Exome sequences and multi‐environment field trials elucidate the genetic basis of adaptation in barley

Broadening the genetic base of crops is crucial for developing varieties to respond to global agricultural challenges such as climate change. Here, we analysed a diverse panel of 371 domesticated lines of the model crop barley to explore the genetics of crop adaptation. We first collected exome sequence data and phenotypes of key life history traits from contrasting multi‐environment common garden trials. Then we applied refined statistical methods, including some based on exomic haplotype states, for genotype‐by‐environment (G×E) modelling. Sub‐populations defined from exomic profiles were coincident with barley's biology, geography and history, and explained a high proportion of trial phenotypic variance. Clear G×E interactions indicated adaptation profiles that varied for landraces and cultivars. Exploration of circadian clock‐related genes, associated with the environmentally adaptive days to heading trait (crucial for the crop's spread from the Fertile Crescent), illustrated complexities in G×E effect directions, and the importance of latitudinally based genic context in the expression of large‐effect alleles. Our analysis supports a gene‐level scientific understanding of crop adaption and leads to practical opportunities for crop improvement, allowing the prioritisation of genomic regions and particular sets of lines for breeding efforts seeking to cope with climate change and other stresses.     

Regulation fo protein kinase C activity by various lipids

Protein kinase C has recently attracted considerable attention because of its importance in the control of cell division, cell differentiation, and signal transduction across the cell membrane. The activity of this enzyme is altered by several lipids such as diacylglycerol, free fatty acids, lipoxins, gangliosides, and sulfatides. These lipids may interact with protein kinase C either directly or through calcium ions and produce their regulatory effect (activation or inhibition) on the activities of the enzymes phosphorylated by this kinase. These processes widen our perspective of the regulation of intercellular and intracelluular communication.Abbreviations used (PK-C) Protein kinase C - (cAMP-PK) cAMP dependent protein kinase - (DAG) diacylglycerol - (PtdSer) phosphatidylserine - (InsP ₃) inositol 1,4,5-trisphosphate - (PtdIns 4,5-P₂) inositol 4,5 bisphosphate - (FFA) free fatty acid - (MBP) myelin basic protein - (ATP) adenosine triphosphate - (GTP) guanine triphosphate - (TPA) 12-tetradecanoylphorbol-13-acetate - (EGF) epidermal growth factor - (PDGF) platelet derived growth factor - (NeuNAc) and N-acetylneuraminic acid     

The importance of predation,substrate and spatial refugia in determining lotic insect distributions

An experiment was conducted to evaluate the interaction between predation, substrate, and spatial refugia in the organization of a stream insect community (Reeds Creek, Pendleton Co., West Virginia). Patterns of insect colonization were compared between fish exclusion cages and open controls that allowed access to vertebrate predators. Each cage contained 4 different substrates that varied in the relative amount of spatial refugia. Fish had little influence on the diversity or abundance of any insect taxa, even when spatial refugia were limited. The only significant effect due to predation, was an increased diversity of large (>8 mm) invertebrates in the absence of predators. However, because these taxa were relatively rare, the overall role of fish predation on insect community structure was minimal.In contrast, substrate had a marked effect on insect colonization. Insects were always more abundant (number/basket) on loose substrates containing large numbers of interstitial spaces, compared to cement-embedded substrates with few refuges available. In addition, invertebrates were more abundant on loose gravel compared to loose cobbles. Howver, when substrate preferencesrd were examined according to insect density (number/m²), loose cobbles were generally the preferred substrate. The present experiment rejects the hypothesis that patterns of substrate colonization can be explained as differential insect mortality by predators, due to varying amounts of refugia. Alternative mechanisms such as differing amounts of trapped detritus and substrate surface area may account for substrate preference.     

Acknowledgments

One of the major causes of worldwide amphibian declines is a skin infection caused by a pathogenic chytrid fungus (Batrachochytrium dendrobatidis). This study documents the interactions between this pathogen and a susceptible amphibian host, the boreal toad (Bufo boreas). The amount of time following exposure until death is influenced by the dosage of infectious zoospores, duration of exposure, and body size of the toad. The significant relation between dosage and the number of days survived (dose-response curve) supports the hypothesis that the degree of infection must reach a particular threshold of about 10⁷–10⁸ zoosporangia before death results. Variation in air temperature between 12°C and 23°C had no significant effect on survival time. The infection can be transmitted from infected to healthy animals by contact with water containing zoospores; no physical contact between animals is required. These results are correlated with observations on the population biology of boreal toads in which mortalities associated with B. dendrobatidis have been identified.     

Characterization of the genome of Pseudomonas aeruginosa bacteriophage phi PLS27 with particular reference to the ends of the DNA.

The DNA of Pseudomonas aeruginosa rough-specific bacteriophage phi PLS27 was studied. The genome size as determined by summing the sizes of restriction fragments was 42.7 kilobase pairs. Of particular interest was the fact that the DNA was insensitive to certain common restriction endonucleases including EcoRI, BamHI, and HindIII. The ends of the phage DNA were cloned and sequenced, revealing direct repeats of 318 nucleotides. The left end of the genome when cloned into the promoter selection vector pKK232-8 exhibited promoter activity in Escherichia coli. Two promoters bearing greater than 70% sequence homology to the plasmid pNM74 TOL operon and PAK pilin promoters were identified.     

