Primordial germ cells (PGCs) are the embryonic precursors of mature egg and sperm cells. In the mouse, following specification at embryonic day (E) 7.25, PGCs proliferate and migrate through the embryonic hindgut towards the genital ridges (future gonads). At E10.5, upon genital ridge entry, developing PGCs undergo epigenetic reprogramming followed by sex differentiation, committing to either oogenesis or spermatogenesis. Signalling cross-talk between PGCs and soma is a key feature of germ cell development. However, to what extent extrinsic signals emanating from the gonadal environment influence key germ cell processes is still not well understood. Here, I describe for the first time a crucial role of a key nutrient and hormone sensing pathway (mTOR) during PGC development. mTOR signals via two distinct multi-protein complexes, mTORC1 and mTORC2. Most of the presented work focuses on mTORC1 and its downstream translational regulators 4E-binding proteins (4E-BPs) and S6 kinases (S6Ks), respectively. Using an immunofluorescence-based approach, I show that in mouse PGCs, mTORC1 signals mainly via 4E-BP1, rather than the S6K1-S6 signalling axis. Interestingly, the observed activation of mTORC1-4E-BP1 signalling in PGCs shortly follows their entry into the genital ridge, suggesting a possible role at this developmental transition. However, global deletion of either 4E-BPs or S6Ks revealed only a minor phenotype in PGCs. Further, my results also point towards activation of AKT, a potential upstream mTORC1 activator in PGCs. This indicates a possible link to mTORC2 signalling. In view of that, I carried out a germline specific conditional deletion of Mtor (using a newly generated Blimp1-iCre mouse line), that leads to the loss of mTORC1 and mTORC2. Preliminary observations show a strong phenotype of very few germ cells surviving at E13.5. In summary, my results suggest a critical role for mTOR signalling during PGC development.