We report J-band MOSFIRE spectroscopy of a low-mass () star-forming galaxy at z = 0.997 showing the detection of [N ii] and [S ii] alongside a strong H line. We derive a gas-phase metallicity of , placing this object in a region of M ∗-Z space that is sparsely populated at this redshift. Furthermore, many existing metallicity measurements in this M ∗-z regime are derived from only [N ii]/H (N2), a diagnostic widely used in high-redshift metallicity studies despite the known strong degeneracy with the ionization parameter and resulting large systematic uncertainty. We demonstrate that even in a regime where [N ii] and [S ii] are at the detection limit and the measurement uncertainty associated with the [N ii]/[S ii] ratio is high (S/N ≈ 3), the more sophisticated Dopita et al. diagnostic provides an improved constraint compared to N2 by reducing the systematic uncertainty due to the ionization parameter. This approach does not, however, dispel uncertainty associated with stochastic or systematic variations in the nitrogen-to-oxygen abundance ratio. While this approach improves upon N2, future progress in extending metallicity studies into this low-mass regime will require larger samples to allow for stochastic variations, as well as careful consideration of the global trends among dwarf galaxies in all physical parameters, not just metallicity.

The RNA-synthesizing machinery of the severe acute respiratory syndrome Coronavirus (SARS-CoV) is composed of 16 non-structural proteins (nsp1-16) encoded by ORF1a/1b. The 148-amino acid nsp10 subunit contains two zinc fingers and is known to interact with both nsp14 and nsp16, stimulating their respective 3'-5' exoribonuclease and 2'-O-methyltransferase activities. Using alanine-scanning mutagenesis, in cellulo bioluminescence resonance energy transfer experiments, and in vitro pulldown assays, we have now identified the key residues on the nsp10 surface that interact with nsp14. The functional consequences of mutations introduced at these positions were first evaluated biochemically by monitoring nsp14 exoribonuclease activity. Disruption of the nsp10-nsp14 interaction abrogated the nsp10-driven activation of the nsp14 exoribonuclease. We further showed that the nsp10 surface interacting with nsp14 overlaps with the surface involved in the nsp10-mediated activation of nsp16 2'-O-methyltransferase activity, suggesting that nsp10 is a major regulator of SARS-CoV replicase function. In line with this notion, reverse genetics experiments supported an essential role of the nsp10 surface that interacts with nsp14 in SARS-CoV replication, as several mutations that abolished the interaction in vitro yielded a replication-negative viral phenotype. In contrast, mutants in which the nsp10-nsp16 interaction was disturbed proved to be crippled but viable. These experiments imply that the nsp10 surface that interacts with nsp14 and nsp16 and possibly other subunits of the viral replication complex may be a target for the development of antiviral compounds against pathogenic coronaviruses.