Loss of SUMO1 in mice affects RanGAP1 localization and formation of PML nuclear bodies, but is not lethal as it can be compensated by SUMO2 or SUMO3
Loss of SUMO1 in mice affects RanGAP1 localization and formation of PML nuclear bodies, but is not lethal as it can be compensated by SUMO2 or SUMO3
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DOI：
10.1242/jcs.038570
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发表时间：
2008-12-15
影响因子：
4
通讯作者：
Kuehn, Michael R.
中科院分区：
文献类型：
--
作者：
Evdokimov, Evgenij;Sharma, Prashant;Kuehn, Michael R.
小泛素样修饰物（SUMO）与靶蛋白的结合调节许多生物学过程，并与肿瘤发生和转移有关。脊椎动物中的三种SUMO同种型SUMO 1和高度相似的SUMO 2和SUMO 3可以与独特的以及重叠的靶蛋白亚群缀合。然而，目前尚不清楚每个家庭成员的作用是否不同，是否存在冗余。在这里，我们描述了一个突变小鼠系，完全缺乏SUMO 1，但令人惊讶的是，是可行的，缺乏任何明显的表型。我们的研究指出SUMO 2和/或SUMO 3的补偿利用SUMO 1靶点的SUMO化。SUMO异构体相互替代的能力对于合理靶向SUMO通路具有重要意义。
Conjugation of the small ubiquitin-like modifier (SUMO) to target proteins regulates numerous biological processes and has been implicated in tumorigenesis and metastasis. The three SUMO isoforms in vertebrates, SUMO1 and the highly similar SUMO2 and SUMO3, can be conjugated to unique as well as overlapping subsets of target proteins. Yet, it is still not clear whether roles for each family member are distinct or whether redundancy exists. Here we describe a mutant mouse line that completely lacks SUMO1, but surprisingly is viable and lacks any overt phenotype. Our study points to compensatory utilization of SUMO2 and/or SUMO3 for sumoylation of SUMO1 targets. The ability of SUMO isoforms to substitute for one another has important implications for rational targeting of the SUMO pathway.