Sourav Ghosh

Well, really happy to see that finally evidence showing VCP ruptures depolarised mitochondria outer membrane, as we have seen that VCP can also extract bacterial surface proteins and rupture cytosolic dwelling pathogens also.

Congratulations! Fantastic findings. Do you also find the hierarchical recruitment of GBP2-4 in these structures?

📢A new effector-triggered immunity role for GBP1! No place for pathogens to hide now that GBP1 can detect extracellular pathogens that hijack the actin cytoskeleton. Surprise*suprise* GBP1 does this independently of LPS! 🧵
biorxiv.org/content/10.1...

So grateful to the AIC team at Janelia! Three surreal weeks packed with months of learning, cutting-edge technology, and inspiring science. Huge thanks to Bob’s for the amazing food—it made everything even sweeter. Truly an experience of a lifetime that I’ll always cherish! 💛
#microscopy #IPALM #ExM

Incredibly honoured and grateful to receive the 2025 Angelika Amon Young Scientist Award! Deep thanks to my supervisor @anirban-banerjee.bsky.social, friends, lab colleagues, Department of Biosciences and Bioengineering, and @iitbombay.bsky.social for their unwavering support. Simply Lovely.

So cool. Congratulations. Maybe after ubiquitination, AR will be pulled out from the chromatin, or it can fall off spontaneously.

Clustering of NLRP3 induced by membrane or protein scaffolds promotes inflammasome assembly - Nature Communications NLRP3 inflammasome activation is critical for the induction of protective immunity, but molecular insights are still lacking. Here, the authors express NLRP3 variants targeted to different cellular lo...

NLRP3 inflammasomes can assemble on most organelles. A beautiful study by Hafner et al demonstrate the flexibility of organelles that can support inflammasome activation. Kudos to the authors on an intriguing study.
www.nature.com/articles/s41...
@ivahb.bsky.social @elvirab.bsky.social

A light-regulated circadian timer optimizes neutrophil bactericidal activity to boost daytime immunity The neutrophil clockwork boosts daytime immunity against bacterial infection.

Tick Tock Neutrophil Clock

Hall Lab (Auckland) with zebrafish model find light boosts the circadian protein Per2, which enhances ROS and hmgb1a expression via a BMAL1–NF-κB enhancer

End result: Better bacterial clearance and survival—a circadian clock-gated boost for daytime innate immune function

Cool insights.

If you're into host-pathogen interactions and cell-autonomous immunity, this is a must-attend! Stellar speaker lineup and exciting science all around. Also, catch work from our lab being presented!"
#immunity #conference #india #embo

Haven’t shared this in a while. But the #ubiquitin and #ubl Starter Pack now includes 116 profiles to follow if you’re interested in the field: signalling, structure and biochemistry, biology, mechanisms, proteostasis, TPD, chemical biology… Check out the list and let me know if you are missing.

ATP functions as a pathogen-associated molecular pattern to activate the E3 ubiquitin ligase RNF213 - Nature Communications RNF213 is an E3 ligase with ATPase activity. Here, the authors show that RNF213 is activated by ATP binding and senses cellular energy states, and reveal a transthiolation mechanism induced by immune ...

Great to see this out. A story that spanned continents, cities and budget codes…

www.nature.com/articles/s41...

Big thanks to all the teams involved!

@clausenlab.bsky.social @e3chembio.bsky.social

Congratulations! So many ways we can sense threats, a detailed and layered system.

Left: Group of three T3SS localizing in the same zone of the bacteria surface. T3SS n°1 and 2 contact, deform, and perforate the vacuole membrane at the same spot. T3SS n°1 needle (83 nm) is long and seems to deviate from basal body axis showing that strong constraints between T3SS and the vacuole at are play. The locally relaxed vacuole to bacteria space (~50–55 nm) potentially limits additional damage by the T3SS n°3 needle (56 nm) that only slightly deforms the membrane. Right: Model of initial vacuolar membrane breaching by T3SS-induced mechanoporation. Shigella actively enters host cells in a specialized endomembrane compartment, the vacuole, that is rapidly injured and ruptured for cytosolic access. After host cell entry, the vacuole membrane is intact and tightly juxtaposed to the surface of Shigella, permitting contact between T3SSs and the endomembrane. In the authors’ proposed model, vacuole membrane injury is supported both by the vacuole tightness and the length of individual T3SSs.

How do intracellular #bacteria breach vacuoles to enter the host cytosol? @leaswistak.bsky.social @matthijnvos.bsky.social @enningalab.bsky.social &co show that #Shigella uses its T3SS system to damage endomembranes via mechanoporation to initiate cytosolic access @plosbiology.org 🧪 plos.io/4jXrr9Z

Chimeric deubiquitinase engineering reveals structural basis for specific inhibition of the mitophagy regulator USP30 - Nature Structural & Molecular Biology Kazi et al. report the crystal structure of the mitochondrial deubiquitinase USP, a clinical stage Parkinson’s disease drug target, in complex with a specific inhibitor. The authors delineate a framew...

Super happy to share that our work on the specific inhibition of USP30 - a clinical stage Parkinson's drug target - is now online at NSMB www.nature.com/articles/s41... Have a read if you fancy chimeric protein engineering or a framework for DUB ligandability. Huge congratulations to Nafizul & team!

Amazing work, congratulations.

This is a poster advertising the LINE scientific symposium aimed at early career researchers working in infection. Displayed is an electron microscope image showing two salmonella bacteria attached to a cells causing the cell membrane to ripple. Below the image, the organisational details about the symposium are shown.

We can see our ECR-focused LINE symposium already on the horizon (9th of June) @crick.ac.uk. shorturl.at/MyWNl 🥳
You can submit your abstracts (talk or poster) until the EXTENDED DEADLINE on the 12th of May here: shorturl.at/7KuXL
Free registration shorturl.at/wLyWY
We're excited to see you there!

Congratulations. How amazing this battle is turning out to be, between host and pathogens.

Shigella flexneri evades LPS ubiquitylation through IpaH1.4-mediated degradation of RNF213 - Nature Structural & Molecular Biology Naydenova, Boyle and Pathe et al. report that Shigella uses the ubiquitin E3 ligase IpaH1.4 to evade lipopolysaccharide ubiquitylation in infected cells by degrading the host E3 ligase RNF213. Using c...

RNF213, a host E3 ligase, ubiquitylates LPS to mark cytosol-invading bacteria for autophagy. But how do cytosol-adapted bacteria escape? We found that Shigella's E3 ligase IpaH1.4 blocks LPS ubiquitylation by degrading RNF213 via the proteasome.
www.nature.com/articles/s41...

Amazing analogy. Thank you for sharing.

Ripping Pathogens to Shreds: How a Cellular Nanomachine Punches a Lethal Blow to Bugs Bacterial pathogens invade our cells in search of nutrients, but cells fight back by tagging these microbes with ubiquitin "death labels", followed by deploying a nanomachine called VCP/p97 that tears...

🚨Got a few minutes over breakfast? 🥣
Here’s a quick peek at what we’ve been up to.
If you don’t have time for the full paper, this summary’s got the essence.
Hope you find it as exciting! 🦠🔬 @natmicrobiol.nature.com @springernature.com
#sciencecom

communities.springernature.com/posts/rippin...

Happy to share my Ph.D work!!
Our latest paper shows VCP/p97 uses its tweezer-like action to tear invading bacteria apart — a powerful cellular defense! 🦠
@natmicrobiol.nature.com
@BsbeIitb @iitbombay @CSIR
This was years of hard work! Thanks all🙌
#microbiology #cellautonomous #immunity #ubiquitin