Changes in iron supply to oceanic plankton are thought to have a significant effect on concentrations of atmospheric carbon dioxide by altering rates of carbon sequestration, a theory known as the 'iron hypothesis'. For this reason, it is important to understand the response of pelagic biota to increased iron supply. Here we report the results of a mesoscale iron fertilization experiment in the polar Southern Ocean, where the potential to sequester iron-elevated algal carbon is probably greatest. Increased iron supply led to elevated phytoplankton biomass and rates of photosynthesis in surface waters, causing a large drawdown of carbon dioxide and macronutrients, and elevated dimethyl sulphide levels after 13 days. This drawdown was mostly due to the proliferation of diatom stocks. But downward export of biogenic carbon was not increased. Moreover, satellite observations of this massive bloom 30 days later, suggest that a sufficient proportion of the added iron was retained in surface waters. Our findings demonstrate that iron supply controls phytoplankton growth and community composition during summer in these polar Southern Ocean waters, but the fate of algal carbon remains unknown and depends on the interplay between the processes controlling export, remineralisation and timescales of water mass subduction.

[1] Several studies have shown the importance of the microbial community in specific aspects of the biogeochemical iron (Fe) cycle such as uptake or regeneration. During FeCycle, a 10-day study of Fe biogeochemistry within an unperturbed mesoscale in situ SF 6 labeled patch of HNLC waters, we investigated the role of both microzooplankton (herbivores and bacterivores) and viruses in regenerating Fe in the upper ocean. In summer 2003 we measured grazer-mediated Fe regeneration rates. The proportion of bacterial Fe released via grazing was severalfold greater than that mobilized from phytoplankton during herbivory. However, as the algal Fe pool (mainly Synechococcus) was severalfold larger than the bacterial pool, the absolute Fe regeneration rates were similar for both herbivores (17 pmol Fe L À1 d À1 ) and bacterivores (20 pmol Fe L À1 d À1 ). In all grazing experiments we observed that 90% (bacterivory) and 25% (herbivory) of the labeled Fe resided in the dissolved fraction after 24 hours. This trend has previously been reported in similar laboratory culture studies, which invoked the formation of dissolved, and/or colloidal metal ligands, associated with digestion, to make the released Fe less bioavailable. This explanation may not be valid for our study as another FeCycle experiment (Maldonado et al., 2005) demonstrated that resident phytoplankton could obtain Fe bound to a wide range of strong-binding ligands. In situ estimates of virally mediated Fe regeneration during FeCycle ranged from 0.4 to 28 pmol L À1 d À1 . It is not known why such a wide range of virally mediated regeneration rates was observed. Such variability prevented a direct comparison on the relative roles of grazers and viruses in Fe recycling. The rates of grazer-mediated regeneration accounted for 30% to >100% of the bacterial and phytoplankton Fe demand measured during FeCycle, indicating the key role of the microbial food web in Fe recycling.

[1] An improved knowledge of iron biogeochemistry is needed to better understand key controls on the functioning of high-nitrate low-chlorophyll (HNLC) oceanic regions. Iron budgets for HNLC waters have been constructed using data from disparate sources ranging from laboratory algal cultures to ocean physics. In summer 2003 we conducted FeCycle, a 10-day mesoscale tracer release in HNLC waters SE of New Zealand, and measured concurrently all sources (with the exception of aerosol deposition) to, sinks of iron from, and rates of iron recycling within, the surface mixed layer. A pelagic iron budget (timescale of days) indicated that oceanic supply terms (lateral advection and vertical diffusion) were relatively small compared to the main sink (downward particulate export). Remote sensing and terrestrial monitoring reveal 13 dust or wildfire events in Australia, prior to and during FeCycle, one of which may have deposited iron at the study location. However, iron deposition rates cannot be derived from such observations, illustrating the difficulties in closing iron budgets without quantification of episodic atmospheric supply. Despite the threefold uncertainties reported for rates of aerosol deposition (Duce et al., 1991), published atmospheric iron supply for the New Zealand region is $50-fold (i.e., 7-to 150-fold) greater than the oceanic iron supply measured in our budget, and thus was comparable (i.e., a third to threefold) to our estimates of downward export of particulate iron. During FeCycle, the fluxes due to short term (hours) biological iron uptake and regeneration were indicative of rapid recycling and were tenfold greater than for new iron (i.e. estimated atmospheric and measured oceanic supply), giving an ''fe'' ratio (uptake of new iron/uptake of new + regenerated iron) of 0.17 (i.e., a range of 0.06 to 0.51 due to uncertainties on aerosol iron supply), and an ''Fe'' ratio (biogenic Fe export/uptake of new + regenerated iron) of 0.09 (i.e., 0.03 to 0.24).Citation: Boyd, P. W., et al. (2005), FeCycle: Attempting an iron biogeochemical budget from a mesoscale SF 6 tracer experiment in unperturbed low iron waters, Global Biogeochem. Cycles, 19, GB4S20,

Abstract.During

DNA double-strand breaks (DSBs) can be repaired by homologous recombination (HR), which can involve Holliday junction (HJ) intermediates that are ultimately resolved by nucleolytic enzymes. An N-terminal fragment of human GEN1 has recently been shown to act as a Holliday junction resolvase, but little is known about the role of GEN-1 in vivo. Holliday junction resolution signifies the completion of DNA repair, a step that may be coupled to signaling proteins that regulate cell cycle progression in response to DNA damage. Using forward genetic approaches, we identified a Caenorhabditis elegans dual function DNA double-strand break repair and DNA damage signaling protein orthologous to the human GEN1 Holliday junction resolving enzyme. GEN-1 has biochemical activities related to the human enzyme and facilitates repair of DNA double-strand breaks, but is not essential for DNA double-strand break repair during meiotic recombination. Mutational analysis reveals that the DNA damage-signaling function of GEN-1 is separable from its role in DNA repair. GEN-1 promotes germ cell cycle arrest and apoptosis via a pathway that acts in parallel to the canonical DNA damage response pathway mediated by RPA loading, CHK1 activation, and CEP-1/p53–mediated apoptosis induction. Furthermore, GEN-1 acts redundantly with the 9-1-1 complex to ensure genome stability. Our study suggests that GEN-1 might act as a dual function Holliday junction resolvase that may coordinate DNA damage signaling with a late step in DNA double-strand break repair.