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Drosophila variable nurse cells encodes arrest defective 1 (ARD1), the catalytic subunit of the major N‐terminal acetyltransferase complex
Author(s) -
Wang Ying,
Mijares Michelle,
Gall Megan D.,
Turan Tolga,
Javier Anna,
Bornemann Douglas J.,
Manage Kevin,
Warrior Rahul
Publication year - 2010
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.22418
Subject(s) - biology , multicellular organism , protein subunit , mutant , genetics , microbiology and biotechnology , gene
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, 2010. © 2010 Wiley‐Liss, Inc.