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Bacteria that assemble in phycospheres surrounding living phytoplankton cells metabolize a substantial proportion of ocean primary productivity. Yet the type and extent of interactions occurring among species that colonize these micron-scale 'hot spot' environments are challenging to study. We identified genes that mediate bacterial interactions in phycosphere communities by culturing a transposon mutant library of copiotrophic bacterium Ruegeria pomeroyi DSS-3 with the diatom Thalassiosira pseudonana CCMP1335 as the sole source of organic matter in the presence or absence of other heterotrophic bacterial species. The function of genes having significant effects on R. pomeroyi fitness indicated explicit cell--cell interactions initiated in the multibacterial phycospheres. We found that R. pomeroyi simultaneously competed for shared substrates while increasing reliance on substrates that did not support the other species' growth. Fitness outcomes also indicated that the bacterium competed for nitrogen in the forms of ammonium and amino acids; obtained purines, pyrimidines, and cofactors via crossfeeding; both initiated and defended antagonistic interactions; and sensed an environment with altered oxygen and superoxide levels. The large genomes characteristic of copiotrophic marine bacteria are hypothesized to enable responses to dynamic ecological challenges occurring at the scale of microns. Here, we discover >200 nonessential genes implicated in the management of fitness costs and benefits of membership in a globally significant bacterial community. bacteria | phytoplankton | phycosphere | community ecology | Transposon Sequencing

Neurons harbor high levels of single-strand DNA breaks (SSBs) that are targeted to neuronal enhancers, but the source of this endogenous damage remains unclear. Using two systems of postmitotic lineage specification--induced pluripotent stem cell-derived neurons and transdifferentiated macrophages--we show that thymidine DNA glycosylase (TDG)-driven excision of methylcytosines oxidized with ten-eleven translocation enzymes (TET) is a source of SSBs. Although macrophage differentiation favors short-patch base excision repair to fill in single-nucleotide gaps, neurons also frequently use the long-patch subpathway. Disrupting this gap-filling process using anti-neoplastic cytosine analogs triggers a DNA damage response and neuronal cell death, which is dependent on TDG. Thus, TET-mediated active DNA demethylation promotes endogenous DNA damage, a process that normally safeguards cell identity but can also provoke neurotoxicity after anticancer treatments.

Methods for the determination of mercury are described using gold nanoparticles functionalized with nitrogen containing cyclic molecules. Detection methods are based on the prevention of nitrogenous compounds induced aggregation of gold nanoparticles by mercury. Histamine, melamine, o-phenylenediamine and uracil induced aggregation of gold nanoparticles. Incubation of histamine, melamine or o-phenylenediamine with mercury resulted in reduction of gold nanoparticles aggregation. Inverse relationship was observed between mercury concentration and aggregation of gold nanoparticles. Dynamic ranges of the methods using histamine, melamine and o-phenylenediamine were 200 nM-7.5 [micro]M, 200 nM-6.0 [micro]M and 200 nM-2.0 [micro]M, respectively. Metals, namely, Pb(II), Co(II), Cr(III), Cu(II), Ni(II), Zn(II), Ca(II), Ba(II) and Cd(II), did not interfere in the assay. However, Ag(I) prevented histamine and o-phenylenediamine induced aggregation of gold nanoparticles. Histamine, melamine and o-phenylenediamine can serve as ligands for the development of sensitive methods for mercury., Author(s): Ansar Khongsit [sup.1], Yudhishthir Singh Rajput [sup.1], Sunita Meena [sup.1], Rajan Sharma [sup.2] Author Affiliations: (1) grid.419332.e, 0000 0001 2114 9718, Animal Biochemistry Division, National Dairy Research Institute, , [...]

CRISPR-Cas9-based base editing allows precise base editing to achieve conversion of adenosine to guanine or cytosine to thymidine. In this issue of Cell, McAuley et al. use adenine base editing to correct a single base-pair mutation causing human CD3[delta] deficiency, demonstrating superior efficiency of genetic correction with reduced undesired genetic alterations compared with standard CRISPR-Cas9 editing. Author Affiliation: (1) Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA * Corresponding author Byline: Harry L. Malech [hmalech@niaid.nih.gov] (1,*), Luigi D. Notarangelo [luigi.notarangelo2@nih.gov] (1,**)