A dual function of V0-ATPase a1 provides an endolysosomal degradation mechanism in Drosophila melanogaster photoreceptors

The vesicular adenosine triphosphatase (v-ATPase) is a proton pump that acidifies intracellular compartments. In addition, mutations in components of the membrane-bound v-ATPase V0 sector cause acidification-independent defects in yeast, worm, fly, zebrafish, and mouse. In this study, we present a dual function for the neuron-specific V0 subunit a1 orthologue v100 in Drosophila melanogaster. A v100 mutant that selectively disrupts proton translocation rescues a previously characterized synaptic vesicle fusion defect and vesicle fusion with early endosomes. Correspondingly, V100 selectively interacts with syntaxins on the respective target membranes, and neither synaptic vesicles nor early endosomes require v100 for their acidification. In contrast, V100 is required for acidification once endosomes mature into degradative compartments. As a consequence of the complete loss of this neuronal degradation mechanism, photoreceptors undergo slow neurodegeneration, whereas selective rescue of the acidification-independent function accelerates cell death by increasing accumulations in degradation-incompetent compartments. We propose that V100 exerts a temporally integrated dual function that increases neuronal degradative capacity.     

The Seasonal Dynamics and Trophic Relations of the Plankton Components in Lake Peipsi (Peipus)

The seasonal dynamics of the biomass and production of phyto-, zoo- and bacterioplankton was investigated during the vegetation periods (from May to November) in 1985 and 1986 in the pelagial of the large eutrophic lake Peipsi (Estonia). The average values of productions per vegetation period for the investigation years were as follows: phytoplanktion − 203.5 gC · m⁻²; bacterioplankton − 37.9 gC · m⁻²; filter-feeding zooplankton − 20.6 gC · m⁻² and predatory zooplankton − 1.5 gC · m⁻². The herbivorous zooplankton production constituted 10.1% of primary production. This ratio indicates a direct relationship between zoo- and phytoplankton in the food chain — filtrators are feeding mostly on living algae and the detrital food chain seems of little importance. The dominance of large forms (Melosira sp., Aphanothece saxicola), in the phytoplankton during the major part of the vegetation period is assumed to be a result of high grazing pressure on small algae. Zooplankton grazing was investigated in situ in a specially constructed twin bathometer. Experimental measurements revealed, that zooplanktion presence in the experimental vessel actually stimulated the phytoplankton growth in many cases — the negative grazing values have been registered. That could be caused by the stimulation effect of nutrients (N, P), excreted by the concentrated zooplankton in the grazing chamber, which led to an increase of the nongrazed phytoplankton production. Bacteria have satisfied the zooplankton food requirements on average by 11%. Grazing on bacteria increased, when grazing on phytoplankton was somehow disturbed.     

The levels of cyclic GMP and glucose 1,6-diphosphate,and the activity of phosphofructokinase,in muscle from normal and dystrophic mice

A striking reduction in the levels of glucose 1,6-diphosphate and an increase in cyclic GMP were found in muscle from dystrophic mice. Concomitant to these changes, the allosteric activity of phosphofructokinase was found to be markedly reduced. These findings could offer an explanation for the observed reduction in glycolysis in the dystrophic muscle.     

Porphyria cutanea tarda: comparison of cases precipitated by alcohol and estrogens.

A group of seven patients with porphyria cutanea tarda (PCT) precipitated by excessive alcohol consumption (A) was compared with a group of nine patients with PCT precipitated by estrogen therapy (B). Comparison was based on clinical signs, biochemical and morphologic evidence of liver disease, results of serum iron studies and response to therapy. Group A patients were men of mean age 57 years; group B patients were women of mean age 39 years who had been taking estrogen orally, either for contraception (in combination with progesterone) or as replacement therapy. Clinical signs were essentially the same in the two groups. Some patients in both groups had biochemical and morphologic evidence of liver disease. Group A patients had elevated values for serum iron and total iron-binding capacity, whereas patients in group B had normal or low values. Cessation of estrogen therapy of less than a year''s duration brought about a spontaneous clinical and biochemical remission in group B patients. Otherwise, phlebotomy seemed to be the therapy of choice in both groups.     

Ultrastructural changes produced in Ehrlich ascites carcinoma cells by ultraviolet-visible radiation in the presence of melanins

Irradiation of Ehrlich ascites carcinoma (EAC) cells in the presence of pheomelanin, i.e., red hair melanin (RHM), has been reported to produce extensive cell lysis. Irradiation in the presence of eumelanin, i.e., black hair melanin (BHM), or irradiation in the absence of either type of melanin did not produce this effect. We observed that RHM particles penetrated the cell membrane without apparent structural damage to the cell or the cell membrane. Irradiation of the cells in the absence of melanin did not produce any changes in the ultrastructure of the cells. Incubation of the cells in the dark in the presence of RHM produced only minor structural, mainly cytoplasmic changes. Irradiation of the cells in the presence of RHM produced extensive ultrastructural changes prior to complete cell lysis; these changes were more severe than the effects of incubation of the cells in the dark in the presence of RHM. When the cells incubated in the dark or irradiated in the presence of latex particles or either one of the eumelanins particles, viz. BHM or synthetic dopa melanin, these particles did not penetrate into the cells or produce any ultrastructural changes. These particles were in fact not even ingested by the cells.     

Human Stem Cell-Derived Neurons Repair Circuits and Restore Neural Function

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