Histone deacetylase inhibition decreases preference without affecting aversion for nicotine

Mutations in the parkin gene cause early-onset, autosomal recessive Parkinson's disease. Parkin functions as an E3 ubiquitin ligase to mediate the covalent attachment of ubiquitin monomers or linked chains to protein substrates. Substrate ubiquitination can target proteins for proteasomal degradation or can mediate a number of non-degradative functions. Parkin has been shown to preserve mitochondrial integrity in a number of experimental systems through the regulation of mitochondrial fission. Upon mitochondrial damage, parkin translocates to mitochondria to mediate their selective elimination by autophagic degradation. The mechanism underlying this process remains unclear. Here, we demonstrate that parkin interacts with and selectively mediates the atypical poly-ubiquitination of the mitochondrial fusion factor, mitofusin 1, leading to its enhanced turnover by proteasomal degradation. Our data supports a model whereby the translocation of parkin to damaged mitochondria induces the degradation of mitofusins leading to impaired mitochondrial fusion. This process may serve to selectively isolate damaged mitochondria for their removal by autophagy.     

2-D DIGE analysis of UV-C radiation-responsive proteins in globe artichoke leaves

Plants respond to ultraviolet stress inducing a self-defence through the regulation of specific gene family members. The UV acclimation is the result of biochemical and physiological processes, such as enhancement of the antioxidant enzymatic system and accumulation of UV-absorbing phenolic compounds (e.g. flavonoids). Globe artichoke is an attractive species for studying the protein network involved in UV stress response, being characterized by remarkable levels of inducible antioxidants. Proteomic tools can assist the evaluation of the expression patterns of UV-responsive proteins and we applied the difference in-gel electrophoresis (DIGE) technology for monitoring the globe artichoke proteome variation at four time points following an acute UV-C exposure. A total of 145 UV-C-modulated proteins were observed and 119 were identified by LC-MS/MS using a ～144,000 customized Compositae protein database, which included about 19,000 globe artichoke unigenes. Proteins were Gene Ontology (GO) categorized, visualized on their pathways and their behaviour was discussed. A predicted protein interaction network was produced and highly connected hub-like proteins were highlighted. Most of the proteins differentially modulated were chloroplast located, involved in photosynthesis, sugar metabolisms, protein folding and abiotic stress. The identification of UV-C-responsive proteins may contribute to shed light on the molecular mechanisms underlying plant responses to UV stress.     

The sweet and bitter sides of galectins in melanoma progression

Melanoma is the leading cause of skin cancer-related deaths, which is due in large part to its aggressive behavior, resistance to therapy, and ability to metastasize to multiple organs such as the lymph nodes, lung, and brain. Melanoma progresses in a stepwise manner from the benign nevus, to radial spreading through the dermis, to a vertical invasive phase, and finally to metastasis. The carbohydrate-binding family of galectins has a strong influence on each phase of melanoma progression through their effects on immune surveillance, angiogenesis, cell migration, tumor cell adhesion, and the cellular response to chemotherapy. Galectins share significant homology in their carbohydrate recognition domain (CRD), which mediates binding to an array of N-glycosylated proteins located on the surface of tumor cells, endothelial cells, T-cells, and to similarly glycosylated extracellular matrix proteins. Galectins are also present within tumor cells where they perform anti-apoptotic functions and enhance intracellular signaling that results in deregulated expression of genes involved in tumor progression. The most extensively studied galectins, galectin-1 and galectin-3, have been shown to have profound effects on melanoma growth and metastasis by influencing many of these biological processes.     

