Balancing Hydraulic Control and Phosphorus Removal in Bioretention Media Amended with Drinking Water Treatment Residuals.

Green stormwater infrastructure like bioretention can reduce stormwater runoff volumes and trap sediments and pollutants. However, bioretention soil media can be both a sink and source of phosphorus (P). We investigated the potential tradeoff between hydraulic conductivity and P sorption capacity in drinking water treatment residuals (DWTRs), with implications for bioretention media design. Batch isotherm and flow-through column experiments were used to quantify the maximum P sorption capacity (Smax) and rate of P sorption for three DWTR sources. Smax values varied greatly among DWTR sources and methodologies, which has implications for regulatory standards. We also conducted a large column experiment to determine the hydraulic and P removal effects of amending bioretention media with solid and mixed layers of DWTRs. When applied to bioretention media, the impact of DWTRs on hydraulic conductivity and P removal depended on layering strategy. Although DWTR addition in solid and mixed layer designs improved P removal, the solid layer restricted water flow and exhibited incomplete P removal, while the mixed layer had no effect on flow and removed ~100% of P inputs. We recommend that DWTRs be mixed with sand in bioretention media to simultaneously achieve stormwater drainage and P reduction goals in green stormwater infrastructure.

Genomic instability due to V(D)J recombination-associated transposition.

The first step in assembling immunoglobulin and T-cell receptors by V(D)J recombination has similarities to transposon excision. The excised transposon-like element then integrates into DNA targets at random in vitro, but whether this activity significantly threatens the genomic integrity of its host has been unclear. Here, we recover examples where the putative transposon associated with V(D)J recombination integrated into the genome of a pre-B-cell line. Transposition accounted for a surprisingly high proportion (one-third) of integrations, while most of the remaining events had parallels to other aberrant V(D)J recombination pathways linked to oncogenic translocation. In total, transposition occurred approximately once every 50,000 V(D)J recombinations. Transposition may thus contribute significantly to genomic instability.

Histone 3 lysine 4 methylation during the pre-B to immature B-cell transition.

The relationship between chromatin modification and lymphocyte development is still poorly understood. Here we show a correlation between methylation of lysine 4 on histone 3 (H3-K4) and activation of several loci required for the pre-B cell to immature B-cell developmental transition. A critical step in this transition is the induction of V(D)J recombination at the Igkappa locus. Upon activation of Igkappa recombination, a >10-fold enrichment of both di- and trimethylated H3-K4 is observed at Jkappa targeting signals, but not at an analogous targeting signal in the T-cell receptor alpha locus or, surprisingly, at several Vkappa signals. However, H3-K4 methylation is restricted to the actively recombining fraction of Jkappa recombination targeting signals, consistent with a direct relationship between H3-K4 methylation and signal activity. Correlations between increased H3-K4 methylation and induction of transcription are also observed at some, but not all, loci where transcription is induced. H3-K4 methylation may therefore be a widely used but not universal means for controlling chromatin activity in this developmental transition.

Sensing of intermediates in V(D)J recombination by ATM.

Ataxia-telangiectasia mutated (ATM) is required for resistance to radiation-induced DNA breaks. Here we use chromatin immunoprecipitation to show that ATM also localizes to breaks associated with V(D)J recombination. ATM recruitment to the recombining locus correlates approximately with recruitment of the break-initiating factor RAG1 and precedes efficient break repair, consistent with localization of ATM to normal recombination intermediates. A product of ATM kinase activity, Ser 18-phosphorylated p53, was detected similarly at these breaks, arguing that ATM phosphorylates target proteins in situ. We suggest routine surveillance of intermediates in V(D)J recombination by ATM helps suppress potentially oncogenic translocations when repair fails.