Intrusion of warm Bering/Chukchi waters onto the shelf in the western Beaufort Sea

Author Posting. © American Geophysical Union, 2009. This article is posted here by permission of American Geophysical Union for personal use, not for redistribution. The definitive version was published in Journal of Geophysical Research 114 (2009): C00A11, doi:10.1029/2008JC004870.Wind-driven changes in the path of warm Bering/Chukchi waters carried by the Alaska Coastal Current (ACC) through Barrow Canyon during late summer are described from high-resolution hydrography, acoustic Doppler current profiler–measured currents, and satellite-measured sea surface temperature imagery acquired from mid-August to mid-September 2005–2007 near Barrow, Alaska. Numerical simulations are used to provide a multidecadal context for these observational data. Four generalized wind regimes and associated circulation states are identified. When winds are from the east or east-southeast, the ACC jet tends to be relatively strong and flows adjacent to the shelf break along the southern flank of Barrow Canyon. These easterly winds drive inner shelf currents northwestward along the Alaskan Beaufort coast where they oppose significant eastward intrusions of warm water from Barrow Canyon onto the shelf. Because these easterly winds promote sea level set down over the Beaufort shelf and upwelling along the Beaufort slope, the ACC jet necessarily becomes weaker, broader, and displaced seaward from the Beaufort shelf break upon exiting Barrow Canyon. Winds from the northeast promote separation of the ACC from the southern flank of Barrow Canyon and establish an up-canyon current along the southern flank that is fed in part by waters from the western Beaufort shelf. When winds are weak or from the southwest, warm Bering/Chukchi waters from Barrow Canyon intrude onto the western Beaufort shelf.This work was supported in 2005 and 2006 by NSF grants OPP-0436131 and OPP-0436166. In 2007, this work received support through Woods Hole Oceanographic Institution- NOAA Cooperative Institute for Climate and Ocean Research Cooperative Agreement NA17RJ1223 and University of Alaska Fairbanks-NOAA Cooperative Institute for Arctic Research Cooperative Agreement NA17RJ1224. Additional support was provided by the James M. and Ruth P. Clark Arctic Research Initiative Fund at the Woods Hole Oceanographic Institution

A new widespread subclass of carbonic anhydrase in marine phytoplankton

Most aquatic photoautotrophs depend on CO2-concentrating mechanisms (CCMs) to maintain productivity at ambient concentrations of CO2, and carbonic anhydrase (CA) plays a key role in these processes. Here we present different lines of evidence showing that the protein LCIP63, identified in the marine diatom Thalassiosira pseudonana, is a CA. However, sequence analysis showed that it has a low identity with any known CA and therefore belongs to a new subclass that we designate as iota-CA. Moreover, LCIP63 unusually prefers Mn2+ to Zn2+ as a cofactor, which is potentially of ecological relevance since Mn2+ is more abundant than Zn2+ in the ocean. LCIP63 is located in the chloroplast and only expressed at low concentrations of CO2. When overexpressed using biolistic transformation, the rate of photosynthesis at limiting concentrations of dissolved inorganic carbon increased, confirming its role in the CCM. LCIP63 homologs are present in the five other sequenced diatoms and in other algae, bacteria, and archaea. Thus LCIP63 is phylogenetically widespread but overlooked. Analysis of the Tara Oceans database confirmed this and showed that LCIP63 is widely distributed in marine environments and is therefore likely to play an important role in global biogeochemical carbon cycling

Differential Host Immune Responses after Infection with Wild-Type or Lab-Attenuated Rabies Viruses in Dogs.

METHODOLOGY/PRINCIPAL FINDINGS: The experimental infection of dogs with TriGAS induced high levels of VNA in the serum, whereas wt RABV infection did not. Dogs infected with TriGAS developed antibodies against the virus including its glycoprotein, whereas dogs infected with DRV-NG11 only developed rabies antibodies that are presumably specific for the nucleoprotein, (N) and not the glycoprotein (G). We show that infection with TriGAS induces early activation of B cells in the draining lymph nodes and persistent activation of DCs and B cells in the blood. On the other hand, infection with DRV-NG11 fails to induce the activation of DCs and B cells and further reduces CD4 T cell production. Further, we show that intrathecal (IT) immunization of TriGAS not only induced high levels of VNA in the serum but also in the CSF while intramuscular (IM) immunization of TriGAS induced VNA only in the serum. In addition, high levels of total protein and WBC were detected in the CSF of IT immunized dogs, indicating the transient enhancement of blood-brain barrier (BBB) permeability, which is relevant to the passage of immune effectors from periphery into the CNS. CONCLUSIONS/SIGNIFICANCE: IM infection of dogs with TriGAS induced the production of serum VNA whereas, IT immunization of TriGAS in dogs induces high levels of VNA in the periphery as well as in the CSF and transiently enhances BBB permeability. In contrast, infection with wt DRV-NG11 resulted in the production of RABV-reactive antibodies but VNA and antibodies specific for G were absent. As a consequence, all of the dogs infected with wt DRV-NG11 succumbed to rabies. Thus the failure to activate protective immunity is one of the important features of RABV pathogenesis in dogs

