QUICK SEARCH:   [advanced] Author: Keyword(s):
Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents

This Article Figures Only Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Sedaghat, Y. Articles by Sonnenfeld, M. J. Search for Related Content PubMed PubMed Citation Articles by Sedaghat, Y. Articles by Sonnenfeld, M. J. Social Bookmarking                         What's this?

The jing Zn-finger transcription factor is a mediator of cellular differentiation in the Drosophila CNS midline and trachea

Yalda Sedaghat^*, Wilson F. Miranda^* and Margaret J. Sonnenfeld

Department of Cellular and Molecular Medicine, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada
^* These authors contributed equally to this work

Author for correspondence (e-mail: msonnenf{at}uottawa.ca)

Accepted 2 March 2002

We establish that the jing zinc-finger transcription factor plays an essential role in controlling CNS midline and tracheal cell differentiation. jing transcripts and protein accumulate from stage 9 in the CNS midline, trachea and in segmental ectodermal stripes. JING protein localizes to the nuclei of CNS midline and tracheal cells implying a regulatory role during their development. Loss of jing-lacZ expression in homozygous sim mutants and induction of jing-lacZ by ectopic sim expression establish that jing is part of the CNS midline lineage. We have isolated embryonic recessive lethal jing mutations that display genetic interactions in the embryonic CNS midline and trachea, with mutations in the bHLH-PAS genes single-minded and trachealess, and their downstream target genes (slit and breathless). Loss- and gain-of-function jing is associated with defects in CNS axon and tracheal tubule patterning. In jing homozygous mutant embryos, reductions in marker gene expression and inappropriate apoptosis in the CNS midline and trachea establish that jing is essential for the proper differentiation and survival of these lineages. These results establish that jing is a key component of CNS midline and tracheal cell development. Given the similarities between JING and the vertebrate CCAAT-binding protein AEBP2, we propose that jing regulates transcriptional mechanisms in Drosophila embryos and promotes cellular differentiation in ectodermal derivatives.

Key words: jing, Zinc finger, CNS midline, Trachea, Drosophila

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?

This article has been cited by other articles:

				H. Kim, K. Kang, and J. Kim AEBP2 as a potential targeting protein for Polycomb Repression Complex PRC2 Nucleic Acids Res., May 1, 2009; 37(9): 2940 - 2950. [Abstract] [Full Text] [PDF]

				X. Sun, T. Morozova, and M. Sonnenfeld Glial and Neuronal Functions of the Drosophila Homolog of the Human SWI/SNF Gene ATR-X (DATR-X) and the jing Zinc-Finger Gene Specify the Lateral Positioning of Longitudinal Glia and Axons Genetics, July 1, 2006; 173(3): 1397 - 1415. [Abstract] [Full Text] [PDF]

				J. Culi, P. Aroca, J. Modolell, and R. S. Mann jing Is Required for Wing Development and to Establish the Proximo-Distal Axis of the Leg in Drosophila melanogaster Genetics, May 1, 2006; 173(1): 255 - 266. [Abstract] [Full Text] [PDF]