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Abstract Marine heatwave (MHW) events have led to acute decreases in primary production and phytoplankton biomass in the surface ocean, particularly at the mid latitudes. In the Northeast Pacific, these anomalous events have occasionally encroached onto the Oregon shelf during the ecologically important summer upwelling season. Increased temperatures reduce the density of offshore waters, and as a MHW is present offshore, coincident downwelling or relaxation may transport warmer waters inshore. As an event persists, new upwelling‐driven blooms may be prevented from extending further offshore. This work focuses on MHWs and coincident events that occurred off Oregon during the summers of 2015–2023. In late summer 2015 and 2019, both documented MHW years, coastal phytoplankton biomass extended on average 6 and 9 km offshore of the shelf break along the Newport Hydrographic Line, respectively. During years not influenced by anomalous warming, coastal biomass extended over 34 km offshore of the shelf break. Reduced biomass also occurs with reduced upwelling transport and nutrient flux during these anomalous warm periods. However, the enhanced front associated with a MHW aids in the compression of phytoplankton closer to shore. Over shorter events, heatwaves propagating far inshore also coincide with reduced chlorophyllaand sea‐surface density at select cross‐shelf locations, further supporting a physical displacement mechanism. Paired with the physiological impacts on communities, heatwave‐reinforced physical confinement of blooms over the inner‐shelf may have a measurable effect on the gravitational flux and alongshore transport of particulate organic carbon. 

ABSTRACT Pseudomonas aeruginosais considered one of the most challenging, drug-resistant, opportunistic pathogens partly due to its ability to synthesize robust biofilms. Biofilm is a mixture of extracellular polymeric substances (EPS) that encapsulates microbial cells, leading to immune evasion, antibiotic resistance, and thus higher risk of infection. In the cystic fibrosis lung environment,P. aeruginosaundergoes a mucoid transition, defined by overproduction of the exopolysaccharide alginate. Alginate encapsulation results in bacterial resistance to antibiotics and the host immune system. Given its role in airway inflammation and chronic infection, alginate is an obvious target to improve treatment forP. aeruginosainfection. Previously, we demonstrated polysaccharide lyase Smlt1473 fromStenotrophomonas maltophiliastrain k279a can catalyze the degradation of multiple polyuronidesin vitro, including D-mannuronic acid (poly-ManA). Poly-ManA is a major constituent ofP. aeruginosaalginate, suggesting that Smlt1473 could have potential application against multidrug-resistantP. aeruginosaand perhaps other microbes with related biofilm composition. In this study, we demonstrate that Smlt1473 can inhibit and degrade alginate fromP. aeruginosa. Additionally, we show that testedP. aeruginosastrains are dominant in acetylated alginate and that all but one have similar M-to-G ratios. These results indicate that variation in enzyme efficacy among the isolates is not primarily due to differences in total EPS or alginate chemical composition. Overall, these results demonstrate Smlt1473 can inhibit and degradeP. aeruginosaalginate and suggest that other factors including rate of EPS production, alginate sequence/chain length, or non-EPS components may explain differences in enzyme efficacy. IMPORTANCEPseudomonas aeruginosais a major opportunistic human pathogen in part due to its ability to synthesize biofilms that confer antibiotic resistance. Biofilm is a mixture of polysaccharides, DNA, and proteins that encapsulate cells, protecting them from antibiotics, disinfectants, and other cleaning agents. Due to its ability to increase antibiotic and immune resistance, the exopolysaccharide alginate plays a large role in airway inflammation and chronicP. aeruginosainfection. As a result, colonization withP. aeruginosais the leading cause of morbidity and mortality in CF patients. Thus, it is an obvious target to improve the treatment regimen forP. aeruginosainfection. In this study, we demonstrate that polysaccharide lyase, Smlt1473, inhibits alginate secretion and degrades established alginate from a variety of mucoidP. aeruginosaclinical isolates. Additionally, Smlt1473 differs from other alginate lyases in that it is active against acetylated alginate, which is secreted during chronic lung infection. These results suggest that Smlt1473 may be useful in treating infections associated with alginate-producingP. aeruginosa, as well as have the potential to reduceP. aeruginosaEPS in non-clinical settings. 

The Neurospora crassa genome has a gene cluster for the synthesis of galactosaminogalactan (GAG). The gene cluster includes the following: (1) UDP-glucose-4-epimerase to convert UDP-glucose and UDP-N-acetylglucosamine to UDP-galactose and UDP-N-acetylgalactosamine (NCU05133), (2) GAG synthase for the synthesis of an acetylated GAG (NCU05132), (3) GAG deacetylase (/NCW-1/NCU05137), (4) GH135-1, a GAG hydrolase with specificity for N-acetylgalactosamine-containing GAG (NCU05135), and (5) GH114-1, a galactosaminidase with specificity for galactosamine-containing GAG (NCU05136). The deacetylase was previously shown to be a major cell wall glycoprotein and given the name of NCW-1 (non-GPI anchored cell wall protein-1). Characterization of the polysaccharides found in the growth medium from the wild type and the GAG synthase mutant demonstrates that there is a major reduction in the levels of polysaccharides containing galactosamine and N-acetylgalactosamine in the mutant growth medium, providing evidence that the synthase is responsible for the production of a GAG. The analysis also indicates that there are other galactose-containing polysaccharides produced by the fungus. Phenotypic characterization of wild-type and mutant isolates showed that deacetylated GAG from the wild type can function as an adhesin to a glass surface and provides the fungal mat with tensile strength, demonstrating that the deacetylated GAG functions as an intercellular adhesive. The acetylated GAG produced by the deacetylase mutant was found to function as an adhesive for chitin, alumina, celite (diatomaceous earth), activated charcoal, and wheat leaf particulates. 

ABSTRACT Whole genome sequencing has revealed that the genome ofStaphylococcus aureuspossesses an uncharacterized 5-gene operon (SAOUHSC_00088–00092 in strain 8325 genome) that encodes factors with functions related to polysaccharide biosynthesis and export, indicating the existence of a new extracellular polysaccharide species. We designate this locus assscfor staphylococcal surface carbohydrate. We found that thesscgenes were weakly expressed and highly repressed by the global regulator MgrA. To characterize Ssc, Ssc was heterologously expressed inEscherichia coliand extracted by heat treatment. Ssc was also conjugated to AcrA fromCampylobacter jejuniinE. coliusing protein glycan coupling technology (PGCT). Analysis of the heat-extracted Ssc and the purified Ssc-AcrA glycoconjugate by tandem mass spectrometry revealed that Ssc is likely a polymer consisting ofN-acetylgalactosamine. We further demonstrated that the expression of thesscgenes inS. aureusaffected phage adsorption and susceptibility, suggesting that Ssc is surface-exposed. IMPORTANCESurface polysaccharides play crucial roles in the biology and virulence of bacterial pathogens.Staphylococcus aureusproduces four major types of polysaccharides that have been well-characterized. In this study, we identified a new surface polysaccharide containing N-acetylgalactosamine (GalNAc). This marks the first report of GalNAc-containing polysaccharide inS. aureus. Our discovery lays the groundwork for further investigations into the chemical structure, surface location, and role in pathogenesis of this new polysaccharide.