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Localization of SUMO-modified Proteins Using Fluorescent Sumo-trapping Proteins
Published on: April 27, 2019
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SUMO2 is essential while SUMO3 is dispensable for mouse embryonic development.
Liangli Wang1, Carolien Wansleeben2, Shengli Zhao3
1Multidisciplinary Neuroprotection Laboratories, Department of Anesthesiology, Duke University Medical Center, Durham, NC, USA.
EMBO Reports
|June 4, 2014
Summary
Small ubiquitin-like modifier (SUMO) conjugation is vital for embryonic development. SUMO2 deficiency causes severe developmental delay and embryonic lethality, indicating SUMO2 expression levels are critical for embryogenesis.
Area of Science:
- Molecular Biology
- Developmental Biology
- Genetics
Background:
- Small ubiquitin-like modifier (SUMO) conjugation is essential for embryogenesis.
- SUMO-conjugating enzyme Ubc9 deficiency leads to early embryonic lethality.
- SUMO1 knockout mice are viable due to SUMO2/3 functional compensation.
Purpose of the Study:
- To investigate the specific roles of SUMO2 and SUMO3 in mouse embryogenesis.
- To determine if functional differences or expression levels of SUMO2/3 are critical for development.
Main Methods:
- Generation of Sumo2- and Sumo3-null mutant mice.
- Phenotypic analysis of knockout mice at various embryonic and postnatal stages.
- Genotyping and comparative analysis of littermates.
Main Results:
- Sumo3(-/-) mice were viable, but Sumo2(-/-) embryos showed severe developmental delay and died around embryonic day 10.5.
- SUMO2 was identified as the predominantly expressed SUMO isoform during embryogenesis.
- Compound heterozygotes (Sumo2(+/-);Sumo3(+/-)) were normal, but Sumo2(+/-);Sumo3(-/-) mice were rare at birth and significantly smaller, indicating a gene dosage effect.
Conclusions:
- SUMO2 plays a critical, non-redundant role in embryogenesis, likely due to its predominant expression.
- The findings suggest that expression levels, rather than inherent functional differences between SUMO2 and SUMO3, are crucial for normal embryonic development.
