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Genes & Dev. 16 (18): 2379-2389

Copyright © 2002 by Cold Spring Harbor Laboratory Press.

Vol. 16, No. 18, pp. 2379-2389, September 15, 2002

Negative regulation of STAT92E by an N-terminally truncated STAT protein derived from an alternative promoter site

Melissa A. Henriksen,1 Aurel Betz,1 Marc V. Fuccillo, and James E. Darnell Jr.2

Laboratory of Molecular Cell Biology, The Rockefeller University, New York, New York 10021, USA

Previously unrecognized mRNAs originating from a dual promoter at the stat92E locus are described. One of these encodes a truncated protein, Delta NSTAT92E, that lacks the N-terminal 133 amino acids. Antibodies detect both the full-length and truncated molecules early in embryogenesis (1-5 h), and mRNA detection by specific RT-PCR reactions accords with the protein distribution. Given that the N termini of mammalian STATs are known to have positive functions in transcriptional activation, we explored the role of Delta NSTAT92E early in embryogenesis. By increasing the Delta NSTAT92E-to-STAT92E ratio in overexpression and RNAi experiments, we observe phenotypes compatible with suppression of wild-type STAT92E activity. We therefore conclude that the short form of STAT92E is a naturally occurring dominant-negative product that can be added to the growing list of negative regulators of STAT activity.

[Key Words: Drosophila melanogaster; STAT92E; alternative promoters; differential splicing]

1 These authors contributed equally to this work.

2 Corresponding author.

GENES & DEVELOPMENT 16:2379-2389 © 2002 by Cold Spring Harbor Laboratory Press  ISSN 0890-9369/02 $5.00

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