Stoichiometric traits of stickleback: Effects of genetic background,rearing environment,and ontogeny

Phenotypes can both evolve in response to, and affect, ecosystem change, but few examples of diverging ecosystem‐effect traits have been investigated. Bony armor traits of fish are good candidates for this because they evolve rapidly in some freshwater fish populations, and bone is phosphorus rich and likely to affect nutrient recycling in aquatic ecosystems. Here, we explore how ontogeny, rearing environment, and bone allocation among body parts affect the stoichiometric phenotype (i.e., stoichiometric composition of bodies and excretion) of threespine stickleback. We use two populations from distinct freshwater lineages with contrasting lateral plating phenotypes (full vs. low plating) and their hybrids, which are mostly fully plated. We found that ontogeny, rearing environment, and body condition were the most important predictors of organismal stoichiometry. Although elemental composition was similar between both populations and their hybrids, we found significant divergence in phosphorus allocation among body parts and in phosphorus excretion rates. Overall, body armor differences did not explain variation in whole body phosphorus, phosphorus allocation, or phosphorus excretion. Evolutionary divergence between these lineages in both allocation and excretion is likely to have important direct consequences for ecosystems, but may be mediated by evolution of multiple morphological or physiological traits beyond plating phenotype.     

The implications of immunopathology for parasite evolution

By definition, parasites harm their hosts, but in many infections much of the pathology is driven by the host immune response rather than through direct damage inflicted by parasites. While these immunopathological effects are often well studied and understood mechanistically in individual disease interactions, there remains relatively little understanding of their broader impact on the evolution of parasites and their hosts. Here, we theoretically investigate the implications of immunopathology, broadly defined as additional mortality associated with the host's immune response, on parasite evolution. In particular, we examine how immunopathology acting on different epidemiological traits (namely transmission, virulence and recovery) affects the evolution of disease severity. When immunopathology is costly to parasites, such that it reduces their fitness, for example by decreasing transmission, there is always selection for increased disease severity. However, we highlight a number of host-parasite interactions where the parasite may benefit from immunopathology, and highlight scenarios that may lead to the evolution of slower growing parasites and potentially reduced disease severity. Importantly, we find that conclusions on disease severity are highly dependent on how severity is measured. Finally, we discuss the effect of treatments used to combat disease symptoms caused by immunopathology.     

THE COEVOLUTIONARY IMPLICATIONS OF HOST TOLERANCE

Host tolerance to infectious disease, whereby hosts do not directly “fight” parasites but instead ameliorate the damage caused, is an important defense mechanism in both plants and animals. Because tolerance to parasite virulence may lead to higher prevalence of disease in a population, evolutionary theory tells us that while the spread of resistance genes will result in negative frequency dependence and the potential for diversification, the evolution of tolerance is instead likely to result in fixation. However, our understanding of the broader implications of tolerance is limited by a lack of fully coevolutionary theory. Here we examine the coevolution of tolerance across a comprehensive range of classic coevolutionary host–parasite frameworks, including equivalents of gene‐for‐gene and matching allele and evolutionary invasion models. Our models show that the coevolution of host tolerance and parasite virulence does not lead to the generation and maintenance of diversity through either static polymorphisms or through “Red‐queen” cycles. Coevolution of tolerance may however lead to multiple stable states leading to sudden shifts in parasite impacts on host health. More broadly, we emphasize that tolerance may change host–parasite interactions from antagonistic to a form of “apparent commensalism,” but may also lead to the evolution of parasites that are highly virulent in nontolerant hosts.     

