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Abstract
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.
Highlights
Segregation of the germline is one of the first events in early embryonic development
Nuclei divide synchronously and migrate towards the periphery of the embryo. Those reaching the posterior pole are incorporated into the germ cells at nuclear cycle 10, whereas somatic cells form during nuclear cycle 14 by an apical-to-basal ingression of a cellularization furrow
We found that carboxy-terminal domain (CTD) Ser 2 phosphorylation of RNA polymerase type II was reduced in posterior somatic cells from 6x[pgc] embryos compared with the wild type (Fig 4E)
Summary
Segregation of the germline is one of the first events in early embryonic development. Consistent with this hypothesis, we observe a decrease in CTD Ser 2 phosphorylation and a concomitant impairment in the transcriptional activation of the cellularization gene slam in posterior somatic cells of tor-mutant and pgc-upregulated embryos. As active transcription is crucial for early blastoderm cellularization, this result further suggests that the pole–hole phenotype in 6x[pgc] embryos is due to general suppression of gene expression in posterior blastoderm nuclei.
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