Cancer stem cells and human malignant melanoma

Cancer stem cells (CSC) have been identified in hematological malignancies and several solid cancers. Similar to physiological stem cells, CSC are capable of self-renewal and differentiation and have the potential for indefinite proliferation, a function through which they may cause tumor growth. Although conventional anti-cancer treatments might eradicate most malignant cells in a tumor, they are potentially ineffective against chemoresistant CSC, which may ultimately be responsible for recurrence and progression. Human malignant melanoma is a highly aggressive and drug-resistant cancer. Detection of tumor heterogeneity, undifferentiated molecular signatures, and increased tumorigenicity of melanoma subsets with embryonic-like differentiation plasticity strongly suggest the presence and involvement of malignant melanoma stem cells (MMSC) in the initiation and propagation of this malignancy. Here, we review these findings in the context of functional properties ascribed to melanocyte stem cells and CSC in other cancers. We discuss the association of deregulated signaling pathways, genomic instability, and vasculogenic mimicry phenomena observed in melanoma subpopulations in light of the CSC concept. We propose that a subset of MMSC may be responsible for melanoma therapy-resistance, tumor invasiveness, and neoplastic progression and that targeted abrogation of a MMSC compartment could therefore ultimately lead to stable remissions and perhaps cures of metastatic melanoma.     

The 4‐pyridylmethyl ester as a protecting group for glutamic and aspartic acids: ‘flipping’ peptide charge states for characterization by positive ion mode ESI‐MS

Use of the 4‐pyridylmethyl ester group for side‐chain protection of glutamic acid residues in solid‐phase peptide synthesis enables switching of the charge state of a peptide from negative to positive, thus making detection by positive ion mode ESI‐MS possible. The pyridylmethyl ester moiety is readily removed from peptides in high yield by hydrogenation. Combining the 4‐pyridylmethyl ester protecting group with benzyl ester protection reduces the number of the former needed to produce a net positive charge and allows for purification by RP HPLC. This protecting group is useful in the synthesis of highly acidic peptide sequences, which are often beset by problems with purification by standard RP HPLC and characterization by ESI‐MS. Copyright © 2014 European Peptide Society and John Wiley & Sons, Ltd.     

Heritability estimates from genomewide relatedness matrices in wild populations: Application to a passerine,using a small sample size

Genomic developments have empowered the investigation of heritability in wild populations directly from genomewide relatedness matrices (GRM). Such GRM‐based approaches can in particular be used to improve or substitute approaches based on social pedigree (PED‐social). However, measuring heritability from GRM in the wild has not been widely applied yet, especially using small samples and in nonmodel species. Here, we estimated heritability for four quantitative traits (tarsus length, wing length, bill length and body mass), using PED‐social, a pedigree corrected by genetic data (PED‐corrected) and a GRM from a small sample (n = 494) of blue tits from natural populations in Corsica genotyped at nearly 50,000 filtered SNPs derived from RAD‐seq. We also measured genetic correlations among traits, and we performed chromosome partitioning. Heritability estimates were slightly higher when using GRM compared to PED‐social, and PED‐corrected yielded intermediate values, suggesting a minor underestimation of heritability in PED‐social due to incorrect pedigree links, including extra‐pair paternity, and to lower information content than the GRM. Genetic correlations among traits were similar between PED‐social and GRM but credible intervals were very large in both cases, suggesting a lack of power for this small data set. Although a positive linear relationship was found between the number of genes per chromosome and the chromosome heritability for tarsus length, chromosome partitioning similarly showed a lack of power for the three other traits. We discuss the usefulness and limitations of the quantitative genetic inferences based on genomic data in small samples from wild populations.     

Association mapping of cold‐induced sweetening in potato using historical phenotypic data

In this study, historical phenotypic data from a potato breeding programme were used with an association mapping approach to identify alleles of candidate genes associated with cold‐induced sweetening of potato. Molecular marker analysis was used to determine allelic variation of candidate genes potentially involved in cold‐induced sweetening. Variations in the UDP‐glucose pyrophosphorylase (UGPase, EC 2.7.7.9) and apoplastic invertase genes (EC 3.2.1.26) were significantly associated with cold‐induced sweetening, and a possible interaction of apoplastic invertase and apoplastic invertase inhibitor was identified. This demonstrates that breeding programme phenotypic data collected over multiple years and environments can be used successfully with pedigree information for association mapping. It also confirms that the UGPase and apoplastic invertase markers are transferable across breeding programmes with distinct germplasm.     

