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Molecular and Cellular Biology, June 2004, p. 5577-5586, Vol. 24, No. 12
0270-7306/04/$08.00+0     DOI: 10.1128/MCB.24.12.5577-5586.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Protein Inhibitor of Activated STAT Y (PIASy) and a Splice Variant Lacking Exon 6 Enhance Sumoylation but Are Not Essential for Embryogenesis and Adult Life

Kelly A. Wong,1 Rachel Kim,1 Heather Christofk,1 Jing Gao,1 Gregory Lawson,2 and Hong Wu1*

Molecular and Medical Pharmacology, Howard Hughes Medical Institute,1 Division of Laboratory Animal Medicine, University of California, Los Angeles, Los Angeles, California 900952

Received 13 January 2004/ Returned for modification 4 February 2004/ Accepted 22 March 2004

Protein inhibitor of activated STAT Y (PIASy) is the shortest member of the PIAS family and has been reported to modulate the transcriptional activities of STAT1, lymphoid enhancer factor 1 (LEF-1), and the androgen receptor. PIAS proteins have also been identified as E3 ligases for the small ubiquitin-like modifier (SUMO) proteins. PIASy in particular has been reported to mediate SUMO-2/3 modification of LEF-1, sequestering it into nuclear bodies, and SUMO-1 ligation to c-Myb, modulating its transcriptional activation properties. We have cloned murine Piasy and a splice variant which omits exon 6, containing the nuclear retention PINIT motif. Cell culture studies indicate that both the full length and the splice variant are localized in the nucleus but differentially enhance SUMO ligation. To further understand the functions of PIASy, we have generated PIASy-deficient mice. Surprisingly, Piasy–/– mice appear phenotypically normal. Activation of STAT1 is not significantly perturbed in Piasy–/– cells, and sumoylation patterns for SUMO-1 or SUMO-3 modification are similar when comparing tissues and embryonic fibroblasts from wild-type and knockout mice. Our study demonstrates that at steady state, PIASy is either dispensable or compensated for by other PIAS family members or by other mechanisms when deleted.

* Corresponding author. Mailing address: Molecular and Medical Pharmacology, Howard Hughes Medical Institute, University of California, Los Angeles, 650 Charles Young Dr. South, CHS 23-234, Los Angeles, CA 90095. Phone: (310) 825-5160. Fax: (310) 267-0242. E-mail: hwu{at}mednet.ucla.edu.

Molecular and Cellular Biology, June 2004, p. 5577-5586, Vol. 24, No. 12
0022-538X/04/$08.00+0     DOI: 10.1128/MCB.24.12.5577-5586.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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