Mississippi River and Sea Surface Height Effects on Oil Slick Migration

Millions of barrels of oil escaped into the Gulf of Mexico (GoM) after the 20 April, 2010 explosion of Deepwater Horizon (DH). Ocean circulation models were used to forecast oil slick migration in the GoM, however such models do not explicitly treat the effects of secondary eddy-slopes or Mississippi River (MR) hydrodynamics. Here we report oil front migration that appears to be driven by sea surface level (SSL) slopes, and identify a previously unreported effect of the MR plume: under conditions of relatively high river discharge and weak winds, a freshwater mound can form around the MR Delta. We performed temporal oil slick position and altimeter analysis, employing both interpolated altimetry data and along-track measurements for coastal applications. The observed freshwater mound appears to have pushed the DH oil slick seaward from the Delta coastline. We provide a physical mechanism for this novel effect of the MR, using a two-layer pressure-driven flow model. Results show how SSL variations can drive a cross-slope migration of surface oil slicks that may reach velocities of order km/day, and confirm a lag time of order 5–10 days between mound formation and slick migration, as observed form the satellite analysis. Incorporating these effects into more complex ocean models will improve forecasts of slick migration for future spills. More generally, large SSL variations at the MR mouth may also affect the dispersal of freshwater, nutrients and sediment associated with the MR plume

Control of Parasitophorous Vacuole Expansion by LYST/Beige Restricts the Intracellular Growth of Leishmania amazonensis

The intracellular protozoan Leishmania replicates in parasitophorous vacuoles (PV) that share many features with late endosomes/lysosomes. L. amazonensis PVs expand markedly during infections, but the impact of PV size on parasite intracellular survival is still unknown. Here we show that host cells infected with L. amazonensis upregulate transcription of LYST/Beige, which was previously shown to regulate lysosome size. Mutations in LYST/Beige caused further PV expansion and enhanced L. amazonensis replication. In contrast, LYST/Beige overexpression led to small PVs that did not sustain parasite growth. Treatment of LYST/Beige over-expressing cells with vacuolin-1 reversed this phenotype, expanding PVs and promoting parasite growth. The opposite was seen with E-64d, which reduced PV size in LYST-Beige mutant cells and inhibited L. amazonensis replication. Enlarged PVs appear to protect parasites from oxidative damage, since inhibition of nitric oxide synthase had no effect on L. amazonensis viability within large PVs, but enhanced their growth within LYST/Beige-induced small PVs. Thus, the upregulation of LYST/Beige in infected cells functions as a host innate response to limit parasite growth, by reducing PV volume and inhibiting intracellular survival

Identification of <i>Drosophila</i> Gene Products Required for Phagocytosis of <i>Leishmania donovani</i>

<div><p>The identity and function of host factors required for efficient phagocytosis and intracellular maintenance of the protozoan parasite <i>Leishmania donovani</i> are poorly understood. Utilising the phagocytic capability of <i>Drosophila</i> S2 cells, together with available tools for modulating gene expression by RNAi, we have developed an experimental system in which to identify host proteins of this type on a genome-wide scale. We have shown that <i>L. donovani</i> amastigotes can be phagocytosed by S2 cells, in which they replicate and are maintained in a compartment with features characteristic of mammalian phagolysosomes. Screening with dsRNAs from 1920 conserved metazoan genes has identified transcripts that, when reduced in expression, cause either increased or decreased phagocytosis. Focussing on genes in the latter class, RNAi-mediated knockdown of the small GTPase Rab5, the prenylated SNARE protein YKT6, one sub-unit of serine palmitoyltransferase (<i>spt2/lace),</i> the Rac1-associated protein Sra1 and the actin cytoskeleton regulatory protein, SCAR, all lead to a significant reduction in parasite phagocytosis. A role for the <i>lace</i> mammalian homologue in amastigote uptake by mammalian macrophages has been verified using the serine palmitoyltransferase inhibitor, myriocin. These observations suggest that this experimental approach has the potential to identify a large number of host effectors required for efficient parasite uptake and maintenance.</p></div