Mostly Microbes and Infection - by David Ojcius

First‑line fecal microbiota transplantation yields rapid improvement in most patients with immune checkpoint inhibitor–mediated colitis. In this cohort, 76.9% responded within a median 1.5 days, with increased microbial diversity and reduced immune‑cell activation after treatment. Multi‑omics profiling highlights potential mechanisms underlying FMT response.

Programmed ribosomal frameshifting acts as a regulatory stress signal that activates GCN2 and shuts down host translation. A minimal SARS‑CoV‑2 frameshift element triggers this response independently of ZAKα and is required for viral propagation. DRG1 and IGF2BP3 mediate GCN2 activation, and the mechanism extends to HIV‑1 and West Nile virus.

GORG‑Dark, a dataset of 9,698 single‑cell genomes from deep‑ocean prokaryoplankton, reveals extensive vertical stratification, unexpected particle‑attached Pelagibacterales, and high Patescibacteria and Nanoarchaeota abundance in marginal seas. Coding analyses uncover chemolithoautotrophy, novel proteorhodopsins, and secondary metabolisms across aphotic lineages.

Incretin therapies now improve multiple obesity‑related diseases, with expanding organ‑specific indications. This review explains their mechanisms, evaluates evidence across conditions, and provides a practical framework for using incretin agents beyond endocrinology—covering drug selection, sequencing, monitoring, safety, long‑term management, and access‑limited prescribing.

Predicted bacteriocin genes reveal potential but not function. This review defines four forms of bacteriocin silence—transcriptional, conditional, phenotypic, and ecological—and outlines a function‑first roadmap using condition‑resolved omics, cue‑dissection, structured assays, and defined consortia to link gene catalogs to real ecological impact.

Researchers identify PfSR1‑MT as a melatonin‑responsive GPCR‑like receptor in Plasmodium falciparum . PfSR1‑MT binds melatonin with high affinity, triggers ECD movement and Ca²⁺ signaling, and is selectively activated by ARL34, which inhibits parasite growth and gametocyte development, highlighting a promising antimalarial target.