The original colours of fossil beetles

Structural colours, the most intense, reflective and pure colours in nature, are generated when light is scattered by complex nanostructures. Metallic structural colours are widespread among modern insects and can be preserved in their fossil counterparts, but it is unclear whether the colours have been altered during fossilization, and whether the absence of colours is always real. To resolve these issues, we investigated fossil beetles from five Cenozoic biotas. Metallic colours in these specimens are generated by an epicuticular multi-layer reflector; the fidelity of its preservation correlates with that of other key cuticular ultrastructures. Where these other ultrastructures are well preserved in non-metallic fossil specimens, we can infer that the original cuticle lacked a multi-layer reflector; its absence in the fossil is not a preservational artefact. Reconstructions of the original colours of the fossils based on the structure of the multi-layer reflector show that the preserved colours are offset systematically to longer wavelengths; this probably reflects alteration of the refractive index of the epicuticle during fossilization. These findings will allow the former presence, and original hue, of metallic structural colours to be identified in diverse fossil insects, thus providing critical evidence of the evolution of structural colour in this group.     

Gill microsomal (Na+,K+)-ATPase from the blue crab Callinectes danae: Interactions at cationic sites

Euryhaline crustaceans tolerate exposure to a wide range of dilute media, using compensatory, ion regulatory mechanisms. However, data on molecular interactions occurring at cationic sites on the crustacean gill (Na⁺,K⁺)-ATPase, a key enzyme in this hyperosmoregulatory process, are unavailable. We report that Na⁺ binding at the activating site leads to cooperative, heterotropic interactions that are insensitive to K⁺. The binding of K⁺ ions to their high affinity sites displaces Na⁺ ions from their sites. The increase in Na⁺ ion concentrations increases heterotropic interactions with the K⁺ ions, with no changes in K_0.5 for K⁺ ion activation at the extracellular sites. Differently from mammalian (Na⁺,K⁺)-ATPases, that from C. danae exhibits additional NH₄⁺ ion binding sites that synergistically activate the enzyme at saturating concentrations of Na⁺ and K⁺ ions. NH₄⁺ binding is cooperative, and heterotropic NH₄⁺ ion interactions are insensitive to Na⁺ ions, but Na⁺ ions displace NH₄⁺ ions from their sites. NH₄⁺ ions also displace Na⁺ ions from their sites. Mg²⁺ ions modulate enzyme stimulation by NH₄⁺ ions, displacing NH₄⁺ ion from its sites. These interactions may modulate NH₄⁺ ion excretion and Na⁺ ion uptake by the gill epithelium in euryhaline crustaceans that confront hyposmotic media.     

Regulation and execution of molecular disassembly and catabolism during senescence

Senescence is a highly orchestrated developmental stage in the life cycle of plants. The onset of senescence is tightly controlled by signaling cascades that initiate changes in gene expression and the synthesis of new proteins. This complement of new proteins includes hydrolytic enzymes capable of executing catabolism of macromolecules, which in turn sets in motion disassembly of membrane molecular matrices, leading to loss of cell function and, ultimately, complete breakdown of cellular ultrastructure. A distinguishing feature of senescence that sets it apart from other types of programmed cell death is the recovery of carbon and nitrogen from the dying tissue and their translocation to growing parts of the plant such as developing seeds. For this to be accomplished, the initiation of senescence and its execution have to be meticulously regulated. For example, the initiation of membrane disassembly has to be intricately linked with the recruitment of nutrients because their ensuing translocation out of the senescing tissue requires functional membranes. Molecular mechanisms underlying this linkage and its integration with the catabolism of macromolecules in senescing tissues are addressed.     

Do we expect natural selection to produce rational behaviour?

