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Activation-induced proteome re-modelling in B cells and the role of mTORC1
In this talk I will summarise our recent work mapping the activated B cell protein landscape. Using high resolution quantitative mass spectrometry we have explored how immune activation and the metabolic checkpoint kinase mTORC1 (mammalian target of rapamycin complex 1) regulate the proteome of B lymphocytes to control B cell differentiation. Triggering the B cell receptor in combination with co-stimulatory signals and cytokines induces considerable proteome re-modelling and our data reveals the metabolic and protein synthesis machinery and environmental sensors that shape B cell fate. We show that mTORC1 activity is critical for the expression of transcription factors that regulate B cell differentiation and metabolism, including aryl hydrocarbon receptor (AHR) and MYC. Inhibiting mTORC1 activity also impairs the expression of nutrient and amino acid transporters. This work provides a detailed map of naïve and immune activated B cell proteomes, and a resource for exploring and understanding the cellular machinery that direct B cell phenotypes.
Date:
7 November 2024, 16:00
Venue:
John Radcliffe Hospital - Main Building, Headington OX3 9DU
Venue Details:
Lecture Room (GPEC)
Speaker:
Dr Andy Howden (University of Dundee)
Organising department:
NDM Experimental Medicine
Organiser:
Dr Matthias Friedrich (University of Oxford)
Organiser contact email address:
matthias.friedrich@ndm.ox.ac.uk
Host:
Dr Matthias Friedrich (University of Oxford)
Booking required?:
Not required
Audience:
Members of the University only
Editor:
Sally Pelling-Deeves
