AI Article Synopsis
- Senescence is a part of how cells stop dividing, which can help prevent tumors and is related to getting older, but it’s also found in babies before they're born.
- Scientists have noticed that some cells in embryos act like they’re in a state of senescence, and these cells are not dividing but help with development.
- The research shows that certain genes help control this process, and when they're missing, it can lead to problems in how the embryo develops.
Article Abstract
Senescence is a form of cell-cycle arrest linked to tumor suppression and aging. However, it remains controversial and has not been documented in nonpathologic states. Here we describe senescence as a normal developmental mechanism found throughout the embryo, including the apical ectodermal ridge (AER) and the neural roof plate, two signaling centers in embryonic patterning. Embryonic senescent cells are nonproliferative and share features with oncogene-induced senescence (OIS), including expression of p21, p15, and mediators of the senescence-associated secretory phenotype (SASP). Interestingly, mice deficient in p21 have defects in embryonic senescence, AER maintenance, and patterning. Surprisingly, the underlying mesenchyme was identified as a source for senescence instruction in the AER, whereas the ultimate fate of these senescent cells is apoptosis and macrophage-mediated clearance. We propose that senescence is a normal programmed mechanism that plays instructive roles in development, and that OIS is an evolutionarily adapted reactivation of a developmental process.
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| http://dx.doi.org/10.1016/j.cell.2013.10.041 | DOI Listing |
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