Molecular genetics of cell death in the nematode Caenorhabditis elegans

In C. elegans, cell death can be readily studied at the cellular, genetic, and molecular levels. Two types of death have been characterized in this nematode: (1) programmed cell death, which occurs as a normal component in development; and (2) pathological cell death which occurs aberrantly as a consequence of mutation. Analysis of mutations that disrupt programmed cell death in various ways has defined a genetic pathway for programmed cell death which includes genes that perform such functions as the determination of which cells die, the execution of cell death, the engulfment of cell corpses, and the digestion of DNA from dead cells. Molecular analysis is providing insightinto the nature of the molecules that function in these aspects of programmed cell death. Characterization of some genes that mutate to induce abnormal cell death has defined a novel gene family called degenerins that encode putative membrane proteins. Dominant alleles of at least two degenerin genes, mec-4 and deg-1, can cause cellular swelling and late onset neurodegeneration of specific groups of cells. © 1992 John Wiley & Sons, Inc.     

Towards a theory of the evolution of butterfly colour patterns under directional and disruptive selection

Two general models for the transspecific evolution of butterfly colour patterns are advanced: directional selection acting equally on both sexes, and disruptive selection involving periods of polymorphism. To consider possible outcomes of me latter process, a morphism notation based on an integrated classification for polymorphism and sexual dimorphism is developed. This notation is used to examine the properties of all morphism transformations possible from the minimal expressions of the nine morphism categories, as reached through defined minimum step changes. The significance of such pathway models is analysed in terms of general properties of butterfly polymorphism. The potential use of pathway models in evolutionary studies is briefly discussed, mainly with respect to phylogenetics, and ideas on the evolution of genetic dominance.     

Evolutionary assembly of cooperating cell types in an animal chemical defense system

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Effects of grazing intensity and grazing exclusion on litter decomposition in the temperate steppe of Nei Mongol,China

Aims Grazing intensity and grazing exclusion affect ecosystem carbon cycling by changing the plant community and soil micro-environment in grassland ecosystems. The aims of this study were: 1) to determine the effects of grazing intensity and grazing exclusion on litter decomposition in the temperate grasslands of Nei Mongol; 2) to compare the difference between above-ground and below-ground litter decomposition; 3) to identify the effects of precipitation on litter production and decomposition. Methods We measured litter production, quality, decomposition rates and soil nutrient contents during the growing season in 2011 and 2012 in four plots, i.e. light grazing, heavy grazing, light grazing exclusion and heavy grazing exclusion. Quadrate surveys and litter bags were used to measure litter production and decomposition rates. All data were analyzed with ANOVA and Pearson’s correlation procedures in SPSS. Important findings Litter production and decomposition rates differed greatly among four plots. During the two years of our study, above-ground litter production and decomposition in heavy-grazing plots were faster than those in light-grazing plots. In the dry year, below-ground litter production and decomposition in light-grazing plots were faster than those in heavy-grazing plots, which is opposite to the findings in the wet year. Short-term grazing exclusion could promote litter production, and the exclusion of light-grazing could increase litter decomposition and nutrient cycling. In contrast, heavy-grazing exclusion decreased litter decomposition. Thus, grazing exclusion is beneficial to the restoration of the light-grazing grasslands, and more human management measures are needed during the restoration of heavy-grazing grasslands. Precipitation increased litter production and decomposition, and below-ground litter was more vulnerable to the inter-annual change of precipitation than above-ground litter. Compared to the light-grazing grasslands, heavy-grazing grasslands had higher sensitivity to precipitation. The above-ground litter decomposition was strongly positively correlated with the litter N content (R² = 0.489, p < 0.01) and strongly negatively correlated with the soil total N content (R² = 0.450, p < 0.01), but it was not significantly correlated with C:N and lignin:N. Below-ground litter decomposition was negatively correlated with the litter C (R² = 0.263, p < 0.01), C:N (R² = 0.349, p < 0.01) and cellulose content (R² = 0.460, p < 0.01). Our results will provide a theoretical basis for ecosystem restoration and the research of carbon cycling.     

A Comparison of Bone Mineral Density and Its Predictors in HIV-Infected and HIV-Uninfected Older Men

ObjectiveBone health in older individuals with HIV infection has not been well studied. This study aimed to compare bone mineral density (BMD), trabecular bone score (TBS), and bone markers between HIV-infected men and age- and body mass index (BMI)-matched HIV-uninfected men aged ≥60 years. We investigated the associations of risk factors related to fracture with BMD, TBS, and bone markers in HIV-infected men.MethodsThis cross-sectional study included 45 HIV-infected men receiving antiretroviral therapy and 42 HIV-uninfected men. Medical history, BMD and TBS measurements, and laboratory tests related to bone health were assessed in all the participants. HIV-related factors known to be associated with bone loss were assessed in the HIV-infected men.ResultsThe mean BMD, TBS, and osteopenia or osteoporosis prevalence were similar among the cases and controls. The HIV-infected men had significantly higher mean N-terminal propeptide of type 1 procollagen and C-terminal cross-linking telopeptide of type I collagen levels. Stepwise multiple linear regression analysis demonstrated that low BMI (lumbar spine, P = .015; femoral neck, P = .018; and total hip, P = .005), high C-terminal cross-linking telopeptide of type I collagen concentration (total hip, P = .042; and TBS, P = .010), and low vitamin D supplementation (TBS, P = .035) were independently associated with low BMD and TBS.ConclusionIn older HIV-infected men with a low fracture risk, the mean BMD and TBS were similar to those of the age- and BMI-matched controls. The mean bone marker levels were higher in the HIV group. Traditional risk factors for fracture, including low BMI, high C-terminal cross-linking telopeptide of type I collagen level, and low vitamin D supplementation, were significant predictors of low BMD and TBS.     

Binding of B‐cell maturation antigen to B‐cell activating factor induces survival of multiple myeloma cells by activating Akt and JNK signaling pathways

B‐cell maturation antigen (BCMA) is expressed on normal and malignant plasma cells and represents a potential target for therapeutic intervention. In this study, we characterized the mechanism underlying the protein kinase B (Akt) and c‐Jun N‐terminal kinase (JNK) pathways and BCMA interactions in regulating multiple myeloma (MM) cell survival. It was found that the expression levels of B cell‐activating factor (BAFF) and BCMA were increased in MM cells as compared with those in normal controls. The proliferation of U266 cells was induced by recombinant human BAFF (rhBAFF) and could also be decreased by BCMA siRNA. The expression of Bcl‐2 protein was up‐regulated, and Bax protein was down‐regulated after rhBAFF treatment, which could be reversed by BCMA siRNA. Similarly, the protein p‐JNK and p‐Akt were activated by rhBAFF and could be changed by BCMA siRNA. In addition, the BCMA mRNA and protein expression levels were decreased after treatment with Akt and JNK pathway inhibitors. These results suggest that Akt and JNK pathways are involved in the regulation of BCMA. A novel BAFF/BCMA signalling pathway in MM may be a new therapeutic target for MM. Copyright © 2016 John Wiley & Sons, Ltd.