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10 p.-5 fig.The question of how neural progenitor cells maintain its self-renewal throughout life is a fundamental problem in cell biology with\udimplications in cancer, aging and neurodegenerative diseases. In this work, we have analyzed the p73 function in embryonic\udneural progenitor cell biology using the neurosphere (NS)-assay and showed that p73-loss has a significant role in the\udmaintenance of neurosphere-forming cells in the embryonic brain. A comparative study of NS from Trp73-/-, p53KO, p53KO;Trp73-/-and their wild-type counterparts demonstrated that p73 deficiency results in two independent, but related, phenotypes: a smaller NS size (related to the proliferation and survival of the neural-progenitors) and a decreased capacity to\udform NS (self-renewal). The former seems to be the result of p53 compensatory activity, whereas the latter is p53 independent.\udWe also demonstrate that p73 deficiency increases the population of neuronal progenitors ready to differentiate into neurons at the expense of depleting the pool of undifferentiated neurosphere-forming cells. Analysis of the neurogenic niches\uddemonstrated that p73-loss depletes the number of neural-progenitor cells, rendering deficient niches in the adult mice.\udAltogether, our study identifies TP73 as a positive regulator of self-renewal with a role in the maintenance of the neurogenic\udcapacity. Thus, proposing p73 as an important player in the development of neurodegenerative diseases and a potential\udtherapeutic target.This work was supported by Grants SAF2009-\ud07897 from Spanish Ministerio de Ciencia e Innovacion (to MCM), Grant from Cajas de Ahorro de Castilla y León (to MCM), and Grants LE030A07 (to MMM) and\udLE015A10-2 (to MCM) from the Junta de Castilla y León.Peer reviewe

p73 deficiency results in impaired self renewal and premature neuronal differentiation of mouse neural progenitors independently of p53