Greater soil microbial biomass loss at low frequency of N addition in an Inner Mongolia grassland

低频率的氮添加使内蒙古草原土壤微生物生物量碳出现更大幅度下降 土壤微生物生物量在生物地球化学循环过程中至关重要,是土壤碳固持的前体物质。人为氮输入深刻地改变了草地土壤微生物生物量。然而,传统氮沉降模拟实验仅通过低频率的氮添加进行,与持续高频率的自然氮沉降相比,对土壤微生物生物量的影响可能存在差异。不同频率的氮添加对土壤微生物生物量的影响尚缺乏可靠的数据支撑。本研究通过在不同的氮添加速率(0–50 g N m−2 yr−1)下,控制氮添加频率(每年2次和12次),研究了土壤微生物生物量碳对不同氮添加频率的响应。研究结果表明,在两种氮添加频率下,随着施氮水平的提高,土壤微生物生物量碳逐渐降低。然而,在低施氮频率下,土壤微生物生物量的下降幅度更大,这说明传统的氮添加实验可能高估了氮沉降对土壤微生物生物量的影响。在低施氮频率下,土壤酸化、无机氮积累、碳氮失衡、地下净初级生产力分配减少和真菌细菌比例降低等情况加剧,导致微生物生物量出现较大幅度下降。在未来研究中,为可靠预测氮沉降对草地生态系统土壤微生物功能和碳循环的影响,不仅要考虑氮添加的剂量,还需要考虑氮添加的频率。     

A Framework for Development and Communication of Absolute Environmental Sustainability Assessment Methods

An absolute environmental sustainability assessment (AESA) addresses whether a production or consumption activity can be considered environmentally sustainable in an absolute sense. This involves a comparison of its environmental pressure to its allocated environmental carrying capacity. AESA methods have been developed in multiple academic fields, each using their own set of concepts and terms with little communication across the fields. A recent growing interest in using AESA methods for decision support calls for a better common understanding of the constituents of an AESA method and how it can be communicated to scientific peers and to potential users. With this aim, we develop a framework for AESA methods, composed of a succession of four assessment steps and involving six methodological choices that must be made by the method developer or the user. We then use the framework to analyze and compare five selected AESA methods that focus on the release of phosphorus and nitrogen to the environment. In this manner, we show that the framework is able to systematically differentiate AESA methods that initially appear to be similar. Intended users of the framework include (1) method developers communicating new AESA methods to academic peers or potential method users and (2) researchers comparing a group of existing AESA methods and communicating their differences to their peers and to potential users looking for guidance on method selection.     

CHANGES IN PHOTOSYNTHESIS IN RESPONSE TO COMBINED IRRADIANCE AND TEMPERATURE STRESS IN CYANOBACTERIAL SURFACE WATERBLOOMS1

Buoyant cyanobacteria, previously mixed throughout the water column, float to the lake surface and form a surface waterbloom when mixing subsides. At the surface, the cells are exposed to full sunlight, and this abrupt change in photon irradiance may induce photoinhibition; at the same time, temperature rises as well. This study investigated the damaging effects of this increase in temperature as well as the ecologically more relevant combination of both an increased temperature and a high photon irradiance. Analysis of surface blooms with oxygen microelectrodes showed that integrated oxygen contents that are dependent on the balance of photosynthetic oxygen evolution and respiratory oxygen uptake decreased when temperature was raised above the lake temperature. Gross rates of photosynthesis were unaffected by temperatures up to of 35°C; hence, a moderate increase in temperature mainly stimulated oxygen uptake. Preincubation of cells of the cyanobacterium Anabaena flos-aquae (Lyngb.) de Brébisson at temperatures up to 35°C did not affect the subsequent measurement of rates of net photosynthesis. Another 5°C rise in temperature severely damaged the photosynthetic apparatus. Failure to restore net rates of photosynthesis was coupled to a strong quenching of the ratio of variable to maximum fluorescence, F_v/F_m, that was the result of a rise in F_o. A combination of high temperature and high photon irradiance was more damaging than high temperature alone. In contrast, low photon irradiances offered substantial protection against heat injury of the photosynthetic apparatus. I conclude from this study that because cyanobacteria usually are acclimated to low average irradiance prior to bloom formation, there is a reasonable risk of chronic photoinhibition. The increase in temperature will enhance the photodamage of cells in the top layer of the bloom. Low photon irradiances in subsurface layers will offer protection against heat injury. If the high temperatures extend to the deepest, dark layers of the bloom, damage in those layers is likely to occur.