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SUMO 2 is essential while SUMO 3 is dispensable for mouse embryonic development
Author(s) -
Wang Liangli,
Wansleeben Carolien,
Zhao Shengli,
Miao Pei,
Paschen Wulf,
Yang Wei
Publication year - 2014
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.15252/embr.201438534
Subject(s) - biology , gene isoform , embryo , sumo protein , microbiology and biotechnology , embryonic stem cell , embryogenesis , mutant , genetics , gene , ubiquitin
Small ubiquitin‐like modifier ( SUMO 1–3) conjugation plays a critical role in embryogenesis. Embryos deficient in the SUMO ‐conjugating enzyme Ubc9 die at the early postimplantation stage. Sumo1 −/− mice are viable, as SUMO 2/3 can compensate for most SUMO 1 functions. To uncover the role of SUMO 2/3 in embryogenesis, we generated Sumo2‐ and Sumo3‐ null mutant mice. Here, we report that Sumo3 −/− mice were viable, while Sumo2 −/− embryos exhibited severe developmental delay and died at approximately embryonic day 10.5 (E10.5). We also provide evidence that SUMO 2 is the predominantly expressed SUMO isoform. Furthermore, although Sumo2 +/− and Sumo2 +/− ;Sumo3 +/− mice lacked any overt phenotype, only 2 Sumo2 +/− ;Sumo3 −/− mice were found at birth in 35 litters after crossing Sumo2 +/− ;Sumo3 +/− with Sumo3 −/− mice, and these rare mice were considerably smaller than littermates of the other genotypes. Thus, our findings suggest that expression levels and not functional differences between SUMO 2 and SUMO 3 are critical for normal embryogenesis.