Complete elimination of hostplant quinolizidine alkaloids by larvae of a polyphagous lycaenid butterfly,Callophrys rubi

Caterpillars of the lycaenid butterfly Callophrys rubi accept a variety of hostplants. When fed inflorescences or leaves of Genista tinctoria (a natural hostplant) or Lupinus polyphyllus (a non-host), the larvae completely eliminate quinolizidine alkaloids ingested from their food in their frass. No alkaloids are stored. Infestation by the parasitoid wasp Distatrix sancus (Braconidae) did not affect alkaloid elimination. The presence of an effective anti-toxin system is discussed with reference to the evolution of hostplant relationships in the genus Callophrys. There is no evidence that in the secondarily myrmecoxenous larvae of C. rubi hostplantderived chemical defense takes the place of former myrmecophily.     

Transposon-induced mutations in two loci of Listeria monocytogenes serotype 1/2a result in phage resistance and lack of N-acetylglucosamine in the teichoic acid of the cell wall.

Teichoic acid-associated N-acetylglucosamine and rhamnose have been shown to serve as phage receptors in Listeria monocytogenes serotype 1/2a. We generated and characterized two single-copy Tn916DeltaE mutants which were resistant to phage A118 and several other serotype 1/2a-specific phages. In one mutant the insertion was immediately upstream of the recently identified ptsHI locus, which encodes two proteins of the phosphoenolpyruvate-dependent carbohydrate uptake system, whereas in the other the insertion was immediately upstream of an operon whose most distal gene was clpC, involved in stress responses and virulence. Transduction experiments confirmed the association of the phage-resistant phenotype of these mutants with the transposon insertion. Phage A118 resistance of the mutants could be attributed to inability of the phage to adsorb onto the mutant cells, and biochemical analysis of cell wall composition showed that the teichoic acids of both mutants were deficient in N-acetylglucosamine. Rhamnose and other teichoic acid and cell wall components were not affected.     

Simulation of Nanoparticle Permeation through a Lipid Membrane

A metric of nanoparticle toxicity is the passive permeability rate through cellular membranes. To assess the influence of nanoparticle morphology on this process, the permeability of buckyball-sized molecules through a representative lipid bilayer was investigated by molecular-dynamics simulation. When C₆₀ was compared with a prototypical opened C₆₀ molecule and a representative combustion-generated particle, C₆₈H₂₉, the calculated free-energy profiles along the permeation coordinate revealed a sizable variation in form and depth. The orientation of the anisotropic molecules was determined by monitoring the principal axis corresponding to the largest moment of inertia, and free rotation was shown to be hindered in the bilayer interior. Diffusion constant values of the permeant molecules were calculated from a statistical average of seven to 10 trajectories at five locations along the permeation coordinate. A relatively minor variation of the values was observed in the bilayer interior; however, local resistance values spanned up to 24 orders of magnitude from the water layer to the bilayer center, due primarily to its exponential dependence on free energy. The permeability coefficient values calculated for the three similarly sized but structurally distinct nanoparticles showed a significant variance. The use of C₆₀ to represent similarly sized carbonaceous nanoparticles for assessments of toxicity is questioned.     

Genomic deletion and promoter methylation status of Hypermethylated in Cancer 1 (HIC1) in mantle cell lymphoma

Mantle cell lymphomas (MCL), characterized by the t(11;14)(q13;q32), frequently carry secondary genetic alterations such as deletions in chromosome 17p involving the TP53 locus. Given that the association between TP53-deletions and concurrent mutations of the remaining allele is weak and based on our recent report that the Hypermethylated in Cancer 1 (HIC1) gene, that is located telomeric to the TP53 gene, may be targeted by deletions in 17p in diffuse large B-cell lymphoma (DLBCL), we investigated whether HIC1 inactivations might also occur in MCL. Monoallelic deletions of the TP53 locus were detected in 18 out of 59 MCL (31%), while overexpression of p53 protein occurred in only 8 out of 18 of these MCL (44%). In TP53-deleted MCL, the HIC1 gene locus was co-deleted in 11 out of 18 cases (61%). However, neither TP53 nor HIC1 deletions did affect survival of MCL patients. In most analyzed cases, no hypermethylation of the HIC1 exon 1A promoter was observed (17 out of 20, 85%). However, in MCL cell lines without HIC1-hypermethylation, the mRNA expression levels of HIC1 were nevertheless significantly reduced, when compared to reactive lymph node specimens, pointing to the occurrence of mechanisms other than epigenetic or genetic events for the inactivation of HIC1 in this entity.     

Epithelioid sarcoma

The first appearance, the 12-year follow-up, and the autopsy of a patient with a strange soft-tissue tumor in the lower leg region are described. Although it was originally taken for a malignant synovial tumor, its peculiar distribution pattern, together with its histologic picture, confirmed the final diagnosis as an epithelioid sarcoma.     

Effect of microtubule-associated proteins on the protofilament number of microtubules assembled in vitro

In order to demonstrate the effect of microtubule-associated proteins on the protofilament number of microtubules, we used different systems of microtubule formation in vitro in which these proteins are either functionally eliminated (by DNA or glycerol) or absent (purified tubulin). The results obtained by electron microscopy of ultrathin-sectioned material indicate that under standard conditions in the presence of microtubule-associated proteins microtubules are formed consisting predominantly of 14 protofilaments. In cases of deficiency of microtubule-associated proteins, the mean value of the protofilament number is lower, and the protofilament number within the microtubule population varies remarkably. On the other hand, the action of microtubule-associated proteins is enhanced by histones resulting in increased protofilament numbers. A model is proposed illustrating that the quality and the quantity of microtubule-associated proteins bound to microtubules determine the curvature between the protofilaments and restrict the variety of their binding angles. In this way the microtubule-associated proteins may be regarded as an important factor in determining the structural fidelity of microtubules.     

Cell degeneration during early development of hymenopteran olfactory sensilla

The imaginal pore plates of Hymenoptera apocrita so far examined embody five or six envelope cells respectively. In early developmental stages, however, supernumerary envelope cells have been found. The results are discussed in the context of cell death as a developmental phenomenon.