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A 42-year-old man presented with 6 months of unexplained left lower quadrant abdominal pain and hematochezia accompanied by weight loss despite extensive evaluations. Stool studies for pathogens were unrevealing, but an abdominal contrast-enhanced computed tomography revealed findings of chronic inferior mesenteric vein thrombosis. Colonoscopy demonstrated ulcerated strictures and gangrene confined to the sigmoid and descending colons, and biopsies confirmed changes of chronic irreversible colon ischemia. A homozygous Factor V Leiden mutation was diagnosed. The patient underwent colectomy and was treated with lifelong anticoagulation. While mesenteric venous thrombosis is a well-recognized cause of colon ischemia in hypercoagulable states, thrombosis of the inferior mesenteric vein is uncommon; when chronic it is rarely clinically apparent. Similarly, while Factor V Leiden mutation is a common hereditary thrombophilia, it uncommonly causes mesenteric venous thrombosis, and homozygotes of the mutation typically present earlier in the fourth decade and with non-mesenteric venous thromboembolism. This case is valuable and adds to the existing literature in describing a rare, clinically atypical, and late index presentation of homozygous Factor V Leiden mutation as chronic inferior mesenteric vein thrombosis yielding irreversible colon ischemia.

Among bacterial toxin-antitoxin systems, to date no antitoxin has been identified that functions by cleaving toxin mRNA. Here we show that YjdO (renamed GhoT) is a membrane lytic peptide that causes ghost cell formation (lysed cells with damaged membranes) and increases persistence (persister cells are tolerant to antibiotics without undergoing genetic change). GhoT is part of a new toxin-antitoxin system with YjdK (renamed GhoS) because in vitro RNA degradation studies, quantitative real-time reverse-transcription PCR and whole-transcriptome studies revealed that GhoS masks GhoT toxicity by cleaving specifically yjdO (ghoT) mRNA. Alanine substitutions showed that Arg28 is important for GhoS activity, and RNA sequencing indicated that the GhoS cleavage site is rich in U and A. The NMR structure of GhoS indicates it is related to the CRISPR-associated-2 RNase, and GhoS is a monomer. Hence, GhoT-GhoS is to our knowledge the first type V toxin-antitoxin system where a protein antitoxin inhibits the toxin by cleaving specifically its mRNA.