Cell fusion induced by ERVWE1 or measles virus causes cellular senescence

Anna Chuprin, Hilah Gal, Tal Biron-Shental, Anat Biran, Aliza Amiel, Shmuel Rozenblatt, Valery Krizhanovsky*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

176 Scopus citations


Cellular senescence limits proliferation of potentially detrimental cells, preventing tumorigenesis and restricting tissue damage. However, the function of senescence in nonpathological conditions is unknown. We found that the human placental syncytiotrophoblast exhibited the phenotype and expressed molecular markers of cellular senescence. During embryonic development, ERVWE1-mediated cell fusion results in formation of the syncytiotrophoblast, which serves as the maternal/fetal interface at the placenta. Expression of ERVWE1 caused cell fusion in normal and cancer cells, leading to formation of hyperploid syncytia exhibiting features of cellular senescence. Infection by the measles virus, which leads to cell fusion, also induced cellular senescence in normal and cancer cells. The fused cells activated the main molecular pathways of senescence, the p53- and p16-pRbdependent pathways; the senescence-associated secretory phenotype; and immune surveillance-related proteins. Thus, fusion-induced senescence might be needed for proper syncytiotrophoblast function during embryonic development, and reuse of this senescence program later in life protects against pathological expression of endogenous fusogens and fusogenic viral infections.

Original languageEnglish
Pages (from-to)2356-2366
Number of pages11
JournalGenes and Development
Issue number21
StatePublished - 1 Nov 2013


  • Cell fusion
  • Cellular senescence
  • ERVWE1
  • Placenta
  • p53
  • pRb


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