We expect that natural selection should result in behavioural rules which perform well; however, animals (including humans) sometimes make bad decisions. Researchers account for these with a variety of explanations; we concentrate on two of them. One explanation is that the outcome is a side effect; what matters is how a rule performs (in terms of reproductive success). Several rules may perform well in the environment in which they have evolved, but their performance may differ in a 'new' environment (e.g. the laboratory). Some rules may perform very badly in this environment. We use the debate about whether animals follow the matching law rather than maximizing their gains as an illustration. Another possibility is that we were wrong about what is optimal. Here, the general idea is that the setting in which optimal decisions are investigated is too simple and may not include elements that add extra degrees of freedom to the situation.     

Long-Term Consequences of Grazing and Burning on Northern Peatland Carbon Dynamics

Abstract Using a 50-year-old field experiment, we investigated the effects of the long-term land management practices of repeated burning and grazing on peatland vegetation and carbon dynamics (C). Plant community composition, C stocks in soils and vegetation, and C fluxes of CO₂, CH₄ and DOC, were measured over an 18-month period. We found that both burning and grazing reduced aboveground C stocks, and that burning reduced C stocks in the surface peat. Both burning and grazing strongly affected vegetation community composition, causing an increase in graminoids and a decrease in ericoid subshrubs and bryophytes relative to unburned and ungrazed controls; this effect was especially pronounced in burned treatments. Soil microbial properties were unaffected by grazing and showed minor responses to burning, in that the C:N ratio of the microbial biomass increased in burned relative to unburned treatments. Increases in the gross ecosystem CO₂ fluxes of respiration and photosynthesis were observed in burned and grazed treatments relative to controls. Here, the greatest effects were seen in the burning treatment, where the mean increase in gross fluxes over the experimental period was greater than 40%. Increases in gross CO₂ fluxes were greatest during the summer months, suggesting an interactive effect of land use and climate on ecosystem C cycling. Collectively, our results indicate that long-term management of peatland has marked effects on ecosystem C dynamics and CO₂ flux, which are primarily related to changes in vegetation community structure.     

Transgene-enforced co-stimulation of CD4+ T cells leads to enhanced and sustained anti-tumor effector functioning

Background The role of co-stimulation in CD4+ T cell activation by professional APC is well established, while less is known of the role co-stimulation plays when CD4+ T cells interact directly with tumor cells. Methods Through genetic engineering of human CD4+ T cells, we tested the hypothesis that integration of co-stimulatory signaling domains within a tumor-targeting chimeric Ag receptor (CAR), the IL-13Ralpha2-specific IL-13-zetakine (IL13zeta), would enhance CD4+ T cell mediated responses against tumors that fail to express ligands for co-stimulatory receptors. Results Compared with CD3zeta-mediated activation alone, CD4+ effector T cells expressing the IL13-CD28-41BBzeta CAR exhibited augmented/sustained MAPK and AKT activity, up-regulated Th1 cytokine production, and enhanced cytolytic potency against tumor targets. Moreover, upon recursive stimulation with tumor, the IL13-CD28-41BBzeta+ cells retained/recycled their lytic function, whereas IL-13zeta+ CD4+ cells became anergic/exhausted. These in vitro observations correlated with enhanced in vivo control of established orthotopic CNS glioma xenografts in immunodeficient mice mediated by adoptively transferred ex vivo-expanded CD4+ T cells expressing the co-stimulatory CAR. Discussion Together these studies demonstrate the importance of integrating co-stimulation with CD3zeta signaling events to activate fully CD4+ anti-tumor effector cells for sustained function in the tumor microenvironment.     

Sexual conflict over parental care promotes the evolution of sex differences in care and the ability to care

Strong asymmetries in parental care, with one sex providing more care than the other, are widespread across the animal kingdom. At present, two factors are thought to ultimately cause sex differences in care: certainty of parentage and sexual selection. By contrast, we here show that the coevolution of care and the ability to care can result in strong asymmetries in both the ability to care and the level of care, even in the absence of these factors. While the coevolution of care and the ability to care does not predict which sex evolves to care more than the other, once other factors give rise to even the slightest differences in the cost and benefits of care between the sexes (e.g. differences in certainty in parentage), a clear directionality emerges; the sex with the lower cost or higher benefit of care evolves both to be more able to care and to provide much higher levels of care than the other sex. Our findings suggest that the coevolution of levels of care and the ability to care may be a key factor underlying the evolution of sex differences in care.     

