Changes in the tail of Ambystoma maculatum at different stages of metamorphosis: observations on tissue remodeling and its relationship to hydrolytic enzymes.

A system for staging A. maculatum during growth and metamorphosis was devised, based on several parameters of body size; body length, tail length and tail width. Animals at various stages of metamorphosis were employed to study the relationship between specific biochemical and histological changes that occur in the tail of this urodele during metamorphosis. The specific and total activity of two hydrolytic enzymes, acid phosphatase and beta-N-acetyl-glucosaminidase, were measured in tail tissues at progressive stages of development. The activities of these enzymes increased in both the fins and muscular portion of the tail during metamorphosis. These activities can be correlated with resorption of the tail fins and the remodeling of tissues in the muscular portion of the tail.     

Induced plant volatiles allow sensitive monitoring of plant health status in greenhouses

A novel approach to support the inspection of greenhouse crops is based on the measurement of volatile organic compounds emitted by unhealthy plants.This approach has attracted some serious interest over the last decade. In pursuit of this interest, we performed several experiments at the laboratory-scale to pinpoint marker volatiles that can be used to indicate certain health problems. In addition to these laboratory experiments, pilot and model studies were performed in order to verify the validity of these marker volatiles under real-world conditions. This paper provides an overview of results and gives an outlook on the use of plant volatiles for plant health monitoring.Key words: plant health, volatiles, plant pathogens, plant infection     

Effect of man-made electromagnetic fields on common <i>Brassicaceae Lepidium sativum</i> (cress d’Alinois) seed germination: a preliminary replication study

Under high levels of radiation (70-100 µW/m2 =175 mV/m), seeds of Brassicaceae Lepidium sativum (cress d’Alinois) never germinated. In fact, the first step of seeds’ germination ‒ e.g. imbibitions of germinal cells ‒ could not occur under radiation, while inside the humid compost such imbibitions occurred and roots slightly developed. When removed from the electromagnetic field, seeds germinated normally. The radiation was, thus, most likely the cause of the non-occurrence of the seeds’ imbibitions and germination.     

Leishmania adaptor protein-1 subunits are required for normal lysosome traffic, flagellum biogenesis, lipid homeostasis, and adaptation to temperatures encountered in the mammalian host

The adaptor protein-1 (AP-1) complex is involved in membrane transport between the Golgi apparatus and endosomes. In the protozoan parasite Leishmania mexicana mexicana, the AP-1 μ1 and σ1 subunits are not required for growth at 27°C but are essential for infectivity in the mammalian host. In this study, we have investigated the function of these AP-1 subunits in order to understand the molecular basis for this loss of virulence. The μ1 and σ1 subunits were localized to late Golgi and endosome membranes of the major parasite stages. Parasite mutants lacking either AP-1 subunit lacked obvious defects in Golgi structure, endocytosis, or exocytic transport. However, these mutants displayed reduced rates of endosome-to-lysosome transport and accumulated fragmented, sterol-rich lysosomes. Defects in flagellum biogenesis were also evident in nondividing promastigote stages, and this phenotype was exacerbated by inhibitors of sterol and sphingolipid biosynthesis. Furthermore, both AP-1 mutants were hypersensitive to elevated temperature and perturbations in membrane lipid composition. The pleiotropic requirements for AP-1 in membrane trafficking and temperature stress responses explain the loss of virulence of these mutants in the mammalian host.     

Cytoplasmic dynein could be key to understanding neurodegeneration

A new mouse mutation, Sprawling, highlights an essential role for the dynein heavy chain in sensory neuron function, but it lacks the ability of other known heavy-chain mutations to ameliorate neurodegeneration due to defective superoxide dismutase.