CNI1/ATL31, a RING-type ubiquitin ligase that functions in the carbon/nitrogen response for growth phase transition in Arabidopsis seedlings.

CNI1/ATL31, a RING-type ubiquitin ligase that functions in the carbon/nitrogen response for growth phase transition in Arabidopsis seedlings.
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DOI:
10.1111/j.1365-313x.2009.04006.x
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发表时间:
2009-12
期刊:
The Plant journal : for cell and molecular biology
影响因子:
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通讯作者:
Takeo Sato;Shugo Maekawa;Shigetaka Yasuda;Yutaka Sonoda;E. Katoh;T. Ichikawa;M. Nakazawa;M. Seki;K. Shinozaki;M. Matsui;Derek B. Goto;A. Ikeda;J. Yamaguchi
Takeo Sato;Shugo Maekawa;Shigetaka Yasuda;Yutaka Sonoda;E. Katoh;T. Ichikawa;M. Nakazawa;M. Seki;K. Shinozaki;M. Matsui;Derek B. Goto;A. Ikeda;J. Yamaguchi
中科院分区:
其他
文献类型:
--
作者:
Takeo Sato;Shugo Maekawa;Shigetaka Yasuda;Yutaka Sonoda;E. Katoh;T. Ichikawa;M. Nakazawa;M. Seki;K. Shinozaki;M. Matsui;Derek B. Goto;A. Ikeda;J. Yamaguchi

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植物能够感知并响应碳(C)和氮(N)代谢物可用性之间的平衡变化,称为C/N响应。在过渡到光自养生长发芽后,如果检测到高的外部C/N比,幼苗的生长被逮捕。为了阐明C/N传感和信号在这个过渡时期的机制,我们筛选了大量的FOX转基因植物,过表达全长cDNA,个人能够继续发芽后严重C/N胁迫下的增长。一个线,cni 1-D(碳/氮不敏感1-显性),被证明有一个抑制的敏感性,C/N条件在生理和分子水平。CNI 1 cDNA编码预测的RING型泛素连接酶,先前注释为ATL 31。ATL 31的过表达被证实是cni 1-D表型的原因,并且该基因的敲除导致萌发后生长期间对C/N条件的超敏反应。使用体外测定系统证实ATL 31蛋白含有泛素连接酶活性。此外,从过表达的蛋白质中去除这种泛素连接酶活性导致突变体表型的丧失。综上所述,这些数据表明,CNI 1/ATL 31活性是所需的植物C/N响应在幼苗生长过渡。
Plants are able to sense and respond to changes in the balance between carbon (C) and nitrogen (N) metabolite availability, known as the C/N response. During the transition to photoautotrophic growth following germination, growth of seedlings is arrested if a high external C/N ratio is detected. To clarify the mechanisms for C/N sensing and signaling during this transition period, we screened a large collection of FOX transgenic plants, overexpressing full-length cDNAs, for individuals able to continue post-germinative growth under severe C/N stress. One line, cni1-D (carbon/nitrogen insensitive 1-dominant), was shown to have a suppressed sensitivity to C/N conditions at both the physiological and molecular level. The CNI1 cDNA encoded a predicted RING-type ubiquitin ligase previously annotated as ATL31. Overexpression of ATL31 was confirmed to be responsible for the cni1-D phenotype, and a knock-out of this gene resulted in hypersensitivity to C/N conditions during post-germinative growth. The ATL31 protein was confirmed to contain ubiquitin ligase activity using an in vitro assay system. Moreover, removal of this ubiquitin ligase activity from the overexpressed protein resulted in the loss of the mutant phenotype. Taken together, these data demonstrated that CNI1/ATL31 activity is required for the plant C/N response during seedling growth transition.