First record of Orbopercularia lichtensteini (Peritrichia: Operculariidae) attached to a hemipteran,Corisella edulis (Nepomorpha: Corixidae), in Hidalgo,Mexico, with notes on its cytology and distributional patterns

Operculariidae includes sessile ciliate species mainly attached to diverse substrates, but records are scarce for their attachment to aquatic true bugs. The goal of this contribution is to provide new cytological data with optical and scanning electron microscopy of Orbopercularia lichtensteini, and some notes about their distribution on a Mexican corixid. We manually collected the corixids in a pond in Mexico during a six-month period, and all individuals were revised to observe the peritrichids. We calculated the abundance and prevalence, with an emphasis on the specific micro-location of the epibiotic peritrich on the host Corisella edulis. A total of 36,205 peritrichids were recorded in 158 corixids. The colonies with fine striated zooids were dichotomously branched and mostly attached to left eyes, but also on other body regions, i.e. left wings and rostrum. We conclude that some morphological colony traits bring some advantages for food particle capture, and aspects of the biology and morphology of Corisella edulis play an important role in determining the spatial distribution of O. lichtensteini.     

Non-apoptotic role of BID in inflammation and innate immunity

Innate immunity is a fundamental defence response that depends on evolutionarily conserved pattern recognition receptors for sensing infections or danger signals. Nucleotide-binding and oligomerization domain (NOD) proteins are cytosolic pattern-recognition receptors of paramount importance in the intestine, and their dysregulation is associated with inflammatory bowel disease. They sense peptidoglycans from commensal microorganisms and pathogens and coordinate signalling events that culminate in the induction of inflammation and anti-microbial responses. However, the signalling mechanisms involved in this process are not fully understood. Here, using genome-wide RNA interference, we identify candidate genes that modulate the NOD1 inflammatory response in intestinal epithelial cells. Our results reveal a significant crosstalk between innate immunity and apoptosis and identify BID, a BCL2 family protein, as a critical component of the inflammatory response. Colonocytes depleted of BID or macrophages from Bid(-/-) mice are markedly defective in cytokine production in response to NOD activation. Furthermore, Bid(-/-) mice are unresponsive to local or systemic exposure to NOD agonists or their protective effect in experimental colitis. Mechanistically, BID interacts with NOD1, NOD2 and the IκB kinase (IKK) complex, impacting NF-κB and extracellular signal-regulated kinase (ERK) signalling. Our results define a novel role of BID in inflammation and immunity independent of its apoptotic function, furthering the mounting evidence of evolutionary conservation between the mechanisms of apoptosis and immunity.     

Catalytic activity of the caspase-8-FLIP(L) complex inhibits RIPK3-dependent necrosis

Caspase-8 has two opposing biological functions--it promotes cell death by triggering the extrinsic pathway of apoptosis, but also has a survival activity, as it is required for embryonic development, T-lymphocyte activation, and resistance to necrosis induced by tumour necrosis factor-α (TNF-α) and related family ligands. Here we show that development of caspase-8-deficient mice is completely rescued by ablation of receptor interacting protein kinase-3 (RIPK3). Adult animals lacking both caspase-8 and RIPK3 display a progressive lymphoaccumulative disease resembling that seen with defects in CD95 or CD95-ligand (also known as FAS and FASLG, respectively), and resist the lethal effects of CD95 ligation in vivo. We have found that caspase-8 prevents RIPK3-dependent necrosis without inducing apoptosis by functioning in a proteolytically active complex with FLICE-like inhibitory protein long (FLIP(L), also known as CFLAR), and this complex is required for the protective function.     

Anti-muscarinic activity of a family of C11N5 compounds isolated from Agelas sponges.

In a search for potential target sites for C11N5 compounds obtained from marine sponges of the genus Agelas we evaluated their interaction with muscarinic acetylcholine receptors from rat brain membranes. In competition experiments with 3H-QNB these compounds displayed the following rank order of potency: sceptrin greater than oroidin greater than or equal to dibromosceptrin greater than or equal to clathrodin. Sceptrin (50 microM) was shown to be a competitive inhibitor of 3H-QNB binding as revealed by Scatchard analysis. The results demonstrate the ability of these compounds to interact with multiple target molecules in the micromolar range.     

