Open AccessSumo-1 Function Is Dispensable in Normal Mouse Development
Author(s) -
Fuping Zhang,
Laura Mikkonen,
Jorma Toppari,
Jorma J. Palvimo,
Irma Thesleff,
Olli A. Jänne
Publication year - 2008
Publication title -
molecular and cellular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.14
H-Index - 327
eISSN - 1067-8824
pISSN - 0270-7306
DOI - 10.1128/mcb.00651-08
Subject(s) - biology , gene targeting , microbiology and biotechnology , wild type , embryo , null allele , gene , genetics , phenotype , mutant
To elucidate SUMO-1 functions in vivo, we targeted by homologous recombination the last three exons of the murineSumo-1 gene.Sumo-1 mRNA abundance was reduced to one-half in heterozygotes and was undetectable inSumo-1 −/− mice, and SUMO-1-conjugated RanGAP1 was detectable in wild-type mouse embryo fibroblasts (MEFs) but not inSumo-1 −/− MEFs, indicating that gene targeting yieldedSumo-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 andSumo-3 mRNAs are also expressed in all tissues, but their abundance was not upregulated inSumo-1 -null mice. The development and function of testis are normal in the absence ofSumo-1 , andSumo-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 ofSumo-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 inSumo-1 +/− orSumo-1 −/− embryos. The ability ofSumo-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.