Happy to share our new preprint “An intragenic FAT1 regulatory element deleted in muscular dystrophy patients drives muscle and mesenchyme expression during development”.
This is a long due follow up of our past discovery of FSHD-associated Copy number variants deleting a putative FAT1 enhancer (Caruso et al., Plos Genetics 2013). We have explored this possibility by investigating the transcriptional activity of this putative enhancer in vivo.
- Nathalie Caruso, Angela K. Zimmermann, Tarana Nigam, Celine Becker, Karelia Lipson, Françoise Helmbacher. “An intragenic FAT1 regulatory element deleted in muscular dystrophy patients drives muscle and mesenchyme expression during development” Biorxiv (2022), September 17 | doi: 10.1101/2022.09.14.507898 | PDF
I’m delighted to share that the manuscript “Astrocyte-intrinsic and extrinsic Fat1 activities regulate astrocyte development and angiogenesis in the retina” is now published in Development (2022) | doi:10.1242/dev.192047 | PDF |
This study uncovers astrocyte-intrinsic and extrinsic Fat1 activities that influence astrocyte migration polarity, proliferation and maturation, the disruption of which impacts retinal vascular development and maintenance of vascular architecture.
Hot off the press! Delighted to share that our publication “Fat1 deletion promotes hybrid EMT state, tumour stemness and metastasis“, led by Ievgenia Pastushenko and Federico Mauri, from the lab of Cedric Blanpain (Laboratory of Stem Cells and Cancer, Université Libre de Bruxelles (ULB)) is now out in Nature. December 16, 2020. DOI: 10.1038/s41586-020-03046-1 | PMID: 33328637 |
This study shows that FAT1 acts as a tumour suppressor gene, its loss promoting initiation and malignant progression of skin and lung squamous cell carcinomas (SCCs). Through a combination of studies using mouse and human SCC models, this works not only uncovers key mechanisms by which FAT1 disruption promotes a hybrid EMT phenotype, with simultaneous acquisition of mesenchymal characteristics and maintenance of epithelial programs, but also identifies drug vulnerabilities and resistances of FAT1-deficient SCCs, the knowledge of which will be key for personalized medicine
In press! Our work in collaboration with the lab of Cynthia Andoniadou (King’s College, London) featuring the roles of FAT & Dachsous Cadherins during pituitary development, is now out at JCI Insight.
Emily J Lodge, Paraskevi Xekouki, Tatiane S Silva, Cristiane Kochi, Carlos A Longui, Fabio R Faucz, Alice Santambrogio, James L Mills, Nathan Pankratz, John Lane, Dominika Sosnowska, Tina Hodgson, Amanda L Patist, Philippa Francis-West, Francoise Helmbacher, Constantine Stratakis, Cynthia L Andoniadou. Requirement of FAT and DCHS protocadherins during hypothalamic-pituitary development. JCI Insight, (2020) Oct 27 |PMID: 33108146 | PDF |
Proud to announce that a review article co-authored with Sigmar Stricker, is now out in Seminars in Cell and Developmental Biology.
Helmbacher, F.#, Stricker, S.#. Tissue cross talks governing limb muscle development and regeneration (Review article). Seminars in Cell and Developmental Biology, (2020), June 7 |PMID: 32517852 | #: co-corresponding | PDF: Helmbacher & Stricker 2020 |
Aix-Marseille University and our CNRS lab are progressively reopening after the Covid-19 lockdown. AMU has announced that we are officially allowed to welcome new interns to start in July. So if you are a student interested by a summer internship with us, we’ll be happy to have you around and offer you a safe environment to start practicing life as a scientist. Contact me for details.
I am thrilled to share the newest preprint, posted on bioRxiv and submitted during the Covid-self-isolation period!
Helmbacher, F. Fat1 regulates astrocyte maturation and angiogenesis in the retina. BioRxiv preprint
As a phase of renovations of the IBDM building has started (plan campus), we (half of the IBDM teams) just moved to our new temporary labs, in a lovely part of the Luminy campus, near the CINAM (the last rectangular building left to the CINAM buildings on the map below).