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Molecular and Cellular Biology, September 2008, p. 5381-5390, Vol. 28, No. 17
0270-7306/08/$08.00+0     doi:10.1128/MCB.00651-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Sumo-1 Function Is Dispensable in Normal Mouse Development{triangledown} ,{ddagger}

Fu-Ping Zhang,1,{dagger} Laura Mikkonen,1,{dagger} Jorma Toppari,2 Jorma J. Palvimo,3 Irma Thesleff,4 and Olli A. Jänne1,5*

Biomedicum Helsinki, Institute of Biomedicine (Physiology), University of Helsinki, FI-00014 Helsinki, Finland,1 Departments of Physiology and Pediatrics, University of Turku, FI-20520 Turku, Finland,2 Department of Medical Biochemistry, University of Kuopio, FI-70211 Kuopio, Finland,3 Institute of Biotechnology, University of Helsinki, FI-00014 Helsinki, Finland,4 Department of Clinical Chemistry, Helsinki University Central Hospital, FI-00290 Helsinki, Finland5

Received 22 April 2008/ Returned for modification 24 May 2008/ Accepted 9 June 2008

To elucidate SUMO-1 functions in vivo, we targeted by homologous recombination the last three exons of the murine Sumo-1 gene. Sumo-1 mRNA abundance was reduced to one-half in heterozygotes and was undetectable in Sumo-1–/– mice, and SUMO-1-conjugated RanGAP1 was detectable in wild-type mouse embryo fibroblasts (MEFs) but not in Sumo-1–/– MEFs, indicating that gene targeting yielded Sumo-1-null mice. Sumo-1 mRNA is expressed in all tissues of wild-type mice, and its abundance is highest in the testis, brain, lungs, and spleen. Sumo-2 and Sumo-3 mRNAs are also expressed in all tissues, but their abundance was not upregulated in Sumo-1-null mice. The development and function of testis are normal in the absence of Sumo-1, and Sumo-1–/– mice of both sexes are viable and fertile. In contrast to a previous report (F. S. Alkuraya et al., Science 313:1751, 2006), we did not observe embryonic or early postnatal demise of Sumo-1-targeted mice; genotypes of embryos and 21-day-old mice were of predicted Mendelian ratios, and there was no defect in lip and palate development in Sumo-1+/– or Sumo-1–/– embryos. The ability of Sumo-1–/– MEFs to differentiate into adipocyte was not different from that of wild-type MEFs. Collectively, our results support the notion that most, if not all, SUMO-1 functions are compensated for in vivo by SUMO-2 and SUMO-3.

* Corresponding author. Mailing address: University of Helsinki, Institute of Biomedicine (Physiology), Biomedicum Helsinki, P.O. Box 63 (Haartmaninkatu 8), FI-00014 Helsinki, Finland. Phone: 358-9-19125040. Fax: 358-9-19125047. E-mail: olli.janne{at}helsinki.fi

{triangledown} Published ahead of print on 23 June 2008.

{ddagger} Supplemental material for this article may be found at http://mcb.asm.org/.

{dagger} F.-P.Z. and L.M. contributed equally to this study.

Molecular and Cellular Biology, September 2008, p. 5381-5390, Vol. 28, No. 17
0270-7306/08/$08.00+0     doi:10.1128/MCB.00651-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



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