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Michiel’s preprint is out!

Michiel’s preprint on the effects of cohesin depletion on rewiring of promoter-enhancer interactions and nascent transcription is out!

https://doi.org/10.1101/2020.02.10.941989

A fruitful collaboration with Gordana Wutz and Wen Tang at Jan-Michael Peters’s lab at the IMP, Matthias Muhar at the IMP’s Zuber lab, and Stefan Schoenfelder and Peter Fraser at Babraham.

Now fingers crossed for the story’s smooth sailing to a journal…

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Two new preprints

Today sees the publication of not just one, but two preprints from our lab and our close collaborators.

The first preprint is work led by Jo Mitchelmore (our group’s first ever PhD student, now at Novartis), in which she has used changes in transcription factor binding affinity at promoter-connected regulatory regions as predictor variables to detect eQTLs. Using this method, she’s uncovered hundreds of novel associations – and a bunch of epromoters, regions that function both as distal enhancers and promoters of other genes. Great collaboration with Chris Wallace and her postdoc Stasiya Grinberg.

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Chicdiff is released!

We have released Chicdiff, an R package for differential analysis of Capture Hi-C data. Joint work by the power team: Jonathan (now at AstraZeneca), William (now back at Cambridge) and Valeriya. The package is available on github, and the preprint describing it is on bioRxiv. If you work with Capture Hi-C data, please try it out and let us know what you think!

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Lina’s paper is out!

Our study of vascular smooth muscle cell heterogeneity using single-cell transcriptomics and lineage tracing is finally out! Co-led by our group’s Lina Dobnikar and Annabel Taylor fro Helle Jørgensen’s lab at Cambridge University.

Vascular smooth muscle cells (VSMCs) from are interesting for at least two reasons: (1) they originate from at least two different embryonic layers, depending on location and (2) in response to inflammation or injury, they lose their muscle cell phenotype and turn into migrating, proliferating fibroblast-like ‘synthetic’ cells.

We found that VSMCs homogeneously bear the footprints of their embryonic origins, but are heterogeneous with respect to other expressed genes. In particular, we found a rare VSMC subpopulation in healthy vessels that express a transcriptional signature (including progenitor marker Sca1) that is prevalent in vascular disease and potentially defines cells in the process of switching to the synthetic state.

Notably, Helle previously showed that only a small proportion of VSMCs expand in response to injury, so being able to catch cells ‘in the act’ of switching may help to understand ‘what makes them tick’.

Link to paper: https://www.nature.com/articles/s41467-018-06891-x.
Link to press release: https://www.babraham.ac.uk/news/2018/11/observation-of-blood-vessel-cells-changes-could-lead-to-early-detection-of-blocked-arteries.

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