Iron clad wetlands: Soil iron-sulfur buffering determines coastal wetland response to salt water incursion

Coastal freshwater wetland chemistry is rapidly changing due to increased frequency of salt water incursion, a consequence of global change. Seasonal salt water incursion introduces sulfate, which microbially reduces to sulfide. Sulfide binds with reduced iron, producing iron sulfide (FeS), recognizable in wetland soils by its characteristic black color. The objective of this study is to document iron and sulfate reduction rates, as well as product formation (acid volatile sulfide (AVS) and chromium reducible sulfide (CRS)) in a coastal freshwater wetland undergoing seasonal salt water incursion. Understanding iron and sulfur cycling, as well as their reduction products, allows us to calculate the degree of sulfidization (DOS), from which we can estimate how long soil iron will buffer against chemical effects of sea level rise. We show that soil chloride, a direct indicator of the degree of incursion, best predicted iron and sulfate reduction rates. Correlations between soil chloride and iron or sulfur reduction rates were strongest in the surface layer (0–3 cm), indicative of surface water incursion, rather than groundwater intrusion at our site. The interaction between soil moisture and extractable chloride was significantly related to increased AVS, whereas increased soil chloride was a stronger predictor of CRS. The current DOS in this coastal plains wetland is very low, resulting from high soil iron content and relatively small degree of salt water incursion. However, with time and continuous salt water exposure, iron will bind with incoming sulfur, creating FeS complexes, and DOS will increase

The influence of sea-water inundation on coupled iron and sulfur cycling in a coastal freshwater wetland

Coastal freshwater wetland chemistry is rapidly changing due to increased frequency of saltwater inundation, a consequence of global change. Seasonal salt water inundation introduces sulfate, which biologically reduces to sulfide via microbial metabolism. Sulfide binds with reduced iron producing iron sulfide (FeS), recognizable in wetland soils by its characteristic black color. The objective of this study is to document rates of iron and sulfate reduction, as well as product formation (acid volatile and chromium reducible sulfide, AVS and CRS) in a coastal freshwater wetland undergoing seasonal salt water inundation. Understanding iron and sulfur cycling, as well as their reduction products allow for calculation of the Degree of Sulfidization (DOS), from which we can estimate how long iron in the sediment will buffer against chemical effects of sea level rise. Soil chloride predicted iron and sulfate reduction rates as it is a direct indicator of inundation extent. Correlations between soil chloride and both reduction rates were stronger at the surface (0-3 cm), indicative of surface water inundation, rather than groundwater intrusion. AVS correlated strongly to soil moisture, however CRS was strongly correlated to soil chloride. For the tidal freshwater TOWeR wetland, the current DOS is very low, which is a result of the high iron content of the Ultisol soils. However with time and continuous inundation, iron will bind to incoming sulfide, creating FeS and DOS will increase. With current conditions, it will take approximately 175 years for the wetland to become sulfidic, and begin to transition to a saltwater marsh. Adviser: Amy J. Burgi

Somatic mosaicism and common genetic variation contribute to the risk of very-early-onset inflammatory bowel disease

Very-early-onset inflammatory bowel disease (VEO-IBD) is a heterogeneous phenotype associated with a spectrum of rare Mendelian disorders. Here, we perform whole-exome-sequencing and genome-wide genotyping in 145 patients (median age-at-diagnosis of 3.5 years), in whom no Mendelian disorders were clinically suspected. In five patients we detect a primary immunodeficiency or enteropathy, with clinical consequences (XIAP, CYBA, SH2D1A, PCSK1). We also present a case study of a VEO-IBD patient with a mosaic de novo, pathogenic allele in CYBB. The mutation is present in ~70% of phagocytes and sufficient to result in defective bacterial handling but not life-threatening infections. Finally, we show that VEO-IBD patients have, on average, higher IBD polygenic risk scores than population controls (99 patients and 18,780 controls; P < 4 × 10-10), and replicate this finding in an independent cohort of VEO-IBD cases and controls (117 patients and 2,603 controls; P < 5 × 10-10). This discovery indicates that a polygenic component operates in VEO-IBD pathogenesis