Dohmann Esther M N, Kuhnle Carola, Schwechheimer Claus
Centre for Plant Molecular Biology, Department of Developmental Genetics, Tübingen University, 72076 Tübingen, Germany.
Plant Cell. 2005 Jul;17(7):1967-78. doi: 10.1105/tpc.105.032870. Epub 2005 May 27.
The COP9 signalosome (CSN) was originally identified based on the constitutively photomorphogenic/de-etiolated/fusca (cop/det/fus) mutants from Arabidopsis thaliana. CSN is evolutionary conserved, and its subunit 5 (CSN5) mediates the deconjugation of NEDD8 from the cullin subunit of E3 ubiquitin ligases (deneddylation). Here, we report on Arabidopsis mutants deficient in CSN5 function. We show that these mutants are phenotypically indistinguishable from the previously described cop/det/fus mutants of other CSN subunits. However, we also show that these mutants retain the CSN complex (lacking CSN5), and this finding is in contrast with the previously described CSN subunit mutants, which lack the CSN complex. We therefore conclude that loss of CSN5 as part of CSN is sufficient to cause the cop/det/fus mutant phenotype. Furthermore, we show that mutants defective in CSN5 as well as mutants defective in CSN are unable to deneddylate the Arabidopsis cullins AtCUL1, AtCUL3A, and AtCUL4. Because these are representative cullin subunits of the three cullin-containing E3 families present in Arabidopsis, we postulate that the cop/det/fus mutant phenotype may be the result of the defects caused by impaired CSN5-dependent deneddylation of cullin-containing E3s.
COP9信号体（CSN）最初是基于拟南芥中组成型光形态建成/去黄化/褐色化（cop/det/fus）突变体而被鉴定出来的。CSN在进化上是保守的，其亚基5（CSN5）介导NEDD8从E3泛素连接酶的cullin亚基上去共轭（去NEDD化）。在此，我们报道了缺乏CSN5功能的拟南芥突变体。我们发现这些突变体在表型上与先前描述的其他CSN亚基的cop/det/fus突变体没有区别。然而，我们还发现这些突变体保留了CSN复合体（缺少CSN5），这一发现与先前描述的缺少CSN复合体的CSN亚基突变体形成对比。因此，我们得出结论，作为CSN一部分的CSN5缺失足以导致cop/det/fus突变体表型。此外，我们表明CSN5缺陷型突变体以及CSN缺陷型突变体均无法使拟南芥cullin蛋白AtCUL1、AtCUL3A和AtCUL4去NEDD化。由于这些是拟南芥中存在的三个含cullin的E3家族的代表性cullin亚基，我们推测cop/det/fus突变体表型可能是由含cullin的E3的CSN5依赖性去NEDD化受损所导致的缺陷的结果。
