Aurora A is involved in central spindle assembly through phosphorylation of Ser 19 in P150Glued

During cytokinesis, closure of the actomyosin contractile ring (CR) is coupled to the formation of a midbody ring (MR), through poorly understood mechanisms. Using time-lapse microscopy of Drosophila melanogaster S2 cells, we show that the transition from the CR to the MR proceeds via a previously uncharacterized maturation process that requires opposing mechanisms of removal and retention of the scaffold protein Anillin. The septin cytoskeleton acts on the C terminus of Anillin to locally trim away excess membrane from the late CR/nascent MR via internalization, extrusion, and shedding, whereas the citron kinase Sticky acts on the N terminus of Anillin to retain it at the mature MR. Simultaneous depletion of septins and Sticky not only disrupted MR formation but also caused earlier CR oscillations, uncovering redundant mechanisms of CR stability that can partly explain the essential role of Anillin in this process. Our findings highlight the relatedness of the CR and MR and suggest that membrane removal is coordinated with CR disassembly.     

Functional complement C1q abnormality leads to impaired immune complexes and apoptotic cell clearance

C1q plays a key role in apoptotic cell and immune complex removal. Its absence contributes to the loss of tolerance toward self structures and development of autoimmunity. C1q deficiencies are extremely rare and are associated with complete lack of C1q or with secretion of surrogate C1q fragments. To our knowledge, we report the first case of a functional C1q abnormality, associated with the presence of a normal C1q molecule. Homozygous GlyB63Ser mutation was found in a patient suffering from lupus with neurologic manifestations and multiple infections. The GlyB63Ser C1q bound to Igs, pentraxins, LPSs, and apoptotic cells, similarly to C1q from healthy donors. However, the interaction of C1r(2)C1s(2) and C1 complex formation was abolished, preventing further complement activation and opsonization by C3. The mutation is located between LysB(61) and LysB(65) of C1q, suggested to form the C1r binding site. Our data infer that the binding of C1q to apoptotic cells in humans is insufficient to assure self-tolerance. The opsonization capacity of C4 and C3 fragments has to be intact to fight infections and to prevent autoimmunity.     

Is the response of coral calcification to seawater acidification related to nutrient loading?

The effect of decreasing aragonite saturation state (Ω_Arag) of seawater (elevated pCO₂) on calcification rates of Acropora muricata was studied using nubbins prepared from parent colonies located at two sites of La Saline reef (La Réunion Island, western Indian Ocean): a back-reef site (BR) affected by nutrient-enriched groundwater discharge (mainly nitrate), and a reef flat site (RF) with low terrigenous inputs. Protein and chlorophyll a content of the nubbins, as well as zooxanthellae abundance, were lower at RF than BR. Nubbins were incubated at ~27°C over 2 h under sunlight, in filtered seawater manipulated to get differing initial pCO₂ (1,440–340 μatm), Ω_Arag (1.4–4.0), and dissolved inorganic carbon (DIC) concentrations (2,100–1,850 μmol kg⁻¹). Increasing DIC concentrations at constant total alkalinity (A_T) resulted in a decrease in Ω_Arag and an increase in pCO₂. A_T at the beginning of the incubations was kept at a natural level of 2,193 ± 6 μmol kg⁻¹ (mean ± SD). Net photosynthesis (NP) and calcification were calculated from changes in pH and A_T during the incubations. Calcification decrease in response to doubling pCO₂ relative to preindustrial level was 22% for RF nubbins. When normalized to surface area of the nubbins, (1) NP and calcification were higher at BR than RF, (2) NP increased in high pCO₂ treatments at BR compared to low pCO₂ treatments, and (3) calcification was not related to Ω_Arag at BR. When normalized to NP, calcification was linearly related to Ω_Arag at both sites, and the slopes of the relationships were not significantly different. The increase in NP at BR in the high pCO₂ treatments may have increased calcification and thus masked the negative effect of low Ω_Arag on calcification. Removing the effect of NP variations at BR showed that calcification declined in a similar manner with decreased Ω_Arag (increased pCO₂) whatever the nutrient loading.     

