Temperature excludes N2-fixing heterocystous cyanobacteria in the tropical oceans

Whereas the non-heterocystous cyanobacteria Trichodesmium spp. are the dominant N2-fixing organisms in the tropical oceans, heterocystous species dominate N2 fixation in freshwater lakes and brackish environments such as the Baltic Sea. So far no satisfactory explanation for the absence of heterocystous cyanobacteria in the pelagic of the tropical oceans has been given, even though heterocysts would seem to represent an ideal strategy for protecting nitrogenase from being inactivated by O2, thereby enabling cyanobacteria to fix N2 and to perform photosynthesis simultaneously. Trichodesmium is capable of N2 fixation, apparently without needing to differentiate heterocysts. Here we show that differences in the temperature dependence of O2 flux, respiration and N2 fixation activity explain how Trichodesmium performs better than heterocystous species at higher temperatures. Our results also explain why Trichodesmium is not successful in temperate or cold seas. The absence of heterocystous cyanobacteria in the pelagic zone of temperate and cold seas, however, requires another explanation.     

Probing carrier dynamics in nanostructures by picosecond cathodoluminescence

Picosecond and femtosecond spectroscopy allow the detailed study of carrier dynamics in nanostructured materials. In such experiments, a laser pulse normally excites several nanostructures at once. However, spectroscopic information may also be acquired using pulses from an electron beam in a modern electron microscope, exploiting a phenomenon called cathodoluminescence. This approach offers several advantages. The multimode imaging capabilities of the electron microscope enable the correlation of optical properties (via cathodoluminescence) with surface morphology (secondary electron mode) at the nanometre scale. The broad energy range of the electrons can excite wide-bandgap materials, such as diamond- or gallium-nitride-based structures that are not easily excited by conventional optical means. But perhaps most intriguingly, the small beam can probe a single selected nanostructure. Here we apply an original time-resolved cathodoluminescence set-up to describe carrier dynamics within single gallium-arsenide-based pyramidal nanostructures with a time resolution of 10 picoseconds and a spatial resolution of 50 nanometres. The behaviour of such charge carriers could be useful for evaluating elementary components in quantum computers, optical quantum gates or single photon sources for quantum cryptography.     

Cell-type-specific replication initiation programs set fragility of the FRA3B fragile site

Common fragile sites have long been identified by cytogeneticists as chromosomal regions prone to breakage upon replication stress. They are increasingly recognized to be preferential targets for oncogene-induced DNA damage in pre-neoplastic lesions and hotspots for chromosomal rearrangements in various cancers. Common fragile site instability was attributed to the fact that they contain sequences prone to form secondary structures that may impair replication fork movement, possibly leading to fork collapse resulting in DNA breaks. Here we show, in contrast to this view, that the fragility of FRA3B--the most active common fragile site in human lymphocytes--does not rely on fork slowing or stalling but on a paucity of initiation events. Indeed, in lymphoblastoid cells, but not in fibroblasts, initiation events are excluded from a FRA3B core extending approximately 700 kilobases, which forces forks coming from flanking regions to cover long distances in order to complete replication. We also show that origins of the flanking regions fire in mid-S phase, leaving the site incompletely replicated upon fork slowing. Notably, FRA3B instability is specific to cells showing this particular initiation pattern. The fact that both origin setting and replication timing are highly plastic in mammalian cells explains the tissue specificity of common fragile site instability we observed. Thus, we propose that common fragile sites correspond to the latest initiation-poor regions to complete replication in a given cell type. For historical reasons, common fragile sites have been essentially mapped in lymphocytes. Therefore, common fragile site contribution to chromosomal rearrangements in tumours should be reassessed after mapping fragile sites in the cell type from which each tumour originates.