Single-cell NAD(H) levels predict clonal lymphocyte expansion dynamics.

Adaptive immunity requires the expansion of high-affinity lymphocytes from a heterogeneous pool. Whereas current models explain this through signal transduction, we hypothesized that antigen affinity tunes discrete metabolic pathways to license clonal lymphocyte dynamics. Here, we identify nicotinamide adenine dinucleotide (NAD) biosynthesis as a biochemical hub for the T cell receptor affinity-dependent metabolome.

Density-dependent resistance protects from its own antimicrobial metabolite, HGA.

To persist in microbial communities, the bacterial pathogen must withstand competition from neighboring bacteria. Here, we find that can antagonize the growth of other species using a secreted inhibitor: HGA (homogentisic acid). Unexpectedly, can itself be inhibited by HGA secreted from neighboring, isogenic strains.