A new article entitled BCL-XL blockage in TNBC models confers vulnerability to inhibition of specific cell cycle regulators has recently been published in Theranostics.
Entitlted “BCL-XL blockage in TNBC models confers vulnerability to inhibition of specific cell cycle regulators“, this article in Theranostics is the result of a collaboration between 5 institutes: IBDM, AMU, Inserm, Weizmann Institute of Science, CRCM, OHSU Knight Cancer Institute. The article is signed by 5 of our CENTURI members: Fahmida Ahmad (IBDM), Olivier Castellanet (IBDM), Bianca Habermann (IBDM), Fabienne Lamballe (IBDM), Flavio Maina (IBDM).
Abstract: Interfaces between cells with distinct genetic identities elicit signals to organize local cell behaviors driving tissue morphogenesis. The Drosophila embryonic axis extension requires planar polarized enrichment of myosin-II powering oriented cell intercalations. Myosin-II levels are quantitatively controlled by GPCR signaling, whereas myosin-II polarity requires patterned expression of several Toll receptors. How Toll receptors polarize myosin-II and how this involves GPCRs remain unknown. Here, we report that differential expression of a single Toll receptor, Toll-8, polarizes myosin-II through binding to the adhesion GPCR Cirl/latrophilin. Asymmetric expression of Cirl is sufficient to enrich myosin-II, and Cirl localization is asymmetric at Toll-8 expression boundaries. Exploring the process dynamically, we reveal that Toll-8 and Cirl exhibit mutually dependent planar polarity in response to quantitative differences in Toll-8 expression between neighboring cells. Collectively, we propose that the cell surface protein complex Toll-8/Cirl self-organizes to generate local asymmetric interfaces essential for planar polarization of contractility.