Events

External attendees, if you wish to attend in person please contact Kelly Nguyen: knguyen@mrc-lmb.cam.ac.uk

Abstract: In Saccharomyces cerevisiae, prolonged cellular stress induces a subset of introns to accumulate post-splicing as stable, linear, spliceosome-protected RNAs. These stable introns sequester splicing components, causing less efficient splicing in these stressed conditions. The mechanism by which these normally ephemeral products of pre-mRNA splicing persist cannot be explained by the current understanding of the splicing pathway, which derives primarily from studies of unstressed cells and their extracts. Here, we determined a cryo-electron microscopy structure of a stable-intron complex purified from saturated-culture conditions. This structure and experimental follow-up show that a Bact-like spliceosome protects stable introns from degradation. Spliceosomes arrive at this Bact-like conformation by reassembling onto linear introns after their excision from pre-mRNAs. Using a genome-wide CRISPRi screen, we also identified genes required for stable-intron accumulation. This screen identified IKS1 as a key regulator of stable-intron accumulation. Loss of Iks1 kinase activity causes depletion of stable introns, whereas perturbation of a putative autoinhibitory helix or overexpression of Iks1 causes stable introns to accumulate in log-phase growth, where they normally would not accumulate. Iks1 phosphorylates proteins involved in proteostasis, including the Ssa1–4 Hsp70 proteins. Hsp70 inhibition is sufficient to induce stable-intron expression, whereas disruption of a predicted physical interaction between Iks1 and Hsp70 reduces stable-intron expression. We propose that Iks1- and Hsp70-dependent regulation of spliceosome components enables the spliceosome to assemble on linear excised introns and protect them from degradation during prolonged stress.

External attendees, if you wish to attend in person please contact Tanmay Bharat: tbharat@mrc-lmb.cam.ac.uk

Abstract to follow

External attendees, if you wish to attend in person please contact Julian Sale: jes@mrclmb.ac.uk

Abstract to follow

External attendees, if you would like to attend, please contact Lori Passmore: passmore@mrc-lmb.cam.ac.uk

Abstract to follow.

External attendees, if you wish to attend in person please contact Felix Randow randow@mrclmb.ac.uk or Leo James@mrclmb.ac.uk

https://mrc-lmb-cam-ac-uk.zoom.us/j/94514662338?pwd=QFmpzVDjmvrrMmV476z2wynx6r2aoA.1

External attendees, if you wish to attend in person please contact Leo James: lcj@mrclmb.ac.uk

Abstract to follow

2-3 July 2026

See website for further information https://www3.mrc-lmb.cam.ac.uk/sites/gsasymposium/

2-3 July 2026

See website for further information https://www3.mrc-lmb.cam.ac.uk/sites/gsasymposium/

Register here: https://www.enterprise.cam.ac.uk/events/new-technologies-and-building-successful-biotechnology-companies-to-treat-disease/#harvey-lodish‑register

Celebrating his return to Cambridge and the MRC Laboratory of Molecular Biology (LMB), we are delighted to welcome Professor Harvey Lodish, Professor of Biology and Biological Engineering at MIT, who undertook his postdoctoral research at the LMB with Drs Sydney Brenner and Francis Crick, for a special lecture and discussion.

The event will explore how fundamental scientific discovery can be translated into real‑world benefit and the role universities play in supporting that journey with integrity, responsibility, and long‑term vision.

Professor Lodish will share insights from his academic career and his experience founding and advising biotechnology companies, including perspectives on mentorship, ethics, and the relationship between research excellence and enterprise. The lecture will be followed by a panel discussion, Q&A, and networking over lunch.

This unique opportunity is open to academics, postdoctoral researchers, and staff from across the Biomedical Campus, including the LMB, Clinical Schools, Milner Therapeutics Institute, and partner organisations

Schedule for the day:
10.00 – Arrival & coffee
10.30 – Welcome
10.45 – Special Lecture with Professor Harvey Lodish: New Technologies and Building Successful Biotechnology Companies to Treat Disease: A Personal History
11.45 – Panel & Q&A
12.30 – Lunch
13.30 – Event close

An informal one day meeting organised by MRC LMB, MRC LMS and Imperial College London examining the application of cutting edge biophysical techniques in complex biological settings. Bringing together scientists in both academia and industry for stimulating talks and discussions how these new and emerging technologies may be able to address challenging questions in the future.

For more information see https://www3.mrc-lmb.cam.ac.uk/sites/nextgen/

External attendees, if you wish to attend in person please contact Tanmay Bharat: tbharat@mrc-lmb.cam.ac.uk

Abstract to follow

External attendees, if you would like to attend in person please contact David Favara: dfavara@mrc-lmb.cam.ac.uk

Adhesion GPCRs are among the most intriguing unresolved problems in receptor biology. The key challenge for their understanding is to decipher their input-output relationship. Their unusual architecture and sensitivity to mechanical and adhesive inputs raise a central question: how are extracellular cues converted into defined signalling outputs? Unlike classical GPCRs, they do not merely bind soluble ligands but instead sense and interpret mechanical stimuli through an elaborate molecular architecture built around the GAIN domain and a cryptic intramolecular agonist. I will present recent work that brings this problem into quantitative focus through through a combination of biophysical measurements and method development: tools for acute, time-controlled receptor activation, strategies for engineered ligand engagement, and force-resolved assays that capture GAIN-domain unfolding, receptor dissociation and mechanochemical signalling. Together, these approaches reveal how adhesion GPCRs convert mechanical and adhesive information into distinct downstream responses. This emerging framework recasts adhesion GPCRs as measurable signalling machines and opens a route towards understanding their roles in neural development, tissue organisation, immunity and cancer with molecular precision.