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Biology subjects

Son, K.

Publications and source records attributed to Son, K..

2 recordsLinked to original sources

Sediment-associated processes drive spatial variation in ecosystem respiration in the Yakima River basin

Hyporheic zones (HZ) can contribute substantially to total stream ecosystem respiration (ERtot). HZ-focused process-based models may, therefore, effectively predict ERtot across sites, yet this remains untested under variable environmental conditions. Here we evaluate whether spatial variation in HZ respiration predicted via a process-based model explains spatial variation in field-estimates of ERtot across 33 sites in the Yakima River basin in Washington State, USA. We found that HZ respiration predictions did not explain spatial variation in field estimates of ERtot. To investigate further, we partitioned ERtot contributions into water column respiration (ERwc) and sediment-associated respiration (ERsed). ERsed contributed >50% of ERtot at 88% of sites, though relative contributions varied substantially. Despite this dominance, modeled HZ respiration explained neither spatial variation in ERtot nor in ERsed, suggesting that the HZ model alone does not capture the drivers of sediment-associated respiration across these sites. Instead, ERsed spatial variation was primarily explained by gross primary production, stream slope, velocity, and total dissolved nitrogen rather than median grain size, a primary control of HZ respiration predicted by the process-based model. Consistent with recent studies, our results indicate that improving basin-scale ERtot predictions requires integrating hydrologic and biogeochemical processes across hyporheic, benthic, and water column zones.

ecology↗

Trabectedin derails transcription-coupled nucleotide excision repair to induce DNA breaks in highly transcribed genes

Most genotoxic anticancer agents fail in tumors with intact DNA repair. Therefore, trabectedin, a unique agent more toxic to cells with active DNA repair, specifically transcription-coupled nucleotide excision repair (TC-NER), provides new therapeutic opportunities. To unlock the potential of trabectedin and inform its application in precision oncology, a full mechanistic understanding of the drugs TC-NER-dependent toxicity is needed. Here, we determined that abortive TC-NER of trabectedin-DNA adducts forms persistent single-strand breaks (SSBs) as the adducts block the second of the two sequential NER incisions. We mapped the 3-hydroxyl groups of SSBs originating from the first NER incision at trabectedin lesions, recording TC-NER on a genome-wide scale. We showed that trabectedin-induced SSBs primarily occur in transcribed strands of active genes and peak near transcription start sites. Frequent SSBs were also found outside gene bodies, connecting TC-NER to divergent transcription from promoters. This work advances the use trabectedin for precision oncology and for studying TC-NER and transcription.

molecular biology↗