The steady-state level of Mg-protoporphyrin IX is not a determinant of plastid-to-nucleus signaling in Arabidopsis

The steady-state level of Mg-protoporphyrin IX is not a determinant of plastid-to-nucleus signaling in Arabidopsis
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DOI:
10.1073/pnas.0803245105
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发表时间:
2008-09-30
影响因子:
11.1
通讯作者:
Nagatani, Akira
Nagatani, Akira
中科院分区:
综合性期刊1区
文献类型:
--
作者:
Mochizuki, Nobuyoshi;Tanaka, Ryouichi;Nagatani, Akira

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质体在植物细胞内的各种细胞活动中起着至关重要的作用,包括光合作用和其他代谢途径。据信质体的功能状态以某种方式由细胞核监测以优化编码质体蛋白的基因的表达。目前主要的质体来源的信号传导模型(“质体信号传导”)提出,Mg-原卟啉IX(MgProto)是一种负信号,当质体发育受到抑制时,它抑制了编码质体定位蛋白的广泛核基因的表达。在这项研究中,我们已经重新评估了这一假设,通过定量的稳态水平的MgProto(以及其相邻的中间体原卟啉IX和MgProto单甲酯[MgProtoMe])在拟南芥植物与改变质体信号转导反应的Lhcb 1,RBCS,HEMA 1,BAM 3和CA 1基因的表达进行监测。此外,我们已经研究了基因表达和MgProto(MgProtoMe)在一系列突变体和条件下,其中稳态水平的MgProto(MgProtoMe)已被修改之间的相关性。总的来说,我们发现MgProto(MgProtoMe)和Lhcb 1表达的稳态水平之间或与任何其他测试的基因之间没有相关性。综合这些结果,我们建议必须对质体信号传导的现有模型进行修正。
The plastid plays a vital role in various cellular activities within plant cells including photosynthesis and other metabolic pathways. It is believed that the functional status of the plastid is somehow monitored by the nucleus to optimize the expression of genes encoding plastid proteins. The currently dominant model for plastid-derived signaling ("plastid signaling'') proposes that Mg-protoporphyrin IX (MgProto) is a negative signal that represses the expression of a wide range of nuclear genes encoding plastid-localized proteins when plastid development is inhibited. In this study, we have re-evaluated this hypothesis by quantifying the steady-state levels of MgProto (as well as its neighboring intermediates protoporphyrin IX and MgProto monomethyl ester [MgProtoMe]) in Arabidopsis plants with altered plastid signaling responses as monitored by expression of the Lhcb1, RBCS, HEMA1, BAM3 and CA1 genes. In addition, we have examined the correlation between gene expression and MgProto (MgProtoMe) in a range of mutants and conditions in which the steady-state levels of MgProto (MgProtoMe) have been modified. Overall we found that there was no correlation between the steady-state levels of MgProto (MgProtoMe) and Lhcb1 expression or with any of the other genes tested. Taking these results together, we propose that the current model on plastid signaling must be revised.