Number of Nuclear Divisions in the Drosophila Blastoderm Controlled by Onset of Zygotic Transcription

SummaryThe cell number of the early Drosophila embryo is determined by exactly 13 rounds of synchronous nuclear divisions, allowing cellularization and formation of the embryonic epithelium [ 1]. The pause in G2 in cycle 14 is controlled by multiple pathways, such as activation of DNA repair checkpoint, progression through S phase, and inhibitory phosphorylation of Cdk1, involving the genes grapes, mei41, and wee1 [ 2, 3, 4, 5, 6, 7 and 8]. In addition, degradation of maternal RNAs [9] and zygotic gene expression [ 10 and 11] are involved. The zinc finger Vielfältig (Vfl) controls expression of many early zygotic genes [ 12 and 13], including the mitotic inhibitor frühstart [ 14 and 15]. The functional relationship of these pathways and the mechanism for triggering the cell-cycle pause have remained unclear. Here, we show that a novel single-nucleotide mutation in the 3′ UTR of the RNPII215 gene leads to a reduced number of nuclear divisions that is accompanied by premature transcription of early zygotic genes and cellularization. The reduced number of nuclear divisions in mutant embryos depends on the transcription factor Vfl and on zygotic gene expression, but not on grapes, the mitotic inhibitor Frühstart, and the nucleocytoplasmic ratio. We propose that activation of zygotic gene expression is the trigger that determines the timely and concerted cell-cycle pause and cellularization.

► A novel RNPII215 mutation reduces the number of nuclear divisions ► Mutant embryos show a precocious onset of zygotic transcription ► The zinc finger Vfl is required for premature cell-cycle pause in mutants