Ecological characteristics of core-use areas used by Bering–Chukchi–Beaufort (BCB) bowhead whales, 2006–2012

© The Author(s), 2014]. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in Progress in Oceanography 136 (2015): 201-222, doi:10.1016/j.pocean.2014.08.012.The Bering–Chukchi–Beaufort (BCB) population of bowhead whales (Balaena mysticetus) ranges across the seasonally ice-covered waters of the Bering, Chukchi, and Beaufort seas. We used locations from 54 bowhead whales, obtained by satellite telemetry between 2006 and 2012, to define areas of concentrated use, termed “core-use areas”. We identified six primary core-use areas and describe the timing of use and physical characteristics (oceanography, sea ice, and winds) associated with these areas. In spring, most whales migrated from wintering grounds in the Bering Sea to the Cape Bathurst polynya, Canada (Area 1), and spent the most time in the vicinity of the halocline at depths <75 m, which are within the euphotic zone, where calanoid copepods ascend following winter diapause. Peak use of the polynya occurred between 7 May and 5 July; whales generally left in July, when copepods are expected to descend to deeper depths. Between 12 July and 25 September, most tagged whales were located in shallow shelf waters adjacent to the Tuktoyaktuk Peninsula, Canada (Area 2), where wind-driven upwelling promotes the concentration of calanoid copepods. Between 22 August and 2 November, whales also congregated near Point Barrow, Alaska (Area 3), where east winds promote upwelling that moves zooplankton onto the Beaufort shelf, and subsequent relaxation of these winds promoted zooplankton aggregations. Between 27 October and 8 January, whales congregated along the northern shore of Chukotka, Russia (Area 4), where zooplankton likely concentrated along a coastal front between the southeastward-flowing Siberian Coastal Current and northward-flowing Bering Sea waters. The two remaining core-use areas occurred in the Bering Sea: Anadyr Strait (Area 5), where peak use occurred between 29 November and 20 April, and the Gulf of Anadyr (Area 6), where peak use occurred between 4 December and 1 April; both areas exhibited highly fractured sea ice. Whales near the Gulf of Anadyr spent almost half of their time at depths between 75 and 100 m, usually near the seafloor, where a subsurface front between cold Anadyr Water and warmer Bering Shelf Water presumably aggregates zooplankton. The amount of time whales spent near the seafloor in the Gulf of Anadyr, where copepods (in diapause) and, possibly, euphausiids are expected to aggregate provides strong evidence that bowhead whales are feeding in winter. The timing of bowhead spring migration corresponds with when zooplankton are expected to begin their spring ascent in April. The core-use areas we identified are also generally known from other studies to have high densities of whales and we are confident these areas represent the majority of important feeding areas during the study (2006–2012). Other feeding areas, that we did not detect, likely existed during the study and we expect core-use area boundaries to shift in response to changing hydrographic conditions.This study is part of the Synthesis of Arctic Research (SOAR) and was funded in part by the U.S. Department of the Interior, Bureau of Ocean Energy Management, Environmental Studies Program through Interagency Agreement No. M11PG00034 with the U.S. Department of Commerce, National Oceanic and Atmospheric Administration (NOAA), Office of Oceanic and Atmospheric Research (OAR), Pacific Marine Environmental Laboratory (PMEL). Funding for this research was mainly provided by U.S. Minerals Management Service (now Bureau of Ocean Energy Management) under contracts M12PC00005, M10PS00192, and 01-05-CT39268, with the support and assistance from Charles Monnett and Jeffery Denton, and under Interagency Agreement No. M08PG20021 with NOAA-NMFS and Contract No. M10PC00085 with ADF&G. Work in Canada was also funded by the Fisheries Joint Management Committee, Ecosystem Research Initiative (DFO), and Panel for Energy Research and Development

