Thomas Ipoutcha

@tomipou.bsky.social

Postdoc at Imperial College, in the @jrPenades lab. Passionate about Phage-bacteria, AMR stories.

I am excited to share that our manuscript titled 'Defining the ESKAPE pathogen prophage repertoire with PHORAGER' is now available online as a preprint in BioRxiv! 🤩 (doi.org/10.64898/202...) Here we present PHORAGER, a Nextflow pipeline for the identification and quality assessment of prophages 🧬

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🚨 New preprint from the lab! 🚨 We show that multireplicon plasmids are true AMR "jack-of-all-trades": Widespread, highly mobile, broad host-range, and packed with resistance genes. Far from random, they form co-evolving associations driven & 𝘮𝘢𝘪𝘯𝘵𝘢𝘪𝘯𝘦𝘥 by IS elements. See Nacho's thread below!👇👇

Multireplicon plasmids emerge under predictable rules and drive the spread of antimicrobial resistance across bacterial hosts

Plasmids are DNA molecules that replicate independently of the bacterial chromosome and are typically associated with the spread of antimicrobial resistance (AMR) and virulence determinants, among other relevant traits. Fusion events between plasmids generate larger, complex backbones that carry two or more replication systems, known as multireplicon plasmids. Despite decades of study, we are still far from understanding how multireplicon plasmids arise, persist, and shape the evolution of AMR. Here, we analyzed 24,000 non-redundant plasmids across bacterial genera and found that more than 30% of them encoded multiple replicons. Compared to single-replicon plasmids, multireplicon plasmids were larger, were enriched in genes encoding antimicrobial, metal, and biocide resistance as well as virulence factors, and showed higher mobility and a broader host range. We also found that multireplicon assembly is not random. Some replicon pairs repeatedly merge into stable multireplicon plasmids, while other pairs rarely fuse even when they commonly coexist intracellularly. We also show that replicon pairs tend to be localized either in close proximity to one another or on opposite poles of the plasmid. We further highlight that multireplicon plasmids can be broadly classified into two groups: long-term coevolving replicon pairs and transient associations that lack a shared evolutionary history. Finally, we reveal the molecular mechanisms underlying multireplicon formation and highlight the role of insertion sequences in their formation and maintenance. Together, our work sheds light on the abundance, gene content, evolutionary patterns, and formation dynamics of multireplicon plasmids and pinpoints their relevance to bacterial evolution and human health. ### Competing Interest Statement The authors have declared no competing interest. Instituto de Salud Carlos III, https://ror.org/00ca2c886, PI23/01945, PFIS - FI22/00265, Miguel Servet - CP22/00164 European Research Council, https://ror.org/0472cxd90, HorizonGT, 101077809 Fundación Ramón Areces, "Ayudas Fundación Ramón Areces para la realización de Tesis Doctorales en Ciencias de la Vida y de la Materia 2025" Coordenação de Aperfeicoamento de Pessoal de Nível Superior, https://ror.org/00x0ma614, 88881.128025/2025-01

biorxiv.org

Ignacio (Nacho) de Quinto@nachodequinto.bsky.social · 4mo ago

What if multireplicon plasmids are not an oddity, but an evolutionary strategy? We found that they are common, more mobile, broader-host-range, and enriched in AMR. Even more interesting: their assembly doesn’t look random. 👀 Paper preprint: www.biorxiv.org/content/10.6... Thread below!🧵👇

This paper started as an idea @albertomarina.bsky.social had many years ago… which of course means he was right all along 😄. Some of us just needed a few years (and a lot of experiments) to catch up. Grateful (and slightly humbled) to be part of this. Thanks Alberto! www.cell.com/cell/fulltex...

Phages communicate across species to shape microbial ecosystems

Gallego-del-Sol et al. show that arbitrium-coding phages can sense non-cognate peptide signals from other phages to regulate lysis-lysogeny decisions. This crosstalk affects lysis-lysogeny outcomes of...

cell.com

➡️ preprint from the lab! Bacteria have loads of antiviral defences in their mobile genetic elements (MGEs). So when MGEs move between bacteria, the defences move with them, generating a fast turnover of defences in bacteria. But what about the antiviral defence turnover in the MGEs themselves? 🤔 🧵👇

biorxiv.org