Altered Mechanical Environment of Bone Cells in an Animal Model of Short- and Long-Term Osteoporosis

Alterations in bone tissue composition during osteoporosis likely disrupt the mechanical environment of bone cells and may thereby initiate a mechanobiological response. It has proved challenging to characterize the mechanical environment of bone cells in vivo, and the mechanical environment of osteoporotic bone cells is not known. The objective of this research is to characterize the local mechanical environment of osteocytes and osteoblasts from healthy and osteoporotic bone in a rat model of osteoporosis. Using a custom-designed micromechanical loading device, we apply strains representative of a range of physical activity (up to 3000 με) to fluorescently stained femur samples from normal and ovariectomized rats. Confocal imaging was simultaneously performed, and digital image correlation techniques were applied to characterize cellular strains. In healthy bone tissue, osteocytes experience higher maximum strains (31,028 ± 4213 με) than osteoblasts (24,921 ± 3,832 με), whereas a larger proportion of the osteoblast experiences strains >10,000 με. Most interestingly, we show that osteoporotic bone cells experience similar or higher maximum strains than healthy bone cells after short durations of estrogen deficiency (5 weeks), and exceeded the osteogenic strain threshold (10,000 με) in a similar or significantly larger proportion of the cell (osteoblast, 12.68% vs. 13.68%; osteocyte, 15.74% vs. 5.37%). However, in long-term estrogen deficiency (34 weeks), there was no significant difference between bone cells in healthy and osteoporotic bone. These results suggest that the mechanical environment of bone cells is altered during early-stage osteoporosis, and that mechanobiological responses act to restore the mechanical environment of the bone tissue after it has been perturbed by ovariectomy.     

Substrate and inhibitor specificities differ between human cytosolic and mitochondrial thioredoxin reductases: Implications for development of specific inhibitors

The cytosolic and mitochondrial thioredoxin reductases (TrxR1 and TrxR2) and thioredoxins (Trx1 and Trx2) are key components of the mammalian thioredoxin system, which is important for antioxidant defense and redox regulation of cell function. TrxR1 and TrxR2 are selenoproteins generally considered to have comparable properties, but to be functionally separated by their different compartments. To compare their properties we expressed recombinant human TrxR1 and TrxR2 and determined their substrate specificities and inhibition by metal compounds. TrxR2 preferred its endogenous substrate Trx2 over Trx1, whereas TrxR1 efficiently reduced both Trx1 and Trx2. TrxR2 displayed strikingly lower activity with dithionitrobenzoic acid (DTNB), lipoamide, and the quinone substrate juglone compared to TrxR1, and TrxR2 could not reduce lipoic acid. However, Sec-deficient two-amino-acid-truncated TrxR2 was almost as efficient as full-length TrxR2 in the reduction of DTNB. We found that the gold(I) compound auranofin efficiently inhibited both full-length TrxR1 and TrxR2 and truncated TrxR2. In contrast, some newly synthesized gold(I) compounds and cisplatin inhibited only full-length TrxR1 or TrxR2 and not truncated TrxR2. Surprisingly, one gold(I) compound, [Au(d2pype)(2)]Cl, was a better inhibitor of TrxR1, whereas another, [(iPr(2)Im)(2)Au]Cl, mainly inhibited TrxR2. These compounds also inhibited TrxR activity in the cytoplasm and mitochondria of cells, but their cytotoxicity was not always dependent on the proapoptotic proteins Bax and Bak. In conclusion, this study reveals significant differences between human TrxR1 and TrxR2 in substrate specificity and metal compound inhibition in vitro and in cells, which may be exploited for development of specific TrxR1- or TrxR2-targeting drugs.