Effects of temperature and water availability on light energy utilization in photosynthetic processes of Deschampsia antarctica

Regional climate change in Antarctica would favor the carbon assimilation of Antarctic vascular plants, since rising temperatures are approaching their photosynthetic optimum (10–19°C). This could be detrimental for photoprotection mechanisms, mainly those associated with thermal dissipation, making plants more susceptible to eventual drought predicted by climate change models. With the purpose to study the effect of temperature and water availability on light energy utilization and putative adjustments in photoprotective mechanisms of Deschampsia antarctica Desv., plants were collected from two Antarctic provenances: King George Island and Lagotellerie Island. Plants were cultivated at 5, 10 and 16°C under well‐watered (WW) and water‐deficit (WD, at 35% of the field capacity) conditions. Chlorophyll fluorescence, pigment content and de‐epoxidation state were evaluated. Regardless of provenances, D. antarctica showed similar morphological, biochemical and functional responses to growth temperature. Higher temperature triggered an increase in photochemical activity (i.e. electron transport rate and photochemical quenching), and a decrease in thermal dissipation capacity (i.e. lower xanthophyll pool, Chl a/b and β carotene/neoxanthin ratios). Leaf mass per unit area was reduced at higher temperature, and was only affected in plants exposed to WD at 16°C and exhibiting lower electron transport rate and amount of chlorophylls. D. antarctica is adapted to frequent freezing events, which may induce a form of physiological water stress. Photoprotective responses observed under WD contribute to maintain a stable photochemical activity. Thus, it is possible that short‐term temperature increases could favor the photochemical activity of this species. However, long‐term effects will depend on the magnitude of changes and the plant's ability to adjust to new growth temperature.     

Bioremediation of oil polluted aquatic systems and soils with novel preparation `Rhoder'

This paper summarises the experience accumulated duringthe field application of biopreparation `Rhoder' (solely or in a combinationwith preliminary mechanical collection of free oil) for remediation of oil polluted aquatic systems and soils in the Moscow region and Western Siberia during 1994–1999.It was demonstrated that `Rhoder' had a very high efficiency (>99%) for bioremediation of the open aquatic surfaces (100 m² bay of the River Chernaya, two 5,000 m² lakes in Vyngayakha) at initial level of oil pollution of 0.4–19.1 g/l. During remediation of the wetland (2,000 m²) in Urai (initial level of oil pollution of 10.5 g/l), a preliminary mechanical collection of oil was applied (75% removal) followed by a triple treatment with `Rhoder'. It resulted in an overall treatment efficiency of 94%. Relatively inferior results of bioremediation of the 10,000 m² wetland in Vyngayakha (65% removal) and the 1,000 m² marshy peat soil in Nizhnevartovsk (19% removal) can be attributed to the very high initial level of oil pollution (24.3 g/l and >750 g/g dry matter, respectively) aggravated by the fact that it was impossible to apply a preliminary mechanical collection of oil on these sites. A possible strategy for remediation of such heavily polluted sitesis discussed.     

Laccase and Lectin Activities of Intracellular Proteins Produced in a Submerged Culture of the Xylotrophic Basidiomycete Lentinus edodes

The white-rot fungus Lentinus edodes produced D: -melibiose-specific lectins and two laccase forms in a lignin-containing medium. The maxima of laccase and lectin activities coincided, falling within the period of active mycelial growth. The enzymes and lectins were isolated and purified by gel filtration followed by anion-exchange chromatography. The L. edodes lectins were found to be able to stabilize the activity of the fungus's own laccases. Lectin activity during the formation of lectin-enzyme complexes remained unchanged.     

