Evolutionary history predicts high‐impact invasions by herbivorous insects

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Cellular turnover of the polyglutamine disease protein ataxin-3 is regulated by its catalytic activity

Ataxin-3, a deubiquitinating enzyme, is the disease protein in spinocerebellar ataxia type 3, one of many neurodegenerative disorders caused by polyglutamine expansion. Little is known about the cellular regulation of ataxin-3. This is an important issue, since growing evidence links disease protein context to pathogenesis in polyglutamine disorders. Expanded ataxin-3, for example, is more neurotoxic in fruit fly models when its active site cysteine is mutated (1). We therefore sought to determine the influence of ataxin-3 enzymatic activity on various cellular properties. Here we present evidence that the catalytic activity of ataxin-3 regulates its cellular turnover, ubiquitination, and subcellular distribution. Cellular protein levels of catalytically inactive ataxin-3 were much higher than those of active ataxin-3, in part reflecting slower degradation. In vitro studies revealed that inactive ataxin-3 was more slowly degraded by the proteasome and that this degradation occurred independent of ubiquitination. Slower degradation of inactive ataxin-3 correlated with reduced interaction with the proteasome shuttle protein, VCP/p97. Enzymatically active ataxin-3 also showed a greater tendency to concentrate in the nucleus, where it colocalized with the proteasome in subnuclear foci. Taken together, these and other findings suggest that the catalytic activity of this disease-linked deubiquitinating enzyme regulates several of its cellular properties, which in turn may influence disease pathogenesis.     

Deletion of complement factor H-related genes CFHR1 and CFHR3 is associated with atypical hemolytic uremic syndrome

Atypical hemolytic uremic syndrome (aHUS) is associated with defective complement regulation. Disease-associated mutations have been described in the genes encoding the complement regulators complement factor H, membrane cofactor protein, factor B, and factor I. In this study, we show in two independent cohorts of aHUS patients that deletion of two closely related genes, complement factor H-related 1 (CFHR1) and complement factor H-related 3 (CFHR3), increases the risk of aHUS. Amplification analysis and sequencing of genomic DNA of three affected individuals revealed a chromosomal deletion of approximately 84 kb in the RCA gene cluster, resulting in loss of the genes coding for CFHR1 and CFHR3, but leaving the genomic structure of factor H intact. The CFHR1 and CFHR3 genes are flanked by long homologous repeats with long interspersed nuclear elements (retrotransposons) and we suggest that nonallelic homologous recombination between these repeats results in the loss of the two genes. Impaired protection of erythrocytes from complement activation is observed in the serum of aHUS patients deficient in CFHR1 and CFHR3, thus suggesting a regulatory role for CFHR1 and CFHR3 in complement activation. The identification of CFHR1/CFHR3 deficiency in aHUS patients may lead to the design of new diagnostic approaches, such as enhanced testing for these genes.     

Predicting spatially heterogeneous invasive spread: Pyracantha angustifolia invading a dry Andean valley in northern Argentina

Biological Invasions - Understanding the drivers of invasive species spread is key to designing optimal management programmes for controlling them. Population models, parameterized from demographic...     

In love and war: The morphometric and phylogenetic basis of ornamentation,and the evolution of male display behavior,in the livebearer genus Poecilia

Exaggerated male traits under sexual selection are often used for both competition and courtship, raising the question of whether ornaments evolved simultaneously for both functions, or if use in one context preceded use in another. Here, we apply a phylogenetic approach to study the evolution of ornamental dorsal fins in male poeciliid fish of the subgenera Mollienesia and Limia, which exhibit convergent development of an enlarged dorsal fin, and often direct erect‐fin displays to male and female conspecifics. Unlike prior categorical assessments of poeciliid adornments, we measure dorsal fin exaggeration with a continuous index of ornamentation. Phylogenetic logistic and generalized least squares regression analyses indicate that high index values are significantly associated with the use of two component postures of courtship and aggressive displays, dorsal fin erection and body curvature, but not with the presence of sexual dichromatism. Male displays initially evolved for male–male aggression in the common ancestor of Mollienesia and Limia, suggesting that this signal originated for competition, then became co‐opted for courtship. These results support the armament‐ornament hypothesis for evolution of exaggerated male traits, and are consistent with an evolutionary shift in the predominant mechanisms of sexual selection from intra‐ to intersexual.     

Towards an interactive,process‐based approach to understanding range shifts: developmental and environmental dependencies matter

Many species are undergoing distributional shifts in response to climate change. However, wide variability in range shifting rates has been observed across taxa, and even among closely‐related species. Attempts to link climate‐mediated range shifts to traits has often produced weak or conflicting results. Here we investigate interactive effects of developmental processes and environmental stress on the expression of traits relevant to range shifts. We use an individual‐based modelling approach to assess how different developmental strategies affect range shift rates under a range of environmental conditions. We find that under stressful conditions, such as at the margins of the species’ fundamental niche, investment in prolonged development leads to the greatest rates of range shifting, especially when longer time in development leads to improved fecundity and dispersal‐related traits. However, under benign conditions, and when traits are less developmentally plastic, shorter development times are preferred for rapid range shifts, because higher generational frequency increases the number of individual dispersal events occurring over time. Our results suggest that the ability of a species to range shift depends not only on their dispersal and colonisation characteristics but also how these characteristics interact with developmental strategies. Benefits of any trait always depended on the environmental and developmental sensitivity of life history trait combinations, and the environmental conditions under which the range shift takes place. Without considering environmental and developmental sources of variation in the expression of traits relevant to range shifts, there is little hope of developing a general understanding of intrinsic drivers of range shift potential.     

Truncated trkB.T1 is dominant negative inhibitor of trkB.TK+-mediated cell survival

Truncated trkB.T1 (T1) neurotrophin receptor inhibits full-length trkB.TK+ (TK+) signaling. At least two possible mechanisms have been proposed for this action: T1 could trap the ligand or function as a dominant negative receptor. To differentiate between these possibilities we have studied survival of serum-deprived PC12-trkB cells stably expressing TK+. PC12-trkB cells were observed to display constitutive trkB kinase activity which leads to survival of a cell subpopulation in the absence of added brain-derived neurotrophic factor (BDNF) and serum. Exogenous BDNF significantly increased cell survival, and this increase was inhibited by BDNF neutralizing antibody. The antibody treatment had no effect on the constitutive TK+ activity. Transfected T1 completely inhibited survival by BDNF or constitutive trkB kinase activity in PC12-trkB cells similarly to tyrosine kinase inhibitor K252a. In addition, T1 coimmunoprecipitated with TK+ and inhibited its autophosphorylation by BDNF. These data suggest that truncated T1 inhibits TK+ signaling by dominant negative action.     

Semiquantitative chemiluminescent detection of UV-B-induced point mutations in the p53 tumor-suppressor gene

The technique of allele-specific PCR (AS-PCR) enables the detection of a small number of mutant alleles in a large number of wild-type (WT) alleles. We used the AS-PCR technique and Southern blotting, using a nonradioactive labeled probe to analyze the formation of point mutations in the tumor-suppressor gene p53 of primary keratinocytes after UV-B irradiation. These permanent mutations resulting from CC dimers occur at distinct "hot-spots", one of which is affected in the human keratinocyte cell line HaCaT. This enabled us to establish the method with a defined positive control template, which also allowed semiquantitative determination of the mutation frequency. This, and the determination of the detection limit, was done with the use of serial dilutions of WT genomic DNA from primary keratinocytes with mutant genomic HaCaT DNA in the AS-PCR assay.