The Structural Basis of the Farnesylated and Methylated KRas4B Interaction with Calmodulin

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Population source affects competitive response and effect in a C4 grass (Panicum virgatum)

Grassland restoration success depends on the development of plant communities that accord with restoration goals. Intraspecific variation in competitiveness may affect community development. For some grassland species, germplasm can be obtained from sources ranging from wild collections to selectively bred cultivars. The extent to which population source affects competitive outcomes in restoration projects is unclear. We addressed this knowledge gap in a glasshouse experiment comparing competitive response and effect among three sources of switchgrass (Panicum virgatum) that are available for restoration: selectively bred cultivars, commercial ecotypes (commercially produced but not deliberately selected), and wild collections. Two strains per source type were grown with four associates chosen to encompass varied functional groups: conspecifics, Bromus inermis, Cirsium arvense, and Solanum ptycanthum. Switchgrass competitive response was evaluated for survival, height, biomass, and shoot:root biomass ratio; competitive effect was assessed as associate survival, height, biomass, and shoot:root ratio. Competitive responses of cultivars and commercial ecotypes were broadly similar, although cultivar biomass exceeded both that of ecotypes and wild collections, and ecotypes had the highest shoot:root ratio. Wild collections were most negatively affected by competition. The shoot:root ratios of all sources were highest when grown with S. ptycanthum, indicating that competitive responses were plastic; plasticity in fitness‐related traits can contribute to persistence in variable environments. Cultivars exerted negative effects on B. inermis. Secondary analyses indicated that all switchgrass sources were most inhibited by the annual S. ptycanthum. To summarize, population source affected multiple aspects of switchgrass competitive ability, when grown against functionally varied associates.     

Wolbachia infection can bias estimates of intralocus sexual conflict

Males and females share most of their genome and develop many of the same traits. However, each sex frequently has different optimal values for these shared traits, creating intralocus sexual conflict. This conflict has been observed in wild and laboratory populations of insects and affects important evolutionary processes such as sexual selection, the maintenance of genetic variation, and possibly even speciation. Given the broad impacts of intralocus conflict, accurately detecting and measuring it is important. A common way to detect intralocus sexual conflict is to calculate the intersexual genetic correlation for fitness, with negative values suggesting conflict. Here, we highlight a potential confounder of this measure—cytoplasmic incompatibility caused by the intracellular parasite Wolbachia. Infection with Wolbachia can generate negative intersexual genetic correlations for fitness in insects, suggestive of intralocus sexual conflict. This is because cytoplasmic incompatibility reduces the fitness of uninfected females mated to infected males, while uninfected males will not suffer reductions in fitness if they mate with infected females and may even be fitter than infected males. This can lead to strong negative intersexual genetic correlations for fitness, mimicking intralocus conflict. We illustrate this issue using simulations and then present Drosophila simulans data that show how reproductive incompatibilities caused by Wolbachia infection can generate signals of intralocus sexual conflict. Given that Wolbachia infection in insect populations is pervasive, but populations usually contain both infected and uninfected individuals providing scope for cytoplasmic incompatibility, this is an important consideration for sexual conflict research but one which, to date, has been largely underappreciated.     

Assessing factors associated with changes in the numbers of birds visiting gardens in winter: Are predators partly to blame?

The factors governing the recent declines observed in many songbirds have received much research interest, in particular whether increases of avian predators have had a negative effect on any of their prey species. In addition, further discussion has centered on whether or not the choice of model formulation has an effect on model inference. The study goal was to evaluate changes in the number of 10 songbird species in relation to a suite of environmental covariates, testing for any evidence in support of a predator effect using multiple model formulations to check for consistency in the results. We compare two different approaches to the analysis of long‐term garden bird monitoring data. The first approach models change in the prey species between 1970 and 2005 as a function of environmental covariates, including the abundance of an avian predator, while the second uses a change–change approach. Significant negative relationships were found between Eurasian Sparrowhawk Accipiter nisus and three of the 10 species analyzed, namely house Sparrow Passer domesticus, starling Sturnus vulgaris, and blue tit Cyanistes caeruleus. The results were consistent under both modeling approaches. It is not clear if this is a direct negative impact on the overall populations of these species or a behavioral response of the prey species to avoid feeding stations frequented by Sparrowhawks (which may in turn have population consequences, by reducing available resources). The species showing evidence of negative effects of Sparrowhawks were three of the four species most at risk to Sparrowhawk predation according to their prevalence in the predator's diet. The associations could be causal in nature, although in practical terms the reduction in the rate of change in numbers visiting gardens accredited to Sparrowhawks is relatively small, and so unlikely to be the main driver of observed population declines.     