Binding of aflatoxins to the 20S proteasome: effects on enzyme functionality and implications for oxidative stress and apoptosis

Aflatoxins (AF) are contaminants of improperly stored foods; they are potent genotoxic and carcinogenic compounds, exerting their effects through damage to DNA. They can also induce mutations that increase oxidative damage. The goal of this study was to evaluate the possibility that a third mechanism could be involved in the carcinogenic action of aflatoxins, namely, direct binding to key enzymes involved in the regulatory pathways of the cell cycle, thereby modulating enzyme functionality. The 20S constitutive and immunoproteasome peptidase and proteolytic activities were assayed in the presence of aflatoxins B1, G1 and M1. All three toxins activated multiple peptidase activities of the proteasome. Aflatoxin (AF) M1 was the most potent activator of proteasome activity, while the constitutive 20S proteasome was specifically stimulated by AFG1. Furthermore, the effects of AFB1 on cultured hepatoma cells were investigated and the various proteasomal activities determined with cell lysates were differently affected. Taking into account the key role of the proteasome in cellular defense against oxidative stress, the carbonyl group content and the activities of antioxidant enzymes in cell lysates were analyzed. The proapoptotic effect of AFB1 was also investigated by measuring caspase-3 activity and cellular levels of p27 and IkappaBalpha.     

Genetic Barriers to Historical Gene Flow between Cryptic Species of Alpine Bumblebees Revealed by Comparative Population Genomics

Evidence is accumulating that gene flow commonly occurs between recently diverged species, despite the existence of barriers to gene flow in their genomes. However, we still know little about what regions of the genome become barriers to gene flow and how such barriers form. Here, we compare genetic differentiation across the genomes of bumblebee species living in sympatry and allopatry to reveal the potential impact of gene flow during species divergence and uncover genetic barrier loci. We first compared the genomes of the alpine bumblebee Bombus sylvicola and a previously unidentified sister species living in sympatry in the Rocky Mountains, revealing prominent islands of elevated genetic divergence in the genome that colocalize with centromeres and regions of low recombination. This same pattern is observed between the genomes of another pair of closely related species living in allopatry (B. bifarius and B. vancouverensis). Strikingly however, the genomic islands exhibit significantly elevated absolute divergence (d_XY) in the sympatric, but not the allopatric, comparison indicating that they contain loci that have acted as barriers to historical gene flow in sympatry. Our results suggest that intrinsic barriers to gene flow between species may often accumulate in regions of low recombination and near centromeres through processes such as genetic hitchhiking, and that divergence in these regions is accentuated in the presence of gene flow.     

Polygyny in the tree swallow Tachycineta bicolor: a result of the cost of searching for an unmated male

The costs imposed by parental care duties on an individual's future survival and reproduction generate conflicts because parents should attempt to minimize their investment in the present brood, and exploit the parental care of the other parent. This conflict is likely to contribute to cases of both polygamy and desertion. Here, we study the costs of polygyny in the tree swallow Tachycineta bicolor , using observations on 52 nests that were attended by polygynous males over 14 y. Both females mated to polygynous males paid reproductive costs at several stages of the nesting cycle. Clutches laid by social mates of polygynous versus monogamous males did not differ in size. However, initial brood sizes for polygynously mated females were lower because a higher proportion of their eggs failed to hatch. Likewise, fledging success was lower and nest predation rates were higher, perhaps reflecting the direct or indirect effects of reduced male attention. These results demonstrate that females pay a productivity cost when breeding with reduced male parental care. In contrast, polygynous males fledge on average more young than monogamous ones and clearly benefit from the association. We suggest that a mate-search cost is leading to the few cases of polygamous males: although females are likely evaluating males for their prospective dedication to the breeding attempt, in a short-lived bird with a short breeding season, the cost to females of searching for a more dedicated male is the risk of not breeding at all.     

