Determination of the number of thioether-linked cysteine residues in cytochromes c and phycobiliproteins.

Hydrolysis of cytochromes c and phycobiliproteins in 6 n HCl containing 0.21 m dimethylsulfoxide at 110°C for 22 h results in the quantitative conversion of cysteinyl, cystinyl, and thioether-linked cysteinyl residues to cysteic acid. Methionine is converted to homocysteic acid in a 10% yield. The number of thioether-linked cysteinyl residues can be calculated, if the number of cysteinyl and cystinyl residues is determined separately as S-carboxymethylcysteine in a 6 n HCl hydrolyzate of reduced, carboxymethylated protein. Data are presented on the number of thioether-linked cysteinyl residues present in R-, B-, and C-phycoerythrins, C- and R-phycocyanins, allophycocyanins, and the subunits of these proteins.     

Cordycepin and xylosyladenine: inhibitors of methylation of nuclear RNA.

Cordycepin and xylosyladenine inhibited methylation of nuclear RNA to a greater extent than RNA synthesis in L1210 cells $\text{in vitro}$. Inhibition of base methylation, 2′-0-methylation and 5′cap methylation was equal to, 2 to 5-fold greater and 1.5-fold greater, respectively than inhibition of RNA synthesis. Cordycepin was more potent than xylosyladenine in inhibiting 2′-0-methylation of cytidine and adenosine, but not guanosine. These results suggest that impirment in the 2′-0-methylation of nuclear RNA may be one of the major effects that limits the biological activity of rRNA and mRNA by these drugs.     

Redefining Genomic Privacy: Trust and Empowerment

Fulfilling the promise of the genetic revolution requires the analysis of large datasets containing information from thousands to millions of participants. However, sharing human genomic data requires protecting subjects from potential harm. Current models rely on de-identification techniques in which privacy versus data utility becomes a zero-sum game. Instead, we propose the use of trust-enabling techniques to create a solution in which researchers and participants both win. To do so we introduce three principles that facilitate trust in genetic research and outline one possible framework built upon those principles. Our hope is that such trust-centric frameworks provide a sustainable solution that reconciles genetic privacy with data sharing and facilitates genetic research.     

Carbon flow through energycane agroecosystems established post‐intensive agriculture

As part of an integrated energy and climate system, biomass production for bioenergy based on the tropical perennial C₄ grass energycane can both offset fossil fuels and store soil carbon (C). We measured energycane yields, root biomass, soil C pools, and soil C stocks in a 4 year field trial and modeled C flow from plants to soils in the surface layer of no‐till energycane planted after more than a century of intensive sugarcane agriculture. Aboveground yields ranged from 16.7 to 19.0 Mg C/ha over the 4 year trial. Although total C stocks did not significantly differ in the surface layer (approx. 0–20 cm) during the study, C in free and occluded light fractions decreased, whereas C in the mineral‐rich dense fraction increased over 4 years. Belowground system inputs, estimated from measurements and informed by convergence in the final soil fraction model, were set to 2.5 Mg C ha^?1 year^?1. With this input value, we estimated that surface soils retained photosynthetically fixed C predominantly within the mineral‐associated organic matter pool for a mean and median transit time of 177 and 110 years, respectively. Although we did not model C flow to deep soil layers (approx. 0–100 cm), observed C accumulation (11.4 Mg C ha^?1 year^?1) and root growth down to 120 cm suggest that soil processes and resulting C sequestration at the surface are likely to persist deeper into the soil profile. Energycane, as a strong candidate for climate change mitigation and land degradation remediation, showed high biomass yields and allocation of resources to roots, with sequestered soil C expected to persist for over a century.     

Focus: 50 Years of DNA Repair: The Yale Symposium Reports: Hypoxia and DNA Repair

Hypoxia is a characteristic feature of solid tumors and occurs very early in neoplastic development. Hypoxia transforms cell physiology in multiple ways, with profound changes in cell metabolism, cell growth, susceptibility to apoptosis, induction of angiogenesis, and increased motility. Over the past 20 years, our lab has determined that hypoxia also induces genetic instability. We have conducted a large series of experiments revealing that this instability occurs through the alteration of DNA repair pathways, including nucleotide excision repair, DNA mismatch repair, and homology dependent repair. Our work suggests that hypoxia, as a key component of solid tumors, can drive cancer progression through its impact on genomic integrity. However, the acquired changes in DNA repair that are induced by hypoxia may also render hypoxic cancer cells vulnerable to tailored strategies designed to exploit these changes.