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              <p>The colonic tissues are abnormally colonized by colibactin-producing Escherichia coli (CoPEC) in colorectal cancer (CRC) patients. Colibactin is a genotoxin produced by enzymes encoded by the pks genomic island. Metabolomic studies have shown that CoPEC infection results in reprogramming of intestinal epithelial cell metabolism, leading to a decrease of L-serine concentration. The aim is to investigate whether L-serine allows CoPEC to better persist in the gastrointestinal tract and/or exert their pro-carcinogenic functions. In vitro, we have shown that CoPEC uses L-serine from the enterocyte via the activation of serine-utilization-operon, which provides to CoPEC a competitive growth advantage in comparison to a commensal strain or its mutant (11G5-Δpks). To highlight the specific role of L-serine, APCmin/+ mice were fed with a Serine Depleted (SD) diet. SD diet induced an early and transient decrease in CoPEC 11G5 bacterial colonization associated with a decrease of DNA damages. In addition, the pro-carcinogenic potential of CoPEC on MC38 grafted-tumors is significantly lower with the SD diet than with the control diet. The impact of L-serine utilization on CoPEC virulence was verified both in vitro and in vivo with a 11G5-ΔtdcA mutant, unable to metabolize serine. Altogether, these data support that CoPEC would use the host L-serine, by activation of its serine operon utilization, to persist and promote its genotoxic and pro-carcinogenic effects. This work allows us to elucidate the mechanisms of action of CoPEC in colonic carcinogenesis and identify potential novel therapeutic targets.</p>
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