Alex Whitworth lab

@labwhitworth.bsky.social

Research group at the MRC Mitochondrial Biology Unit, University of Cambridge. Interested in all things neurodegeneration, mitochondrial dysfunction, in vivo genetics, Drosophila, mitophagy, mtDNA, calcium, gut-brain axis etc

It was a pleasure to present our emerging story @cambridgeflyclub.bsky.social. Great feedback from an engaged and enthusiastic audience of young (and some not so young 😜) fly researchers. Now let’s hear from some ECRs…

Cambridge Fly Club@cambridgeflyclub.bsky.social · 3w ago

💡 First, Dr Alex Whitworth @labwhitworth.bsky.social, explored the emerging concept of the gut–brain axis in neurodegeneration. His talk highlighted how Drosophila models provide insights into gut homeostasis, systemic inflammation, and their links to neurodegenerative diseases such as Parkinson’s.

Revised preprint on mitochondria in central brain of Drosophila now online: much new analysis + details of largest resource for analyzing neuronal mitochondria generated so far, with ~6M mitochondria, >20k neurons, >5k cell types. Much thanks to all coauthors, enjoy! www.biorxiv.org/content/10.1...

Connectomic Analysis of Mitochondria in the Central Brain of Drosophila

Mitochondria are integral to the metabolism and cell biology of a neuron. Electron microscopy images of fly brain volumes, taken for connectomics, can be analyzed for mitochondria as well as the cells...

biorxiv.org

We're hiring a Postdoctoral Research Associate at the MRC Mitochondrial Biology Unit @mrc-mbu.bsky.social Cambridge Join our ARIA Precision Mitochondria project with Bitrobius Genetics to develop novel technologies for mitochondrial DNA delivery and genome engineering www.cam.ac.uk/jobs/researc...

Research Associate (Fixed Term)

The Medical Research Council Mitochondrial Biology Unit (MRC MBU), University of Cambridge wishes to appoint a post-doctoral Research Associate to join the research group of Prof. Michal Minczuk at th...

cam.ac.uk

Great review on an exciting field - emerging technologies to treat mitochondrial diseases, which have potential application to other conditions such as neurodegeneration.

London Mitochondrial Centre@londonmito.bsky.social · 2mo ago

We are pleased to share a new review published in Cell Reports Medicine @cellpress.bsky.social: “Emerging therapeutic strategies for mitochondrial DNA-related diseases” Full article: doi.org/10.1016/j.xc... #Mitochondria #mtDNA #GeneTherapy #GenomeEditing #RareDiseases #TranslationalMedicine

Was intrigued when I saw this initiative launched a little while back. Delighted to see it is working well. Maybe it’ll be the beginning of redressing the balance of power with the publishing houses and help support ECRs and junior faculty.

Daniel Gorelick@danielgorelick.bsky.social · 2mo ago

Paying peer reviewers works. Expanded Fast & Fair experiment @biologyopen.bsky.social: • 5.5 vs 37.7 working days to decision with reviews • ~3 vs ~9 reviewer invitations per manuscript • no reduction in editor-assessed review quality • similar acceptance rates www.biorxiv.org/content/10.6...

Scatter plot showing that Fast & Fair peer review reached first decision with reviews much faster than conventional peer review: mean 5.5 versus 37.7 working days. Most Fast & Fair manuscripts met the 7-working-day target, while conventional manuscripts were slower and more variable, up to 116 working days.

Interesting. Miro-Milton/TRAK interaction not necessary for mito trafficking?? www.biorxiv.org/content/10.6...

The Interaction Between Miro and TRAK is not Required for Bulk Mitochondrial Trafficking

In metazoans, mitochondria optimally distribute to sites of need through long-range transport events on microtubules. The prevailing model for this trafficking mechanism is that the tail-anchored calcium-binding GTPase, Miro, recruits cytosolic TRAK and associated molecular motors to the outer mitochondrial membrane. Therefore, Miro is proposed to be an obligate adaptor for TRAK required for bulk mitochondrial transport, a process that is considered particularly important for long-range trafficking in neurons, and thus, for viability. Here, we impaired Miro-TRAK interaction in vivo by introducing a point mutation into the Drosophila TRAK orthologue Milton, that impairs its interaction with Miro, based on recent structural evidence. Flies harbouring this point mutation are viable to adulthood. Moreover, neurons carrying this mutation exhibit little to no observable reduction in axonal mitochondria. Mutant flies, however, display progressive loss of motor function with age and reduced lifespan. We therefore call into question the long-standing view that Miro plays an obligatory role in mitochondrial trafficking and challenge the canonical model for mitochondrial transport. ### Competing Interest Statement The authors have declared no competing interest.

biorxiv.org

🚨 Registration is open! 🚨 Join us for "Mitochondria Vol. 3: Mitochondrial Plasticity in Metabolism and Signalling", a free-of-charge international conference organized by the CRC 1218! 🗓 When: 05–07 October 2026 📍 Where: MTI, UzK Cologne, Germany 👉 Register now: mitochondria-volume3.uni-koeln.de

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