The role of the hemiparasitic annual Rhinanthus minor in determining grassland community structure

Summary Rhinanthus minor (yellow-rattle) is a widespread hemiparasitic plant of grassland habitats throughout Great Britain. It is usually considered to be indicative of species-rich grassland, but in a survey of 14 habitats throughout Britain it was found that R. minor at the time of flowering normally occupied relatively low-diversity patches within areas of high diversity as determined by the number of species, Simpson's Index and the Shannon-Wiener Index. Following the death of adult plants of R. minor in the summer it was shown that the pattern of species diversity changed such that by the time R. minor germinated in the following spring the differences between the areas containing and not containing R. minor were much less distinct. A perturbation experiment in which R. minor was removed from four sites indicated that the effect of the removal of R. minor on the development of community structure over the next year was to increase species diversity on three of the sites and decrease it on the fourth. Those species which responded to the removal of R. minor by an increase in abundance were shown to be preferred hosts. All three lines of evidence point to the fact R. minor has a significant effect on the species diversity of the communities in which it grows by selectively parasitizing components of the flora and modifying the competitive relationships between plants. However, as the communities generally responded to the removal of R. minor by an increase in diversity and as the general survey indicated that R. minor is generally associated with areas of low diversity it would appear that the plants which are selectively parasitized are generally not the competitive dominants in the community.     

The burden of common infectious disease syndromes at the clinic and household level from population-based surveillance in rural and urban Kenya

Background

Characterizing infectious disease burden in Africa is important for prioritizing and targeting limited resources for curative and preventive services and monitoring the impact of interventions.

Methods

From June 1, 2006 to May 31, 2008, we estimated rates of acute lower respiratory tract illness (ALRI), diarrhea and acute febrile illness (AFI) among >50,000 persons participating in population-based surveillance in impoverished, rural western Kenya (Asembo) and an informal settlement in Nairobi, Kenya (Kibera). Field workers visited households every two weeks, collecting recent illness information and performing limited exams. Participants could access free high-quality care in a designated referral clinic in each site. Incidence and longitudinal prevalence were calculated and compared using Poisson regression.

Results

Incidence rates resulting in clinic visitation were the following: ALRI — 0.36 and 0.51 episodes per year for children <5 years and 0.067 and 0.026 for persons ≥5 years in Asembo and Kibera, respectively; diarrhea — 0.40 and 0.71 episodes per year for children <5 years and 0.09 and 0.062 for persons ≥5 years in Asembo and Kibera, respectively; AFI — 0.17 and 0.09 episodes per year for children <5 years and 0.03 and 0.015 for persons ≥5 years in Asembo and Kibera, respectively. Annually, based on household visits, children <5 years in Asembo and Kibera had 60 and 27 cough days, 10 and 8 diarrhea days, and 37 and 11 fever days, respectively. Household-based rates were higher than clinic rates for diarrhea and AFI, this difference being several-fold greater in the rural than urban site.

Conclusions

Individuals in poor Kenyan communities still suffer from a high burden of infectious diseases, which likely hampers their development. Urban slum and rural disease incidence and clinic utilization are sufficiently disparate in Africa to warrant data from both settings for estimating burden and focusing interventions.     

Increased formation of short-chain organic acids after chronic ethanol administration and its interaction with the carnitine pool in rat

Organic acidurias are genetic disorders of mitochondrial metabolism that lead to the accumulation of organic acids in tissues and biological fluids. It has been demonstrated that interaction of carnitine with the cellular coenzyme A (CoA) pool, through the production of acyl-carnitines, is potentially critical for maintaining normal cellular metabolism under condition of impaired acyl-CoA use and that exposure of humans and other mammals to ethanol leads to impairment of mitochondrial function. The aim of the present study was to evaluate the role of chronic administration of ethanol on urinary excretion of short-chain organic acids and endogenous carnitines in rats. The data reported show that chronic administration of ethanol significantly increases urinary excretion of propionate, methylmalonate, as well as free acetate, butyrate, pyruvate, lactate, and beta-hydroxybutyrate. Chronic administration of propranolol abolished ethanol-dependent accumulation of propionate, suggesting involvement of beta-adrenergic mechanisms. Increased formation of propionate and methylmalonate was associated with decreased plasma carnitine levels and with increased excretion of specific acyl-carnitines, corresponding to the accumulating acyl groups. Our data indicate that chronic alcohol ingestion induces increased excretion of selected organic acids and that the endogenous carnitine pool might exert a protective role against the deleterious effects of accumulating short-chain organic acids.     

Level of Toll-like receptor agonist exposure differentially determines chemokine production in humans

Toll-like receptor (TLR) agonists, ubiquitously present in the environment, are key players in activating synthesis of cytokines and chemokines that control normal and pathophysiological processes, including multiple inflammatory diseases. TLR2 and TLR4 respond to bacterial cell wall products. We examined the impact of TLR activation on human immune capacity using stimuli ranging from the low levels seen in most environments to the high concentrations widely used for in vitro studies. Peripheral blood mononuclear cells from 117 healthy children were activated with lipopolysaccharide (TLR4 ligand) or peptidoglycan (TLR2 ligand) over a million-fold range of concentrations. Resulting interleukin-6, CCL2, and CCL22 production were quantified by ELISA. The intensity of cytokine production elicited was linearly related to the intensity of the stimulus up to maximal responses. In marked contrast, chemokine production was not linearly related to agonist concentration. Responses rose with increasing stimulation, and then were markedly reduced (40%-100%, p < 0.0001) in response to the high levels of TLR stimulation most commonly cited. Thus, the levels of TLR4 and TLR2 agonists typically used for in vitro interrogation of immune capacity yield results clearly distinct from those obtained using commonly occurring environmental levels of TLR ligands. These findings demonstrate the importance of utilizing TLR ligands at concentrations more closely mimicking environmental levels when assessing immune capacity.