Mesoscale features create hotspots of carbon uptake in the Antarctic Circumpolar Current

The influence of eddy structures on the seasonal depletion of dissolved inorganic carbon (DIC) and carbon dioxide (CO2) disequilibrium was investigated during a trans-Atlantic crossing of the Antarctic Circumpolar Current (ACC) in austral summer 2012. The Georgia Basin, downstream of the island of South Georgia (54-55°S, 36-38°W) is a highly dynamic region due to the mesoscale activity associated with the flow of the Subantarctic Front (SAF) and Polar Front (PF). Satellite sea-surface height and chlorophyll-a anomalies revealed a cyclonic cold core that dominated the northern Georgia Basin that was formed from a large meander of the PF. Warmer waters influenced by the SAF formed a smaller anticyclonic structure to the east of the basin. Both the cold core and warm core eddy structures were hotspots of carbon uptake relative to the rest of the ACC section during austral summer. This was most amplified in the cold core where greatest CO2 undersaturation (-78 µatm) and substantial surface ocean DIC deficit (5.1 mol m-2) occurred. In the presence of high wind speeds, the cold core eddy acted as a strong sink for atmospheric CO2 of 25.5 mmol m-2 day-1. Waters of the warm core displayed characteristics of the Polar Frontal Zone (PFZ), with warmer upper ocean waters and enhanced CO2 undersaturation (-59 µatm) and depletion of DIC (4.9mol m-2). A proposed mechanism for the enhanced carbon uptake across both eddy structures is based on the Ekman eddy pumping theory: (i) the cold core is seeded with productive (high chlorophyll-a) waters from the Antarctic Zone and sustained biological productivity through upwelled nutrient supply that counteracts DIC inputs from deep waters; (ii) horizontal entrainment of low-DIC surface waters (biological uptake) from the PFZ downwell within the warm core and cause relative DIC-depletion in the upper water column. The observations suggest that the formation and northward propagation of cold core eddies in the region of the PF could project low-DIC waters towards the site of Antarctic Intermediate Water formation and enhance CO2 drawdown into the deep ocean

Anopheles Imd Pathway Factors and Effectors in Infection Intensity-Dependent Anti-Plasmodium Action

The Anopheles gambiae immune response against Plasmodium falciparum, an etiological agent of human malaria, has been identified as a source of potential anti-Plasmodium genes and mechanisms to be exploited in efforts to control the malaria transmission cycle. One such mechanism is the Imd pathway, a conserved immune signaling pathway that has potent anti-P. falciparum activity. Silencing the expression of caspar, a negative regulator of the Imd pathway, or over-expressing rel2, an Imd pathway-controlled NFkappaB transcription factor, confers a resistant phenotype on A. gambiae mosquitoes that involves an array of immune effector genes. However, unexplored features of this powerful mechanism that may be essential for the implementation of a malaria control strategy still remain. Using RNA interference to singly or dually silence caspar and other components of the Imd pathway, we have identified genes participating in the anti-Plasmodium signaling module regulated by Caspar, each of which represents a potential target to achieve over-activation of the pathway. We also determined that the Imd pathway is most potent against the parasite's ookinete stage, yet also has reasonable activity against early oocysts and lesser activity against late oocysts. We further demonstrated that caspar silencing alone is sufficient to induce a robust anti-P. falciparum response even in the relative absence of resident gut microbiota. Finally, we established the relevance of the Imd pathway components and regulated effectors TEP1, APL1, and LRIM1 in parasite infection intensity-dependent defense, thereby shedding light on the relevance of laboratory versus natural infection intensity models. Our results highlight the physiological considerations that are integral to a thoughtful implementation of Imd pathway manipulation in A. gambiae as part of an effort to limit the malaria transmission cycle, and they reveal a variety of previously unrecognized nuances in the Imd-directed immune response against P. falciparum

Insect Neuropeptide Bursicon Homodimers Induce Innate Immune and Stress Genes during Molting by Activating the NF-κB Transcription Factor Relish

