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PhD Student in the Plasmid Biology and Evolution (PBE) and Evolution of Microbiomes and Mobile Genetic Elements (EMMGE) labs. Bioinformatician and Biologist hybrid 💻🧬

In celebration of good friends and collaborators Erin Gloag @sirmicrobe.bsky.social, Dan Wozniak and @nanamikubota.bsky.social, here's a cool new study about rapid P. aeruginosa adaptation in wounds, with some hidden phage phun as bonus. journals.asm.org/doi/10.1128/...

A big shoutout to all the authors involved in this work!!! @asantoslopez.bsky.social , @sanmillan.bsky.social , @jorgesastred.bsky.social , @javierdelafuente.bsky.social , C. Costas, A. Alonso-del-Valle, M. Hernández and R. Cantón

New paper out! 🔈 Genomic Characterization of the RyC collection: 50 Multidrug Resistant Clinical Isolates of Escherichia coli and Klebsiella spp. 50 MDR gut isolates, 2 sequencing platforms, 4 “omes,” and 1 mission: provide a resource to decode AMR and MGE dynamics www.biorxiv.org/content/10.6...

New book "A Primer for Experimental Evolution" with coauthors Michael Rose, Margarida Matos, and Joe Graves. www.worldscientific.com/worldscibook... A compact primer for students and colleagues interested in planning and designing experiments to address questions in evolutionary biology.

🚨 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!👇👇

New paper out! 🔈🔈📣📣 Plasmids promote antimicrobial resistance through Insertion Sequence-mediated gene inactivation. Combining experimental and computational approaches, we unveil how two of the most prevalent bacterial MGE accelerate the evolution of AMR. 🧵👇🏻 www.biorxiv.org/content/10.1...

Our new manuscript is out! A bit of everything cool: Plasmids ✅ Insertion Sequences ✅ AMR Evolution ✅ Microbial Communities ✅ Databases analyses ✅ Mathematical modeling ✅ See the scientific thread below of Jorge Sastre, who has brilliantly led this work with @palomarodera.bsky.social

Looking forward to seeing everyone, new and old, at the Microbial Population Biology GRS + GRC in just a couple days! go.bsky.app/GGxRjzC

Latest from the lab! Between clinical S. aureus, most gene transfer mechanisms are blocked, yet lateral transduction remains highly efficient. Restriction modification-defective strains act as gateways for horizontal gene transfer, enabling DNA flow across populations. rdcu.be/fbNQK

The science was cutting edge, and the company was unparalleled- thank you everyone for such a welcoming and thrilling #GRCMicroPop! Looking forward to cyberstalking all your google scholar profiles ❤️

We demonstrate that in a porcine full-thickness thermal injury wound model, a Pseudomonas aeruginosa mutant deficient in biofilm formation undergoes adaptive evolution by acquiring mutations that alter the outer membrane, either type IV pili (T4P) or lipopolysaccharide (LPS) mutations, that restores the deficient biofilm phenotype. We also observe a striking degree of mutational parallelism, at both the biosynthetic pathway and gene level, indicating the strong selective pressures experienced by these pathways during chronic wound infection.

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

Nature Communications - The efficiency of horizontal gene transfer between different bacterial lineages is often unclear. Here, Figueroa et al. show that lateral transduction is the primary driver...

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!🧵👇