MAPKs. Translocation and activation of cPLA(2), as well as Ca(2+) accumulation in sarcoplasmic reticulum stores sensitive to caffeine and amplification of [Ca(2+)](i) cycling in response to beta(2)-AR agonists, were blocked by inhibitors of the p38 or p42/44 MAPK pathway (SB203580 and PD98059, respectively), suggesting a role of both MAPK subtypes in beta(2)-AR stimulation. In contrast, beta(1)-AR stimulation of [Ca(2+)](i) cycling was rather limited by the MAPKs, clearly proving the divergence between beta(2)-AR and beta(1)-AR signaling systems. This study presents the first evidence for the coupling of beta(2)-AR to cardiac cPLA(2) and points out the key role of the MAPK pathway in the intracellular signaling elicited by positive inotropic beta(2)-AR agonists in heart.