Loss of the CONSTITUTIVE PHOTOMORPHOGENIC9 signalosome subunit 5 is sufficient to cause the cop/det/fus mutant phenotype in Arabidopsis
Loss of the CONSTITUTIVE PHOTOMORPHOGENIC9 signalosome subunit 5 is sufficient to cause the cop/det/fus mutant phenotype in Arabidopsis
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DOI：
10.1105/tpc.105.032870
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发表时间：
2005-07-01
期刊：
影响因子：
11.6
通讯作者：
Schwechheimer, C
中科院分区：
文献类型：
--
作者：
Dohmann, EMN;Kuhnle, C;Schwechheimer, C
COP 9信号体（CSN）最初是基于来自拟南芥的组成型光形态发生/去黄化/褐色（cop/det/fus）突变体鉴定的。CSN是进化保守的，其亚基5（CSN 5）介导NEDD 8从E3泛素连接酶的cullin亚基的去缀合（去eddylation）。在这里，我们报告拟南芥突变体CSN 5功能缺陷。我们发现，这些突变体是表型上无法区分从先前描述的COP/DET/FUS突变体的其他CSN亚基。然而，我们还表明，这些突变体保留CSN复合物（缺乏CSN 5），这一发现是在与先前描述的CSN亚基突变体，缺乏CSN复合物。因此，我们得出结论，CSN 5作为CSN的一部分的丢失足以引起cop/det/fus突变表型。此外，我们发现，CSN 5缺陷的突变体以及CSN缺陷的突变体不能deneddylate拟南芥cullin AtCUL 1，AtCUL 3A，和AtCUL 4。因为这些是代表cullin亚基的三个cullin含有E3家族存在于拟南芥中，我们假设，cop/det/fus突变体表型可能是由受损的CSN 5依赖性去eddylation的cullin含有E3的缺陷造成的结果。
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.