Segregation of the germline is a fundamental event during early development. In Drosophila, germ cells are specified at the posterior pole of the embryo by the germplasm. As zygotic expression is activated, germ cells remain transcriptionally silent owing to the polar granule component (Pgc), a small peptide present in germ cells. Somatic cells at both the embryonic ends are specified by the torso (Tor) receptor tyrosine kinase, and in tor mutants the somatic cells closer to the germ cells fail to cellularize correctly. Here, we show that extra wild-type gene copies of pgc cause a similar cellularization phenotype, and that both excessive pgc and a lack of tor are associated with an impairment of transcription in somatic cells. Moreover, a lack of pgc partly ameliorates the cellularization defect of tor mutants, thus revealing a functional antagonism between pgc and tor in the specification of germline and somatic properties. As transcriptional quiescence is a general feature of germ cells, similar mechanisms might operate in many organisms to 'protect' somatic cells that adjoin germ cells from inappropriately succumbing to such quiescence.