Genetics, Vol. 160, 547-560, February 2002, Copyright © 2002

The Drosophila Gene taranis Encodes a Novel Trithorax Group Member Potentially Linked to the Cell Cycle Regulatory Apparatus

Stéphane Calgaroa, Muriel Boubea, David L. Cribbsa, and Henri-Marc Bourbona
a Centre de Biologie du Développement, Université Paul Sabatier, 31062 Toulouse Cedex, France

Corresponding author: Henri-Marc Bourbon, UMR5547 du CNRS, Université Paul Sabatier, 118 Route de Narbonne, 31062 Toulouse, France., bourbon{at}cict.fr (E-mail)

Communicating editor: T. C. KAUFMAN

Genes of the Drosophila Polycomb and trithorax groups (PcG and trxG, respectively) influence gene expression by modulating chromatin structure. Segmental expression of homeotic loci (HOM) initiated in early embryogenesis is maintained by a balance of antagonistic PcG (repressor) and trxG (activator) activities. Here we identify a novel trxG family member, taranis (tara), on the basis of the following criteria: (i) tara loss-of-function mutations act as genetic antagonists of the PcG genes Polycomb and polyhomeotic and (ii) they enhance the phenotypic effects of mutations in the trxG genes trithorax (trx), brahma (brm), and osa. In addition, reduced tara activity can mimic homeotic loss-of-function phenotypes, as is often the case for trxG genes. tara encodes two closely related 96-kD protein isoforms (TARA-{alpha}/-ß) derived from broadly expressed alternative promoters. Genetic and phenotypic rescue experiments indicate that the TARA-{alpha}/-ß proteins are functionally redundant. The TARA proteins share evolutionarily conserved motifs with several recently characterized mammalian nuclear proteins, including the cyclin-dependent kinase regulator TRIP-Br1/p34SEI-1, the related protein TRIP-Br2/Y127, and RBT1, a partner of replication protein A. These data raise the possibility that TARA-{alpha}/-ß play a role in integrating chromatin structure with cell cycle regulation.




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