Cellular senescence in embryonic development

15/11/2013
Cellular senescence determines the end of the cell cycle and is involved in processes in which cell damage is produced: it is a mechanism which deactivates proliferation in the case of cancer and during ageing. The research published in Cell, directed by Manuel Serrano, researcher at the Spanish National Cancer Research Centre, demonstrates that this biological process also occurs in the embryonic development phase in mammals.
The research included the collaboration of UAB researchers Jesús Ruberte (CBATEG and the Department of Animal Anatomy) and Alfonso Rodríguez-Baeza (Department of Morphological Sciences, Anatomy Area and Human Embryology) and shows that during the degeneration of the mesonephros, a transitory embryonic kidney, and in the formation of the inner ear, cellular senescence contributes to the remodelling of these organs.
From the viewpoint of mechanisms, the embryonic senescence is dependent of the p21 gene, but independent of the p53 gene and DNA damage, and is regulated by the TGF-ß/SMAD and PI3K/FOXO pathways. Later, the embryonic tissues are infiltrated by macrophages, which eliminate senescent cells, thus allowing the tissues to reorganise and giving way to the formation of adult organs.
Conceptually, this research adds cellular senescence to the list of key processes contributing to embryonic development such as cell proliferation, differentiation, migration and death. It also gives way to the possibility of the hypothesis that cell senescence appears during evolution as a mechanism capable of remodelling embryonic organs, and which later in the adult period adapts to regenerate damaged cells.
Original article: Programmed cell senescence during mammalian embryonic development. Daniel Muños-Espín, Marta Cañamero, Antonio Maraver, Gonzalo Gómez-López, Julio Contreras, Silvia Murillo-Cuesta, Alfonso Rodríguez-Baeza, Isabel Varela-Nieto, Jesús Ruberte, Manuel Collado, Manuel Serrano. Cell (2013). DOI: http://dx.doi.org/10.1016/j.cell.2013.10.019