Corals shed bacteria as a potential mechanism of resilience to organic matter enrichment

Understanding the mechanisms of resilience of coral reefs to anthropogenic stressors is a critical step toward mitigating their current global decline. Coral–bacteria associations are fundamental to reef health and disease, but direct observations of these interactions remain largely unexplored. Here, we use novel technology, high-speed laser scanning confocal microscopy on live coral (Pocillopora damicornis), to test the hypothesis that corals exert control over the abundance of their associated bacterial communities by releasing (‘shedding'') bacteria from their surface, and that this mechanism can counteract bacterial growth stimulated by organic inputs. We also test the hypothesis that the coral pathogen Vibrio coralliilyticus can evade such a defense mechanism. This first report of direct observation with high-speed confocal microscopy of living coral and its associated bacterial community revealed a layer (3.3–146.8 μm thick) on the coral surface where bacteria were concentrated. The results of two independent experiments showed that the bacterial abundance in this layer was not sensitive to enrichment (5 mg l⁻¹ peptone), and that coral fragments exposed to enrichment released significantly more bacteria from their surfaces than control corals (P<0.01; 35.9±1.4 × 10⁵ cells cm⁻² coral versus 1.3±0.5 × 10⁵ cells cm⁻² coral). Our results provide direct support to the hypothesis that shedding bacteria may be an important mechanism by which coral-associated bacterial abundances are regulated under organic matter stress. Additionally, the novel ability to watch this ecological behavior in real-time at the microscale opens an unexplored avenue for mechanistic studies of coral–microbe interactions.     

A taxonomy of transcriptomic cell types across the isocortex and hippocampal formation

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On a likelihood-based goodness-of-fit test of the beta-binomial model

When faced with proportion data that exhibit extra-binomial variation, data analysts often consider the beta-binomial distribution as an alternative model to the more common binomial distribution. A typical example occurs in toxicological experiments with laboratory animals, where binary observations on fetuses within a litter are often correlated with each other. In such instances, it may be of interest to test for the goodness of fit of the beta-binomial model; this effort is complicated, however, when there is large variability among the litter sizes. We investigate a recent goodness-of-fit test proposed by Brooks et al. (1997, Biometrics 53, 1097-1115) but find that it lacks the ability to distinguish between the beta-binomial model and some severely non-beta-binomial models. Other tests and models developed in their article are quite useful and interesting but are not examined herein.     

Analytical method for the determination of sphinganine and sphingosine in serum as a potential biomarker for fumonisin exposure

The toxins produced by Fusarium moniliforme, which include fumonisins, are possible human carcinogens. Fumonisins are inhibitors of de novo sphingolipid biosynthesis. Alterations of the ratio of sphinganine (Sa) to sphingosine (So) in urine and serum has been proposed as a possible biomarker of exposure to this toxin. A new method was developed for their analysis in tissues and urine. This work describes the further adaptation of the method to the analysis of Sa and So in serum and its validation in sera of untreated and fumonisin B₁ (FB₁) treated rats and mice. No significant differences in the Sa/So ratios were observed in the FB₁ treated rats. In mice, the increase was only of marginal statistical significance. Determination of Sa/So ratios in human sera could readily be made in small volumes (from 0.3 to 0.5 ml) of serum.     

Immunity to the extracellular domain of Nogo-A modulates experimental autoimmune encephalomyelitis

Nogo-66, the extracellular 66 aa loop of the Nogo-A protein found in CNS myelin, interacts with the Nogo receptor and has been proposed to mediate inhibition of axonal regrowth. It has been shown that immunization with Nogo-A promotes recovery in animal models of spinal cord injury through induction of Ab production. In this report, studies were performed to characterize the immune response to Nogo-66 and to determine the role of Nogo in experimental autoimmune encephalomyelitis (EAE). Immunization of EAE-susceptible mouse strains with peptides derived from Nogo-66 induced a CNS immune response with clinical and pathological similarities to EAE. The Nogo-66 peptides elicited strong T cell responses that were not cross-reactive to other encephalitogenic myelin Ags. Using a large scale spotted microarray containing proteins and peptides derived from a wide spectrum of myelin components, we demonstrated that Nogo-66 peptides also generated a specific Ab response that spreads to several other encephalitogenic myelin Ags following immunization. Nogo-66-specific T cell lines ameliorated established EAE, via Nogo-66-specific Th2 cells that entered the CNS. These results indicate that some T cell and B cell immune responses to Nogo-66 are associated with suppression of ongoing EAE, whereas other Nogo-66 epitopes can be encephalitogenic.     

Characterization and identification of 6 mutagens in opium pyrolysates implicated in oesophagel cancer in Iran

Previous epidemiological studies have indicated an association between the ingestion of opium pyrolysates, dietary deficiencies, and a high incidence of oesophageal cancer in subjects in north-east Iran. Laboratory studies have shown that pyrolysates of opium and particularly of morphine, a major opium alkaloid, are highly mutagenic in bacteria and induce sister-chromatid exchanges in mammalian cells after metabolic activation. We now report the ability of these pyrolysates to transform Syrian hamster embryo cells in culture and present some evidence for their carcinogenicity in mice and hamsters following topical, subcutaneous, intratracheal and intragastric administration. 6 of the most abundant mutagenic compounds present in morphine pyrolysate were isolated and purified by high-performance liquid chromatography and characterized by gas chromatography/mass spectrometry and ¹H-Fourier transform nuclear magnetic resonance spectroscopy. These hitherto unknown compounds, all containing a hydroxy-phenanthrene moiety, were identified as: 3-methyl-3H-naphth[1,2-e]indol-10-ol; 1,2-dihydro-3-methyl-3H-naphth[1,2-e]indol-10-ol; 6-methylaminophenanthren-3-ol; 2-methylphenanthro[3,4-d][1,3]oxazol-10-ol; 2,3-dimethyl-3H-phenanthro[3,4-d]imidazol-10-ol and 2-methyl-3H-phenanthro[3,4-d]imidazol-10-ol. Mutagenicity in Salmonella typhimurium TA98 of these compounds increased in the order listed, the last compound being 35 times more active than benzo[a]pyrene. The mechanisms, by which these mutagens are formed and metabolically activated are discussed.