Synergy between the KEAP1/NRF2 and PI3K Pathways Drives Non-Small-Cell Lung Cancer with an Altered Immune Microenvironment

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Modulation of an IDP binding mechanism and rates by helix propensity and non-native interactions: association of HIF1α with CBP

Intrinsically disordered proteins that acquire their three dimensional structures only upon binding to their targets are very important in cellular signal regulation. While experimental studies have been made on the structures of both bound (structured) and unbound (disordered) states, less is known about the actual folding-binding transition. Coarse grained simulations using native-centric (i.e. Gō) potentials have been particularly useful in addressing this problem, given the large search space for IDP binding, but have well-known deficiencies in reproducing the unfolded state structure and dynamics. Here, we investigate the interaction of HIF1α with CBP using a hierarchy of coarse-grained models, in each case matching the binding affinity at 300 K to the experimental value. Starting from a pure Gō-like model based on the native structure of the complex we go on to consider a more realistic model of helix propensity in the HIF1α, and finally the effect of non-native interactions between binding partners. We find structural disorder (i.e."fuzziness") in the bound state of HIF1α in all models which is supported by the results of atomistic simulations. Correcting the over-stabilized helices in the unbound state gives rise to a more cooperative folding-binding transition (destabilizing partially bound intermediates). Adding non-native contacts lowers the free energy barrier for binding to an almost barrierless scenario, leading to higher binding/unbinding rates relative to the other models, in better agreement with the near diffusion-limited binding rates measured experimentally. Transition state structures for the three models are highly disordered, supporting a fly-casting mechanism for binding.     

INTERCELLULAR ADHESIONS IN THE POLLEN-STIGMA SYSTEM: POLLEN CAPTURE,GRAIN BINDING,AND TUBE ATTACHMENTS

Four independent pollen-stigma binding forces are differentiated after pollen contacts stigmas of Brassica oleracea var. capitata. Identification is based on their different rates and sequence of appearance during gametophyte development; on their differential occurrence after compatible and incompatible pollinations; and on their different stabilities to NaOH and hexane. The first binding force develops most rapidly, begins seconds after pollen-stigma contact, is complete within minutes, occurs on compatible or incompatible papillae, and dissociates in methanol. A second slower binding reaction begins about 15 min after contact, continues for at least 90 min (when pollen tubes emerge), results in a binding structure termed the ocreatine, develops only on compatible papillae, and is dissociated by NaOH. A third attractive mechanism binds the tip of the emerging tube to a cuticle, is detected only on incompatible papillae, and is not dissociated by NaOH or methanol. Ocreatine formation and tube development beyond the emergence stage are prevented by the incompatibility response. A fourth attraction mechanism occurs between the surfaces of papilla and elongating tubes. Reviews of physical and biochemical evidence indicate that van der Waals forces and enzymatically mediated lipid polymerization are alternatives to agglutination as mechanisms for binding male gametophyte to papilla.     

Tatlockia micdadei (Pittsburgh pneumonia agent) growth kinetics may explain its infrequent isolation from water and the low prevalence of Pittsburgh pneumonia.

Sediment and indigenous microflora taken from water distribution systems has been shown to promote the survival of Legionella pneumophila. The effect of sediment and indigenous microflora on Tatlockia micdadei (Pittsburgh pneumonia agent, PPA) was evaluated by growth curve experiments. Symbiosis between PPA and environmental bacteria was demonstrated by satellitism experiments. Unlike L. pneumophila, the concentration of PPA remained stationary in test tube suspensions containing both microflora and sediment. The difference in the ecology between the two organisms may explain the infrequent environmental recovery of PPA and, ultimately, the epidemiologic differences between Legionnaires disease and Pittsburgh pneumonia.     

Effectiveness of handwashing agents in eliminating Staphylococcus aureus from gloved hands.

The recent emphasis on gloving has resulted in accounts of healthcare workers washing gloves instead of changing them. This study evaluated the efficacy of soap and three germicidal agents in decontaminating latex and vinyl medical gloves that were experimentally contaminated with Staphylococcus aureus. Gloves were tested for perforations before and after the glove-washing procedure. Results of this study demonstrated that contamination was reduced from the glove surfaces. Although the routine washing of gloved hands cannot be recommended, it may be carried out under limited circumstances.