The Drosophila EGF receptor gene homolog: conservation of both hormone binding and kinase domains

Chicken v-erB probe was used to isolate a unique clone of Drosophila melanogaster DNA. It maps by in situ hybridization to position 57F on chromosome 2. A complete nucleotide sequence of the coding region has been obtained. The putative Drosophila EGF receptor protein is similar in overall organization to the human homolog. It shows three distinct domains: an extracellular putative EGF binding domain, a hydrophobic transmembrane region, and a cytoplasmic kinase domain. The overall amino acid homology is 41% in the extracellular domain and 55% in the kinase domain. Two cysteine-rich regions, a hallmark of the human ligand-binding domain, have also been conserved. Fusion of the coding sequences of the kinase and extracellular domains generating the receptor gene must have occurred over 800 million years ago.     

Factors determining the development of algal and bacterial blooms in the Dead Sea: a study of simulation experiments in outdoor ponds

Abstract To simulate the occurrence of bacterial and algal blooms in the Dead Sea, we filled 5.6 m³ outdoor ponds with mixtures of Dead Sea water and Mediterranean water, at different seasons, and studied the effect of salinity and of addition of glycerol, glucose and different concentrations of phosphate on the rate and extent of bacterial and algal growth. Addition of phosphate appeared to be essential for the development of mass blooms of both the green alga Dunaliella and of the red halobacteria. In the presence of phosphate the growth rates were high only when the Dead Sea water was diluted by at least 25–35% with Mediterranean water. Also, at low temperatures (14–17°C) mass blooms of bacteria and algae occurred, but growth rates were reduced, and the maximal salinity at which growth was observed shifted to a lower value. Glucose, glycerol and a Dunaliella bloom all proved to be suitable carbon sources for mass development of halobacteria.     

Photooxidative Death in Blue-Green Algae

When incubated in the light under 100% oxygen, wild-type blue-green algae (Anacystis nidulans, Synechococcus cedrorum) die out rapidly at temperatures of 4 to 15 C, and at 35 C (or at 26 C in the case of S. cedrorum) in the absence of CO(2). Photosynthesis is impaired in these cells long before they die. Blocking of photosystem II at high temperatures in the presence of CO(2) sensitizes the algae to photooxidative death. Photooxidative death and bleaching of photosynthetic pigments are separable phenomena. Photooxidative conditions were demonstrated in Israeli fish ponds using A. nidulans as the test organism during dense summer blooms, when dissolved CO(2) is low, and in winter, when water temperatures generally drop below 15 C. This finding suggests that photooxidative death may be responsible for the sudden decomposition of blue-green blooms in summer, and may be a factor in the absence of blue-green blooms in winter.     

Protein turnover and cell-cycle initiation in yeast

The effects of short pulses of cycloheximide on the traversal of the G1 phase of the cell cycle of the yeast Saccharomyces cerevisiae were examined. Cells were released from a block at the regulatory stage of G1, termed ‘start’, and pulsed with cycloheximide. Delays in budding which were considerably longer than the length of the pulse were observed. During the delay the cells remained blocked at ‘start’. No delay in budding was observed after cycloheximide pulses, when cells were released from a cdc 24 block which arrests the budding process but not ‘start’. Overall protein synthesis did not show an additional delay after the pulse. The extra lag following cycloheximide pulses appears to reflect a unique feature of ‘start’. It may be accounted for by a requirement at ‘start’ for a labile protein with a half-life time of about 6 min.     

Complete genome sequence of the erythromycin-producing bacterium Saccharopolyspora erythraea NRRL23338

Saccharopolyspora erythraea is used for the industrial-scale production of the antibiotic erythromycin A, derivatives of which play a vital role in medicine. The sequenced chromosome of this soil bacterium comprises 8,212,805 base pairs, predicted to encode 7,264 genes. It is circular, like those of the pathogenic actinomycetes Mycobacterium tuberculosis and Corynebacterium diphtheriae, but unlike the linear chromosomes of the model actinomycete Streptomyces coelicolor A3(2) and the closely related Streptomyces avermitilis. The S. erythraea genome contains at least 25 gene clusters for production of known or predicted secondary metabolites, at least 72 genes predicted to confer resistance to a range of common antibiotic classes and many sets of duplicated genes to support its saprophytic lifestyle. The availability of the genome sequence of S. erythraea will improve insight into its biology and facilitate rational development of strains to generate high-titer producers of clinically important antibiotics.     

A New Fungal Diterpene Induces VDAC1-dependent Apoptosis in Bax/Bak-deficient Cells

The pro-apoptotic Bax and Bak proteins are considered central to apoptosis, yet apoptosis occurs in their absence. Here, we asked whether the mitochondrial protein VDAC1 mediates apoptosis independently of Bax/Bak. Upon screening a fungal secondary metabolite library for compounds inducing apoptosis in Bax/Bak-deficient mouse embryonic fibroblasts, we identified cyathin-R, a new cyathane diterpenoid compound able to activate apoptosis in the absence of Bax/Bak via promotion of the VDAC1 oligomerization that mediates cytochrome c release. Diphenylamine-2-carboxilic acid, an inhibitor of VDAC1 conductance and oligomerization, inhibited cyathin-R-induced VDAC1 oligomerization and apoptosis. Similarly, Bcl-2 overexpression conferred resistance to cyathin-R-induced apoptosis and VDAC1 oligomerization. Silencing of VDAC1 expression prevented cyathin-R-induced apoptosis. Finally, cyathin-R effectively attenuated tumor growth and induced apoptosis in Bax/Bak-deficient cells implanted into a xenograft mouse model. Hence, this study identified a new compound promoting VDAC1-dependent apoptosis as a potential therapeutic option for cancerous cells lacking or presenting inactivated Bax/Bak.