Evolutionary history predicts high‐impact invasions by herbivorous insects

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N-terminal truncation of antiapoptotic MCL1, but not G2/M-induced phosphorylation, is associated with stabilization and abundant expression in tumor cells

The antiapoptotic BCL2 family member MCL1 is normally up- and down-modulated in response to environmental signals and conditions, but is constitutively expressed in cancer where it promotes cell survival and drug resistance. A post-translational modification identified here, truncation at the N terminus, was found to act along with previously described ERK- and GSK3-induced phosphorylation events to regulate the turnover of the MCL1 protein and thus its availability for antiapoptotic effects. Although both N-terminally truncated and full-length MCL1 contain sequences enriched in proline, glutamic acid, serine, and threonine and were susceptible to proteasomal degradation, the truncated form decayed less rapidly and was maintained for an extended period in the presence of ERK activation. This was associated with extended cell survival because the truncated form of MCL1 (unlike those of BCL2 and BCLX) retained antiapoptotic activity. N-terminal truncation slightly increased the electrophoretic mobility of MCL1 and differed from the phosphorylation/band shift to decreased mobility, which occurs in the G2/M phase and was not found to affect MCL1 turnover. The N-terminally truncated form of MCL1 was expressed to varying extents in normal lymphoid tissues and was the predominant form present in lymphomas from transgenic mice and human tumor lines of B-lymphoid origin. The degradation versus stabilized expression of antiapoptotic MCL1 is thus controlled by N-terminal truncation as well as by ERK- and GSK3 (but not G2/M)-induced phosphorylation. These modifications may contribute to dysregulated MCL1 expression in cancer and represent targets for promoting its degradation to enhance tumor cell death.     

Phosphorylation of Parkin by the cyclin-dependent kinase 5 at the linker region modulates its ubiquitin-ligase activity and aggregation

Mutations in Parkin are responsible for a large percentage of autosomal recessive juvenile parkinsonism cases. Parkin displays ubiquitin-ligase activity and protects against cell death promoted by several insults. Therefore, regulation of Parkin activities is important for understanding the dopaminergic cell death observed in Parkinson disease. We now report that cyclin-dependent kinase 5 (Cdk5) phosphorylates Parkin both in vitro and in vivo. We found that highly specific Cdk5 inhibitors and a dominant negative Cdk5 construct inhibited Parkin phosphorylation, suggesting that a significant portion of Parkin is phosphorylated by Cdk5. Parkin interacts with Cdk5 as observed by co-immunoprecipitation experiments of transfected cells and rat brains. Phosphorylation by Cdk5 decreased the auto-ubiquitylation of Parkin both in vitro and in vivo. We identified Ser-131 located at the linker region of Parkin as the major Cdk5 phosphorylation site. The Cdk5 phosphorylation-deficient S131A Parkin mutant displayed a higher auto-ubiquitylation level and increased ubiquitylation activity toward its substrates synphilin-1 and p38. Additionally, the S131A Parkin mutant more significantly accumulated into inclusions in human dopaminergic cells when compared with the wild-type Parkin. Furthermore, S131A Parkin mutant increased the formation of synphilin-1/alpha-synuclein inclusions, suggesting that the levels of Parkin phosphorylation and ubiquitylation may modulate the formation of inclusion bodies relevant to the disease. The data indicate that Cdk5 is a new regulator of the Parkin ubiquitin-ligase activity and modulates its ability to accumulate into and modify inclusions. Phosphorylation by Cdk5 may contribute to the accumulation of toxic Parkin substrates and decrease the ability of dopaminergic cells to cope with toxic insults in Parkinson disease.     

Integration of biological networks and gene expression data using Cytoscape

Cytoscape is a free software package for visualizing, modeling and analyzing molecular and genetic interaction networks. This protocol explains how to use Cytoscape to analyze the results of mRNA expression profiling, and other functional genomics and proteomics experiments, in the context of an interaction network obtained for genes of interest. Five major steps are described: (i) obtaining a gene or protein network, (ii) displaying the network using layout algorithms, (iii) integrating with gene expression and other functional attributes, (iv) identifying putative complexes and functional modules and (v) identifying enriched Gene Ontology annotations in the network. These steps provide a broad sample of the types of analyses performed by Cytoscape.     

Affinity precipitation an option for early capture in bioprocessing

Affinity precipitation is a bioseparation technique where the affinity ligand is coupled to a stimuliresponsive polymer. Stimuli-responsive polymers show abrupt, yet reversible, phase transition (precipitation) in response to a small change in an environmental parameter. The corresponding ligand conjugates can be used to co-precipitate and thereby capture and isolate target molecules from complex solutions such as culture supernatants and cell lysates. The approach is compatible with a 'discardibles only' type of downstream process and can be scaled over several orders of magnitude. This report discusses the set-up and development of affinity precipitation procedures, the related instrumentation and scale up, as well as applications for the isolation of proteins and polynucleotides.