Mutations in the Drosophila variable nurse cells (vnc) gene result in female sterility and oogenesis defects, including egg chambers with too many or too few nurse cells. We show that vnc corresponds to Arrest Defective1 (Ard1) and encodes the catalytic subunit of NatA, the major N-terminal acetyl-transferase complex. While N-terminal acetylation is one of the most prevalent covalent protein modifications in eukaryotes, analysis of its role in development has been challenging since mutants that compromise NatA activity have not been described in any multicellular animal. Our data show that reduced ARD1 levels result in pleiotropic oogenesis defects including abnormal cyst encapsulation, desynchronized cystocyte division, disrupted nurse cell chromosome dispersion, and abnormal chorion patterning, consistent with the wide range of predicted NatA substrates. Furthermore, we find that loss of Ard1 affects cell survival/ proliferation and is lethal for the animal, providing the first demonstration that this modification is essential in higher eukaryotes. Developmental Dynamics 239:2813-2827,

Drosophila variable nurse cells (vnc) egg chamber with a binucleate oocyte resulting from an extra nuclear division after oocyte specification. Nuclear lamin staining (green) allows visualization of oocyte nuclei that have a much lower DNA content than polyploid nurse cell nuclei (blue). F‐actin (red) reveals cell outlines and ring canals that link nurse cell and oocyte cytoplasm. From Warrior et al., Developmental Dynamics 239:2813–2827, 2010.