Diatom carbon export enhanced by silicate upwelling in the North East Atlantic.

Diatom carbon export enhanced by silicate upwelling in the northeast Atlantic John T. Allen1,2, Louise Brown1,3, Richard Sanders1, C. Mark Moore1, Alexander Mustard1, Sophie Fielding1, Mike Lucas1, Michel Rixen4, Graham Savidge5, Stephanie Henson1 and Dan Mayor1 Top of pageDiatoms are unicellular or chain-forming phytoplankton that use silicon (Si) in cell wall construction. Their survival during periods of apparent nutrient exhaustion enhances carbon sequestration in frontal regions of the northern North Atlantic. These regions may therefore have a more important role in the 'biological pump' than they have previously been attributed1, but how this is achieved is unknown. Diatom growth depends on silicate availability, in addition to nitrate and phosphate2, 3, but northern Atlantic waters are richer in nitrate than silicate4. Following the spring stratification, diatoms are the first phytoplankton to bloom2, 5. Once silicate is exhausted, diatom blooms subside in a major export event6, 7. Here we show that, with nitrate still available for new production, the diatom bloom is prolonged where there is a periodic supply of new silicate: specifically, diatoms thrive by 'mining' deep-water silicate brought to the surface by an unstable ocean front. The mechanism we present here is not limited to silicate fertilization; similar mechanisms could support nitrate-, phosphate- or iron-limited frontal regions in oceans elsewhere.

Organisational controls, typologies and time scales of paraglacial gravel-dominated coastal systems

The fundamental controls on the initiation and development of gravel-dominated deposits (beaches and barriers) on paraglacial coasts are particle size and shape, sediment supply, storm wave activity (primarily runup), relative sea-level (RSL) change, and terrestrial basement structure (primarily as it affects accommodation space). This paper examines the stochastic basis for barrier organisation as shown by variation in gravel barrier architecture. We recognise punctuated self-organisation of barrier development that is disrupted by short phases of barrier instability. The latter results from positive feedback causing barrier breakdown when sediment supply is exhausted. We examine published typologies for gravel barriers and advocate a consolidated perspective using rate of RSL change and sediment supply. We also consider the temporal variation in controls on barrier development. These are examined in terms of a simple behavioural model (BARCH) for prograding gravel barrier architecture and its sensitivity to such controls. The nature of macroscale (102–103 years) gravel barrier development, including inherited characteristics that influence barrier genesis, as well as forcing from changing RSL, sediment supply, headland control and barrier inertia, is examined in the context of long-surviving barriers along the southern England coastline.

A complex zinc finger controls the enzymatic activities of nidovirus helicases.

Nidoviruses (Coronaviridae, Arteriviridae, and Roniviridae) encode a nonstructural protein, called nsp10 in arteriviruses and nsp13 in coronaviruses, that is comprised of a C-terminal superfamily 1 helicase domain and an N-terminal, putative zinc-binding domain (ZBD). Previously, mutations in the equine arteritis virus (EAV) nsp10 ZBD were shown to block arterivirus reproduction by disrupting RNA synthesis and possibly virion biogenesis. Here, we characterized the ATPase and helicase activities of bacterially expressed mutant forms of nsp10 and its human coronavirus 229E ortholog, nsp13, and correlated these in vitro activities with specific virus phenotypes. Replacement of conserved Cys or His residues with Ala proved to be more deleterious than Cys-for-His or His-for-Cys replacements. Furthermore, denaturation-renaturation experiments revealed that, during protein refolding, Zn2+ is essential for the rescue of the enzymatic activities of nidovirus helicases. Taken together, the data strongly support the zinc-binding function of the N-terminal domain of nidovirus helicases. nsp10 ATPase/helicase deficiency resulting from single-residue substitutions in the ZBD or deletion of the entire domain could not be complemented in trans by wild-type ZBD, suggesting a critical function of the ZBD in cis. Consistently, no viral RNA synthesis was detected after transfection of EAV full-length RNAs encoding ATPase/helicase-deficient nsp10 into susceptible cells. In contrast, diverse phenotypes were observed for mutants with enzymatically active nsp10, which in a number of cases correlated with the activities measured in vitro. Collectively, our data suggest that the ZBD is critically involved in nidovirus replication and transcription by modulating the enzymatic activities of the helicase domain and other, yet unknown, mechanisms.