A conditional knockout of Trp53 shows rescue of apoptosis but implies a slower recovery of double strand breaks

P53 a well-known tumor suppressor gene has emerged as a key player in neurological development including synaptic plasticity, neuronal differentiation, and apoptosis (1,2). In this research, we aimed to investigate the role of p53 in inhibitory neurons in the MGE. This region is one of the sources of inhibitory neurons (3,4). To reveal the role of p53 in the developing brain we will investigate p53 binding protein 1 and apoptosis. To activate a p53-mediated response, a single dose of X-ray irradiation of 1 Gy was applied to pregnant mice. The embryos are harvested 2h, 6h, and 24h after irradiation. Cleaved caspase 3 and 53BP1 were evaluated by performing immunohistochemistry on
embryonal brain tissue. 24h post-irradiation, inactivation of Trp53 showed a higher amount of DSBs compared to wild-type mice. This was compared with earlier research performed by Mfossa et al. in which the role of p53 in excitatory NPCs is investigated. Trp53 inactivation showed rescue of apoptotic cells. Further research is crucial on other aspects of p53 such as cell cycle arrest, DNA repair, differentiation, and senescence.