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Biology subjects

Celotti, M.

Publications and source records attributed to Celotti, M..

2 recordsLinked to original sources

Human embryo implantation involves Syncytin-2/MFSD2A-mediated heterokaryon formation with maternal endometrium

Human embryo implantation involves attachment of the blastocyst to the endometrial epithelium to subsequently gain access to the underlying stromal compartment. The blastocyst is believed to cross the epithelium either by migration through, or upon apoptosis of, the endometrial epithelial cell layer. Yet, how the blastocyst exactly traverses the endometrial epithelium remains unknown. Here, we describe an in vitro implantation model of human blastoids and hormonally matured endometrial organoids amenable to high-resolution live imaging. We demonstrate that the initial step of implantation is mediated by the direct fusion of blastoid cells with endometrial epithelial cells. Blastoids express the fusion proteins Syncytin-1 and -2, while the endometrial epithelium mainly expresses the fusion co-receptor for Syncytin-2, called MFSD2A. CRISPR-induced loss of MFSD2A in the endometrial epithelium prevents blastoids from attaching and abolishes fusion. Together, these findings support a model in which fetal-maternal cell fusion constitutes the critical initiating mechanism of human embryo implantation, with endometrial MFSD2A playing an indispensable role in this process.

developmental biology↗

Intra-epithelial non-canonical Activin A signalling safeguards prostate progenitor quiescence

The healthy prostate is a relatively quiescent tissue. Yet, prostate epithelium overgrowth is a common condition during ageing, associated with urinary dysfunction and tumorigenesis. For over thirty years, TGF-{beta} ligands have been known to induce cytostasis in a large variety of epithelia, but the intracellular pathway mediating this signal in the prostate, as well as its relevance for quiescence, have remained elusive. Here, using mouse prostate organoids to model epithelial progenitors, we found that intra-epithelial non-canonical Activin A signalling inhibited cell proliferation in a Smad-independent manner. Mechanistically, Activin A triggered Tak1 and p38 MAPK activity, leading to p16 and p21 nuclear import. Spontaneous evasion from this quiescent state occurred upon prolonged culture, due to reduced Activin A secretion, a condition associated with DNA replication stress and aneuploidy. Organoids capable to escape quiescence in vitro were also able to implant with increased frequency into immunocompetent mice. Our study demonstrates that non-canonical Activin A signalling safeguards epithelial quiescence in the healthy prostate, with potential implications for the understanding of cancer initiation, and the development of therapies targeting quiescent tumour progenitors.

cancer biology↗