Increasing p16INK4a expression decreases forebrain progenitors and neurogenesis during ageing

Mammalian ageing is associated with reduced regenerative capacity in tissues that contain stem cells. It has been proposed that this is at least partially caused by the senescence of progenitors with age; however, it has not yet been tested whether genes associated with senescence functionally contribute to physiological declines in progenitor activity. Here we show that progenitor proliferation in the subventricular zone and neurogenesis in the olfactory bulb, as well as multipotent progenitor frequency and self-renewal potential, all decline with age in the mouse forebrain. These declines in progenitor frequency and function correlate with increased expression of p16INK4a, which encodes a cyclin-dependent kinase inhibitor linked to senescence. Ageing p16INK4a-deficient mice showed a significantly smaller decline in subventricular zone proliferation, olfactory bulb neurogenesis, and the frequency and self-renewal potential of multipotent progenitors. p16INK4a deficiency did not detectably affect progenitor function in the dentate gyrus or enteric nervous system, indicating regional differences in the response of neural progenitors to increased p16INK4a expression during ageing. Declining subventricular zone progenitor function and olfactory bulb neurogenesis during ageing are thus caused partly by increasing p16INK4a expression.     

Inhibitory action ofγ-aminobutyric acid (GABA) onAscaris muscle

Zusammenfassung Die somatische Muskulatur vonAscaris lumbricoides wird durch-Aminobuttersäure in Konzentrationen von 10^–6-10^–5 M völlig gehemmt. Eine hnliche Hemmung wird durch Piperazin (10^–3 M) erzielt. Beide Substanzen steigern die Cl-Permeabilität der Muskelmembran.

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On leave of absence from the Instituto de Biofísica, Universidade do Brazil, Rio de Janeiro (Brazil).     

Sea urchin elongation factor 1δ (EF1δ) and evidence for cell cycle-directed localization changes of a sub-fraction of the protein at M phase

Eukaryotic elongation factor 1 (eEF1) is a translational multimolecular complex reported in higher eukaryotes to be a target of CDK1/cyclin B, the universal regulator of M phase, but whose role in the cell cycle remains to be determined. A specific polyclonal antibody was produced and used to characterize the delta subunit of sea urchin elongation factor 1 (SgEF1) in early embryos, a powerful model for investigating cell cycle regulation. The SgEF1 protein was present in unfertilized eggs as two isoforms of 35 and 37 kDa, issued from two different mRNAs. The two canonical eEF1 partners, eEF1 and eEF1, were shown to co-immunoprecipitate with the SgEF1 isoforms. Both isoforms were associated in a macromolecular complex, which resolved upon gel filtration chromatography at a molecular weight > 400 kDa, suggesting association with other yet unidentified partners. After fertilization, the amount as well as the ratio of both SgEF1 isoforms remained constant during the first cell division as judged by Western blotting. Immunofluorescence analysis showed that a pool of the protein concentrated as a ring at the embryo nuclear location around the period of nuclear envelope breakdown and was visualized later as two large spheres around the mitotic spindle poles. Thus, the eEF1 protein shows cell cycle-specific localization changes in sea urchin embryos.Received 27 May 2003; received after revision 1 July 2003; accepted 4 July 2003     

Detection of HLA-E and -G DNA alleles for population and disease studies

HLA-E and -G genes show a restricted polymorphism encoding for molecules whose variability is limited at the peptide binding site. Fourteen alleles that give rise to only three productive proteins for HLA-G (*0101, *0103 and *0104) and five alleles with three different proteins for HLA-E (*0101, *0102 and *0103) have been described. Expression of these molecules is low and found in many tissues for HLA-E; HLA-G protein is expressed in extravillous trophoblast cells and thymic epithelium. Molecular studies have shown how HLA-G and HLA-E bind to natural killer (NK) cells immunoglobulin and lectin-type inhibitory receptors. HLA-E may act as a sentinel of the cell; if classical class I and HLA-G are being expressed, HLA-E molecules may reach the cell surface and inhibit the lysis by NK cells. Most findings are consistent with the hypothesis that HLA-E and -G proteins may be tolerogenic molecules at either the T-cell receptor (TcR) (inflammation, graft rejection) or NK level, switching off cells which usually attack foreign (including foetus) or self (autoimmune) antigens. A low HLA-E and -G polymorphism is observed in humans, and their allele frequencies are mostly homogeneous in the populations tested so far. Many studies to detect these alleles are now being performed in isolated populations and also in pregnancy-associated pathologies. In the present paper, standard and detailed techniques to detect HLA-E and -G DNA polymorphism are reported and discussed. Received 14 July 1999; received after revision 25 August 1999; accepted 25 August 1999