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Biology subjects

Nehring, R. B.

Publications and source records attributed to Nehring, R. B..

2 recordsLinked to original sources

Estimating densities of larval Salmonflies (Pteronarcys californica) through multiple pass removal of post-emergent exuvia in Colorado rivers.

Traditional methods of collecting and sorting benthic macroinvertebrate samples are useful for stream biomonitoring and ecological studies; however, these methods are time consuming, expensive, and require taxonomic expertise. Estimating larval densities through collection of post-emergent exuvia can be a practical and time efficient alternative. We evaluated the use of multiple pass depletion techniques of the post-emergent exuvia of Pteronarcys californica to estimate larval densities at ten sites in three Colorado rivers. Exuvia density was highly correlated with both final-instar larval density (R2 = 0.90) and total larval density (R2 = 0.88) and the multiple pass removal technique performed well. Exuvia surveys found P. californica at three low density sites where benthic sampling failed to detect it. At moderate and high density sites the exuvia surveys always produced lower density estimates than benthic surveys. Multiple pass depletion estimates of exuvia proved to be an accurate and efficient technique at estimating larval densities and provided an effective alternative for traditional benthic sampling when objectives are monitoring P. californica and detecting populations, especially at low density sites.

ecology↗

Bacteria-to-human protein networks reveal origins of endogenous DNA damage

DNA damage provokes mutations and cancer, and results from external carcinogens or endogenous cellular processes. Yet, the intrinsic instigators of DNA damage are poorly understood. Here we identify proteins that promote endogenous DNA damage when overproduced: the DNA-damaging proteins (DDPs). We discover a large network of DDPs in Escherichia coli and deconvolute them into six DNA-damage-causing function clusters, demonstrating DDP mechanisms in three: reactive-oxygen increase by transmembrane transporters, chromosome loss by replisome binding, and replication stalling by transcription factors. Their 284 human homologs are over-represented among known cancer drivers, and their expression in tumors predicts heavy mutagenesis and poor prognosis. Half of tested human homologs, when overproduced in human cells, promote DNA damage and mutation, with DNA-damaging mechanisms like those in E. coli. Together, our work reveals DDP networks that provoke endogenous DNA damage and may indicate functions of many human known and newly implicated cancer-promoting proteins.

cancer biology↗