BACKGROUND: Bursicon is a heterodimer neuropeptide composed of two cystine knot proteins, bursicon α (burs α) and bursicon β (burs β), that elicits cuticle tanning (melanization and sclerotization) through the Drosophila leucine-rich repeats-containing G protein-coupled receptor 2 (DLGR2). Recent studies show that both bursicon subunits also form homodimers. However, biological functions of the homodimers have remained unknown until now. METHODOLOGY/PRINCIPAL FINDINGS: In this report, we show in Drosophila melanogaster that both bursicon homodimers induced expression of genes encoding antimicrobial peptides (AMPs) in neck-ligated adults following recombinant homodimer injection and in larvae fat body after incubation with recombinant homodimers. These AMP genes were also up-regulated in 24 h old unligated flies (when the endogenous bursicon level is low) after injection of recombinant homodimers. Up-regulation of AMP genes by the homodimers was accompanied by reduced bacterial populations in fly assay preparations. The induction of AMP expression is via activation of the NF-κB transcription factor Relish in the immune deficiency (Imd) pathway. The influence of bursicon homodimers on immune function does not appear to act through the heterodimer receptor DLGR2, i.e. novel receptors exist for the homodimers. CONCLUSIONS/SIGNIFICANCE: Our results reveal a mechanism of CNS-regulated prophylactic innate immunity during molting via induced expression of genes encoding AMPs and genes of the Turandot family. Turandot genes are also up-regulated by a broader range of extreme insults. From these data we infer that CNS-generated bursicon homodimers mediate innate prophylactic immunity to both stress and infection during the vulnerable molting cycle

Rudra Interrupts Receptor Signaling Complexes to Negatively Regulate the IMD Pathway

Insects rely primarily on innate immune responses to fight pathogens. In Drosophila, antimicrobial peptides are key contributors to host defense. Antimicrobial peptide gene expression is regulated by the IMD and Toll pathways. Bacterial peptidoglycans trigger these pathways, through recognition by peptidoglycan recognition proteins (PGRPs). DAP-type peptidoglycan triggers the IMD pathway via PGRP-LC and PGRP-LE, while lysine-type peptidoglycan is an agonist for the Toll pathway through PGRP-SA and PGRP-SD. Recent work has shown that the intensity and duration of the immune responses initiating with these receptors is tightly regulated at multiple levels, by a series of negative regulators. Through two-hybrid screening with PGRP-LC, we identified Rudra, a new regulator of the IMD pathway, and demonstrate that it is a critical feedback inhibitor of peptidoglycan receptor signaling. Following stimulation of the IMD pathway, rudra expression was rapidly induced. In cells, RNAi targeting of rudra caused a marked up-regulation of antimicrobial peptide gene expression. rudra mutant flies also hyper-activated antimicrobial peptide genes and were more resistant to infection with the insect pathogen Erwinia carotovora carotovora. Molecularly, Rudra was found to bind and interfere with both PGRP-LC and PGRP-LE, disrupting their signaling complex. These results show that Rudra is a critical component in a negative feedback loop, whereby immune-induced gene expression rapidly produces a potent inhibitor that binds and inhibits pattern recognition receptors

Supplementary Material for: <b><i>Francisella </i></b>Is Sensitive to Insect Antimicrobial Peptides

<i>Francisella tularensis</i> causes the zoonotic disease tularemia. Arthropod vectors are important transmission routes for the disease, although it is not known how <i>Francisella</i> survives the efficient arthropod immune response. Here, we used <i>Drosophila melanogaster</i> as a model host for <i>Francisella</i> infections and investigated whether the bacteria are resistant to insect humoral immune responses, in particular to the antimicrobial peptides (AMPs) secreted into the insect hemolymph. Moreover, we asked to what extent such resistance might depend on lipopolysaccharide (LPS) structure and surface characteristics of the bacteria. We analyzed <i>Francisella novicida</i> mutant strains in genes, directly or indirectly involved in specific steps of LPS biosynthesis, for virulence in wild-type and <i>Relish</i>^<i>E20</i> immune-deficient flies, and tested selected mutants for sensitivity to AMPs in vitro. We demonstrate that <i>Francisella</i> is sensitive to specific fly AMPs, i.e. Attacin, Cecropin, Drosocin and Drosomycin. Furthermore, six bacterial genes, <i>kpsF, manB, lpxF, slt, tolA </i>and<i> pal</i>, were found to be required for resistance to <i>Relish</i>-dependent immune responses, illustrating the importance of structural details of <i>Francisella</i> lipid A and Kdo core for interactions with AMPs. Interestingly, a more negative surface charge and lack of O-antigen did not render mutant bacteria more sensitive to cationic AMPs and did not attenuate virulence in flies