Micronuclei, genetic polymorphisms and cardiovascular disease mortality in a nested case-control study in Italy

AIM: To validate the predictive value of micronuclei (MN) in peripheral blood lymphocytes (PBL) and glutathione-S-transferases (GSTs) polymorphisms (GSTM1 and GSTT1) for mortality risk (MR) of cardiovascular diseases (CVD). METHODS: Blood samples from 1650 healthy subjects selected from the general population were collected between June 1991 and November 1993, and slides were immediately prepared for MN assessment. The vital status, or the cause of death, was monitored for all subjects until January 2005. At the end of the follow-up, 111 deaths were recorded and 39 CVD cases were observed (age range=42-88 years). Two thousand binucleated (BN) cells/subject were scored for the MN assay and GSTs genotypes were assessed on the DNA extracted from the blood or serum samples. RESULTS: A significantly higher MN frequency was recorded for the case group in comparison with the control group (n=67, Kruskall-Wallis test, p=0.006) and GSTT1 null genotype was significantly less frequent in CVD patients (chi(2)-test, p=0.036). The influence of other factors were evaluated using a unconditional logistic regression that confirmed a significant association of GSTT1 positive genotype with an increased OR for CVD (OR=6.29, 95% CI 1.32-29.95) beside a significant effect of age (OR=1.13, 95% CI 1.03-1.26 year(-1)). Finally, subjects with an higher MN frequency showed a higher MR for CVD (Log-rank test, p=0.001). CONCLUSIONS: MN confirmed to be a suitable cytogenetic biomarker for early prediction of CVD death. The GSTT1 positive genotype is associated with an increased MR for CVD.     

In vitro induction of neoantigen-specific T cells in myelodysplastic syndrome,a disease with low mutational burden

Therapies that utilize immune checkpoint inhibition work by leveraging mutation-derived neoantigens and have shown greater clinical efficacy in tumors with higher mutational burden. Whether tumors with a low mutational burden are susceptible to neoantigen-targeted therapy has not been fully addressed. To examine the feasibility of neoantigen-specific adoptive T-cell therapy, the authors studied the T-cell response against somatic variants in five patients with myelodysplastic syndrome (MDS), a malignancy with a very low tumor mutational burden. DNA and RNA from tumor (CD34⁺) and normal (CD3⁺) cells isolated from the patients’ blood were sequenced to predict patient-specific MDS neopeptides. Neopeptides representing the somatic variants were used to induce and expand autologous T cells ex vivo, and these were systematically tested in killing assays to determine the proportion of neopeptides yielding neoantigen-specific T cells. The authors identified a total of 32 somatic variants (four to eight per patient) and found that 21 (66%) induced a peptide-specific T-cell response and 19 (59%) induced a T-cell response capable of killing autologous tumor cells. Of the 32 somatic variants, 11 (34%) induced a CD4⁺ response and 11 (34%) induced a CD8⁺ response that killed the tumor. These results indicate that in vitro induction of neoantigen-specific T cells is feasible for tumors with very low mutational burden and that this approach warrants investigation as a therapeutic option for such patients.     

T cell activation induces CuZn superoxide dismutase (SOD)-1 intracellular re-localization,production and secretion

Reactive oxygen species (ROS) behave as second messengers in signal transduction for a series of receptor/ligand interactions. A major regulatory role is played by hydrogen peroxide (H₂O₂), more stable and able to freely diffuse through cell membranes. Copper–zinc superoxide dismutase (CuZn-SOD)-1 is a cytosolic enzyme involved in scavenging oxygen radicals to H₂O₂ and molecular oxygen, thus representing a major cytosolic source of peroxides. Previous studies suggested that superoxide anion and H₂O₂ generation are involved in T cell receptor (TCR)-dependent signaling. Here, we describe that antigen-dependent activation of human T lymphocytes significantly increased extracellular SOD-1 levels in lymphocyte cultures. This effect was accompanied by the synthesis of SOD-1-specific mRNA and by the induction of microvesicle SOD-1 secretion. It is of note that SOD-1 increased its concentration specifically in T cell population, while no significant changes were observed in the “non-T” cell counterpart. Moreover, confocal microscopy showed that antigen-dependent activation was able to modify SOD-1 intracellular localization in T cells. Indeed, was observed a clear SOD-1 recruitment by TCR clusters. The ROS scavenger N-acetylcysteine (NAC) inhibited this phenomenon. Further studies are needed to define whether SOD-1-dependent superoxide/peroxide balance is relevant for regulation of T cell activation, as well as in the functional cross talk between immune effectors.