Ultrastructure de l'œuf de Triatoma infestans Klug

Summary The thick rigid chorion of the egg of Triatoma secreted by the follicle cells shows two porous layers: an aerial layer in the exochorion, an alveolar one in the endochorion. The anterior part of the eggshell is closed up by an operculum which is heaved up by the hatching larva. The operculum has no alveolar layer. The air enters through the numerous holes of the shell surface into the aerial layer and through the micropyles into the alveolar layer. The egg has no respiratory plastron.The follicle cells produce also a vitelline envelope whose structure shows a rapid condensation at fertilization time. During its development the embryo secretes two layers: serosal and embryonic cuticle.At high humidities, at low temperatures the egg is able to increase its weight during the early stages of embryogenesis, and this increase stops when the serosal cuticle is secreted. In a dry atmosphere the egg loses water but can develop if the temperature is higher than 20°C.The little permeability of the egg is related to the structure of its envelopes. The chorion and the vitelline envelope prevent the water from getting out of the egg. The serosal cuticle seems to be opposed to the penetration of the water into the egg. The role of the embryonic cuticle is probably limited in the transit of water.

Nous remercions Messieurs les Professeurs Maillet et Folliot qui ont mis le microscope R.C.A. à notre disposition, Madame Allo et Mademoiselle Le Gac, technicienne au microscope à balayage J.S.M. S1, pour leur collaboration technique.     

Local hepatic immune response in rats during primary infection with Fasciola hepatica

The distribution of lymphocyte subpopulations (TCD4+, TCD8+, TCD43+ and Ig+ cells), macrophages and eosinophils were analysed in the inflammatory infiltrates associated with hepatic lesions and in hepatic lymph nodes (HLN) from rats experimentally infected with F. hepatica and necropsied 1, 2, 3, 4, 6 and 8 week post infection (WPI). We also investigated the fixation of immunoglobulin isotypes on migrating flukes in the liver. As early as 1WPI, portal tract areas surrounding migratory tunnels were infiltrated with immune and inflammatory cells. The dominant cells were eosinophils and to lesser extent, macrophages and lymphocytes (TCD4+, TCD8+ and B). Most of the inflammatory and immune cells reached the posterior part of flukes, whereas in front of the parasites these cells were fewer in number. Except for eosinophils, no immune cells penetrated through granuloma consisting of hepatic necrotic cells. As early as 1WPI, IgM could be detected in the liver, and to a lesser extent IgA, IgG2a and IgG2b. At 2WPI, IgE and IgG1 began being detected. IgG2c was detectable at 3WPI. In HLN, we observed numerous microscopic follicles in the cortical zone with proliferation of germinal centres and medullary cords. The protective role of infiltrating cell populations and immunoglobulin isotypes and possible mechanisms of immune evasion by the parasite are discussed.     

Are Immigrants and Nationals Born to Immigrants at Higher Risk for Delayed or No Lifetime Breast and Cervical Cancer Screening? The Results from a Population-Based Survey in Paris Metropolitan Area in 2010

Objectives

This study aims to compare breast cancer screening (BCS) and cervical cancer screening (CCS) practices of French women born to French parents with those of immigrants and nationals born to immigrants, taking their socioeconomic status into account.

Methods

The study is based on data collected in 2010 in the Paris metropolitan area among a representative sample of 3000 French-speaking adults. For women with no history of breast or cervical cancer, multivariate logistic regressions and structural equation models were used to investigate the factors associated with never having undergone BCS or CCS.

Results

We confirmed the existence of a strong gradient, with respect to migration origin, for delaying or never having undergone BCS or CCS. Thus, being a foreign immigrant or being French of immigrant parentage were risk factors for delayed and no lifetime screening. Interestingly, we found that this gradient persisted (at least partially) after adjusting for the women’s socioeconomic characteristics. Only the level of income seemed to play a mediating role, but only partially. We observed differences between BCS and CCS which suggest that organized CCS could be effective in reducing socioeconomic and/or ethnic inequities.

Conclusion

Socioeconomic status partially explained the screening nonparticipation on the part of French women of immigrant origin and foreign immigrants. This was more so the case with CCS than with BCS, which suggests that organized prevention programs might reduce social inequalities.     

Proteasomal degradation of human release factor eRF3a regulates translation termination complex formation

In eukaryotes, eRF1 and eRF3 are associated in a complex that mediates translation termination. The regulation of the formation of this complex in vivo is far from being understood. In mammalian cells, depletion of eRF3a causes a reduction of eRF1 level by decreasing its stability. Here, we investigate the status of eRF3a when not associated with eRF1. We show that eRF3a forms altered in their eRF1-binding site have a decreased stability, which increases upon cell treatment with the proteasome inhibitor MG132. We also show that eRF3a forms altered in eRF1 binding as well as wild-type eRF3a are polyubiquitinated. These results indicate that eRF3a is degraded by the proteasome when not associated with eRF1 and suggest that proteasomal degradation of eRF3a controls translation termination complex formation by adjusting the eRF3a level to that of eRF1.