Microbial hitchhikers on intercontinental dust: catching a lift in Chad

Ancient mariners knew that dust whipped up from deserts by strong winds travelled long distances, including over oceans. Satellite remote sensing revealed major dust sources across the Sahara. Indeed, the Bodélé Depression in the Republic of Chad has been called the dustiest place on earth. We analysed desert sand from various locations in Chad and dust that had blown to the Cape Verde Islands. High throughput sequencing techniques combined with classical microbiological methods showed that the samples contained a large variety of microbes well adapted to the harsh desert conditions. The most abundant bacterial groupings in four different phyla included: (a) Firmicutes—Bacillaceae, (b) Actinobacteria—Geodermatophilaceae, Nocardiodaceae and Solirubrobacteraceae, (c) Proteobacteria—Oxalobacteraceae, Rhizobiales and Sphingomonadaceae, and (d) Bacteroidetes—Cytophagaceae. Ascomycota was the overwhelmingly dominant fungal group followed by Basidiomycota and traces of Chytridiomycota, Microsporidia and Glomeromycota. Two freshwater algae (Trebouxiophyceae) were isolated. Most predominant taxa are widely distributed land inhabitants that are common in soil and on the surfaces of plants. Examples include Bradyrhizobium spp. that nodulate and fix nitrogen in Acacia species, the predominant trees of the Sahara as well as Herbaspirillum (Oxalobacteraceae), a group of chemoorganotrophic free-living soil inhabitants that fix nitrogen in association with Gramineae roots. Few pathogenic strains were found, suggesting that African dust is not a large threat to public health.     

A transfer function approach to measuring cell inheritance

Background  

The inheritance of cellular material between parent and daughter cells during mitosis is highly influential in defining the properties of the cell and therefore the population lineage. This is of particular relevance when studying cell population evolution to assess the impact of a disease or the perturbation due to a drug treatment. The usual technique to investigate inheritance is to use time-lapse microscopy with an appropriate biological marker, however, this is time consuming and the number of inheritance events captured are too low to be statistically meaningful.     

Abundance and feeding of microheterotrophic flagellates from a eutrophic lake

The growth of planktonic bacteria from a eutrophic lake was evaluated with microflagellate predators present and absent. Differential filtration (50 and 8 µm filters) was used to exclude ciliates and larger zoo-and phytoplankton from replicate experimental cultures. Additional filtration (1 µm filter) excluded heterotrophic microflagellates from a second set of experimental cultures, producing cultures that contained either bacteria and microflagellates or only bacteria. Growth of bacteria and microflagellates was evaluated by epifluorescent microscopy from repeated sampling over approximately 200 h. Bacterial numbers were reduced in the presence of microflagellates, and microflagellates were observed to contain bacterial prey. However, microflagellate numbers were high (about 10⁶ cells ml^-1) and were less than an order of magnitude lower than bacterial numbers. Bacteria growing in the presence of microflagellates did not show predator-prey population oscillations but had in-phase oscillations in numbers, suggesting that microflagellate predation in freshwater may not control numbers of planktonic bacteria. Clearance rates of heterotrophic microflagellates, estimated to be only 30 body volumes hr^-1, were insufficient to maintain flagellate growth, suggesting that other energy sources may be needed to maintain microflagellates in eutrophic freshwater ecosystems.     

A mechanism for acute aluminium toxicity in fish

Aluminium is acutely toxic to fish in acid waters. The gill is the principal target organ and death is due to a combination of ionoregulatory, osmoregulatory and respiratory dysfunction. The toxic mechanism has hitherto received little direct consideration and is unknown. In this paper the mechanism of acute aluminium toxicity is approached from a chemical perspective. Symptomatic evidence of toxicity is taken from the literature and combined with our own research to elucidate a biochemically sound model to describe a possible mechanism of acute aluminium toxicity in fish. The proposed model delineates the chemical conditions immediately adjacent to the gill surface and emphasizes their importance in aluminium's toxic mode of action. The mechanism is shown to be bipartite. Aluminium binding to functional groups both apically located at the gill surface and intracellularly located within lamellar epithelial cells disrupts the barrier properties of the gill epithelium. The concomitant iono- and osmoregulatory dysfunction results in accelerated cell necrosis, sloughing and death of the fish. The mechanism of epithelial cell death is proposed as a general mechanism of aluminium-induced accelerated cell death.