Morphology of the spermatozoa of the Microhylidae (Anura, Amphibia)

Microhylid spermatozoa show the autapomorphic condition of possessing a thin post-mitochondrial cytoplasmic collar. Their spermatozoa are apomorphic in several respects. They have lost the distinct nuclear shoulder, endonuclear canal and axial perforatorium observed in urodeles, caecilians and primitive frogs, possess a conical perforatorium and apomorphically lack any fibres associated with the axoneme. The spermatozoa of Cophixalus , however, differ in several respects from those of the other microhylids examined. Cophixalus spermatozoa are longer in almost all measurements, the acrosome vesicle is cylindrical and does not completely cover the putative perforatorium, the perforatorium is asymmetrical and composed of fine fibres, the nucleus is strongly attenuated and narrower, and the mitochondria are elongate. The absence of fibres associated with the axoneme is an apomorphic condition shared with the Ranidae, Rhacophoridae and Pipidae.     

The anaerobic degradation of aromatic compounds by a denitrifying bacterium

Summary Six strains of Rhizobium, present as bacteroids, in Lotus nodules were studied by electron microscopy. Three inclusion bodies frequently detected are described and their distribution among the strains is given. Cytochemical techniques indicated that they have, as principal components, polyphosphate, lipid and neutral polysaccharide, probably glycogen, respectively.     

The chain length of the glycans in bacterial cell walls (Short Communication)

The glycan chain length of peptidoglycan was measured by reduction with NaB³H₄ and isolation of the resulting muramitol, indicative of the length of the chains as biosynthesized, and glucosaminol, which measured the length of the chains after rupture by endo-β-N-acetylglucosaminidases. Measurement of the non-reducing terminal N-acetylglucosamine by Smith degradation confirmed the result.     

Quorum-sensing cross talk: isolation and chemical characterization of cyclic dipeptides from Pseudomonas aeruginosa and other Gram-negative bacteria

In cell-free Pseudomonas aeruginosa culture supernatants, we identified two compounds capable of activating an N-acylhomoserine lactone (AHL) biosensor. Mass spectrometry and NMR spectroscopy revealed that these compounds were not AHLs but the diketopiperazines (DKPs), cyclo(DeltaAla-L-Val) and cyclo(L-Pro-L-Tyr) respectively. These compounds were also found in cell-free supernatants from Proteus mirabilis, Citrobacter freundii and Enterobacter agglomerans [cyclo(DeltaAla-L-Val) only]. Although both DKPs were absent from Pseudomonas fluorescens and Pseudomonas alcaligenes, we isolated, from both pseudomonads, a third DKP, which was chemically characterized as cyclo(L-Phe-L-Pro). Dose-response curves using a LuxR-based AHL biosensor indicated that cyclo(DeltaAla-L-Val), cyclo(L-Pro-L-Tyr) and cyclo(L-Phe-L-Pro) activate the biosensor in a concentration-dependent manner, albeit at much higher concentrations than the natural activator N-(3-oxohexanoyl)-L-homoserine lactone (3-oxo-C6-HSL). Competition studies showed that cyclo(DeltaAla-L-Val), cyclo(L-Pro-L-Tyr) and cyclo(L-Phe-L-Pro) antagonize the 3-oxo-C6-HSL-mediated induction of bioluminescence, suggesting that these DKPs may compete for the same LuxR-binding site. Similarly, DKPs were found to be capable of activating or antagonizing other LuxR-based quorum-sensing systems, such as the N-butanoylhomoserine lactone-dependent swarming motility of Serratia liquefaciens. Although the physiological role of these DKPs has yet to be established, their activity suggests the existence of cross talk among bacterial signalling systems.     

Mouse models of rhinovirus-induced disease and exacerbation of allergic airway inflammation

Rhinoviruses cause serious morbidity and mortality as the major etiological agents of asthma exacerbations and the common cold. A major obstacle to understanding disease pathogenesis and to the development of effective therapies has been the lack of a small-animal model for rhinovirus infection. Of the 100 known rhinovirus serotypes, 90% (the major group) use human intercellular adhesion molecule-1 (ICAM-1) as their cellular receptor and do not bind mouse ICAM-1; the remaining 10% (the minor group) use a member of the low-density lipoprotein receptor family and can bind the mouse counterpart. Here we describe three novel mouse models of rhinovirus infection: minor-group rhinovirus infection of BALB/c mice, major-group rhinovirus infection of transgenic BALB/c mice expressing a mouse-human ICAM-1 chimera and rhinovirus-induced exacerbation of allergic airway inflammation. These models have features similar to those observed in rhinovirus infection in humans, including augmentation of allergic airway inflammation, and will be useful in the development of future therapies for colds and asthma exacerbations.