James Connolly

@ruamicro.bsky.social

MRC Career Development Fellow at Newcastle University. Studying how pathogens control their genes

"In a patient with a staghorn calculus, chronic urinary tract infection with Klebsiella pneumoniae enabled within-patient evolution of virulence properties that facilitated dissemination of infection, leading to a brain abscess." Don't mess with Klebs. #UTISky #UTI #IDSky

Andreas Peschel @andreaspeschel.bsky.social · 2w ago

What drives hypervirulence and resistance of the ESKAPE pathogen Klebsiella pneumoniae? Check this exciting story by @dzif.bsky.social Prof. Christoph Ernst Klebsiella Brain Abscess and Evolution of Heterovirulence in the Urinary Tract | New England Journal of Medicine www.nejm.org/doi/10.1056/...

1/ Excited to share a new preprint! My PhD student Claire asked why neonatal mice become resistant to experimental cholera as they age. Turns out, early-life acquisition of maternally transmitted lactobacilli helps protect against experimental cholera www.biorxiv.org/content/10.6...

Early-life acquisition of Lactobacillaceae protects against experimental cholera

Cholera causes severe diarrheal illness in young children, but the mechanisms underlying age-dependent susceptibility remain unclear. Experimental cholera in neonatal mice recapitulates age-dependent ...

biorxiv.org

Out after a lot of hard work from many people. When we first found arabinanase enzymes in mycobacteria we started looking into their roles in cell remodelling & pathogenesis. Did not expect to find that some species had weaponised them to kill competitors! Myco are endlessly surprising. #glycotime

Patrick Moynihan@pmoyniha.bsky.social · last mo.

New paper in collaboration with @proftracypalmer.bsky.social, @lislowe.bsky.social and many more. We show that mycobacteria produce Type VII secreted anti-bacterial protein toxins. Excited to explore this new area of mycobacterial biology. www.nature.com/articles/s41...

Cool new plasmid work from Joe Wade's lab at the Wadsworth Center! Lots of conjugative plasmids encode Histone-like nucleoid-structuring protein (H-NS) proteins, and there's increasing evidence they somehow specifically bind to the plasmids that encode them #microsky #plasmidsky

Joe Wade@joe-wade.bsky.social · last mo.

New preprint from our lab, in collaboration with the Santiago/Ruiz-Perez group at UVA. We found a plasmid-encoded DNA-binding protein that preferentially binds its own plasmid! www.biorxiv.org/content/10.6... Thread:

Really lovely work, Marjon & team, puts us closer to being able to decipher #UTI diagnosis based on sequencing - currently difficult in my view, with dozens of strains detected and never being entire sure what the pathogen(s) is/are. We need to understand entire signatures better. #UTISky #IDSky

Marjon de Vos@lizscurious.bsky.social · last mo.

Cross-study metagenomics analysis reveals distinct microbial signatures of urinary tract infections www.biorxiv.org/content/10.6... #UTISky

Happy to share the last publication of @bobytaillefer.bsky.social, showing that #T6SS heterogeneity is an attenuation strategy to optimizes the trade-off between competitive killing and survival.

PLOS Biology@plosbiology.org · 2mo ago

The T6SS is a widespread nanoweapon deployed by #bacteria, but why is it deployed heterogeneously? @cascaleslab.bsky.social &co show that #Ecoli adopt distinct #T6SS attacker "ON" & defender "OFF" roles to optimize survival, a key strategy in microbial warfare @plosbiology.org 🧪 plos.io/3S5dL45

Top: Representative confocal fields of the 3 types of TssC-GFP-TssK microcolonies (homogeneous ON, heterogeneous, homogeneous OFF). Scale bars, 10 μm. Bottom:  Model for the role of T6SS phenotypic heterogeneity in EAEC. Top: The Psci1 promoter integrates Fur- and Dam-dependent regulation, generating ON (T6SS⁺, yellow) and OFF (T6SS⁻, blue) subpopulations at a reversible equilibrium. Bottom left: OFF (blue) cells, which do not express T6SS, do not kill competitors but avoid triggering such defences (1). Due to the absence of killing activity, OFF cells are unable to colonize the niche (2). Bottom centre: While ON (yellow) cells assemble and deploy functional T6SS (1) and kill susceptible competitors (2), they provoke retaliatory attacks from defensive T6SS⁺ species (gray) and are eliminated and fail to colonize the niche (3). Bottom right: Heterogeneous ON/OFF population (1) optimizes colonization by killing neighboring cells (2). While ON (yellow) cells are eliminated by counterattacks by defensive T6SS+ species (gray), OFF (blue) cells resist (3) and can ensure a continuous supply of ON cells (4-5) while limiting population-wide exposure to retaliation.