CD8+ T-cell specificity is compromised at a defined MHCI/CD8 affinity threshold

The CD8 co-receptor engages peptide-major histocompatibility complex class I (pMHCI) molecules at a largely invariant site distinct from the T-cell receptor (TCR)-binding platform and enhances the sensitivity of antigen-driven activation to promote effective CD8+ T-cell immunity. A small increase in the strength of the pMHCI/CD8 interaction (~1.5-fold) can disproportionately amplify this effect, boosting antigen sensitivity by up to two orders of magnitude. However, recognition specificity is lost altogether with more substantial increases in pMHCI/CD8 affinity (~10-fold). In this study, we used a panel of MHCI mutants with altered CD8-binding properties to show that TCR-mediated antigen specificity is delimited by a pMHCI/CD8 affinity threshold. Our findings suggest that CD8 can be engineered within certain biophysical parameters to enhance the therapeutic efficacy of adoptive T-cell transfer irrespective of antigen specificity

CD8+ T-­cell specificity is compromised at a defined major histocompatibility complex class I/CD8 affinity threshold

The CD8 co-receptor engages peptide-major histocompatibility complex class I (pMHCI) molecules at a largely invariant site distinct from the T-cell receptor (TCR)-binding platform and enhances the sensitivity of antigen-driven activation to promote effective CD8+ T-cell immunity. A small increase in the strength of the pMHCI/CD8 interaction (~1.5-fold) can disproportionately amplify this effect, boosting antigen sensitivity by up to two orders of magnitude. However, recognition specificity is lost altogether with more substantial increases in pMHCI/CD8 affinity (~10-fold). In this study, we used a panel of MHCI mutants with altered CD8-binding properties to show that TCR-mediated antigen specificity is delimited by a pMHCI/CD8 affinity threshold. Our findings suggest that CD8 can be engineered within certain biophysical parameters to enhance the therapeutic efficacy of adoptive T-cell transfer irrespective of antigen specificity

CD8+ T-cell specificity is compromised at a defined MHCI/CD8 affinity threshold

The CD8 coreceptor engages peptide-major histocompatibility complex class I (pMHCI) molecules at a largely invariant site distinct from the T-cell receptor (TCR) binding platform and enhances the sensitivity of antigen-driven activation to promote effective CD8+ T-cell immunity. A small increase in the strength of the pMHCI/CD8 interaction (~ 1.5-fold) can disproportionately amplify this effect, boosting antigen sensitivity by up to two orders of magnitude. However, recognition specificity is lost altogether with more substantial increases in pMHCI/CD8 affinity (~ 10-fold). In this study, we used a panel of MHCI mutants with altered CD8 binding properties to show that TCR-mediated antigen specificity is delimited by a pMHCI/CD8 affinity threshold. Our findings suggest that CD8 can be engineered within certain biophysical parameters to enhance the therapeutic efficacy of adoptive T-cell transfer irrespective of antigen specificity. The pMHCI/CD8 interaction controls specificit

Klebsiella pneumoniae peptide hijacks a Streptococcus pneumoniae permease to subvert pneumococcal growth and colonization.

Treatment of pneumococcal infections is limited by antibiotic resistance and exacerbation of disease by bacterial lysis releasing pneumolysin toxin and other inflammatory factors. We identified a previously uncharacterized peptide in the Klebsiella pneumoniae secretome, which enters Streptococcus pneumoniae via its AmiA-AliA/AliB permease. Subsequent downregulation of genes for amino acid biosynthesis and peptide uptake was associated with reduction of pneumococcal growth in defined medium and human cerebrospinal fluid, irregular cell shape, decreased chain length and decreased genetic transformation. The bacteriostatic effect was specific to S. pneumoniae and Streptococcus pseudopneumoniae with no effect on Streptococcus mitis, Haemophilus influenzae, Staphylococcus aureus or K. pneumoniae. Peptide sequence and length were crucial to growth suppression. The peptide reduced pneumococcal adherence to primary human airway epithelial cell cultures and colonization of rat nasopharynx, without toxicity. We identified a peptide with potential as a therapeutic for pneumococcal diseases suppressing growth of multiple clinical isolates, including antibiotic resistant strains, while avoiding bacterial lysis and dysbiosis