Allocation of Heme Is Differentially Regulated by Ferrochelatase Isoforms in Arabidopsis Cells.

Allocation of Heme Is Differentially Regulated by Ferrochelatase Isoforms in Arabidopsis Cells.
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DOI:
10.3389/fpls.2016.01326
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发表时间:
2016
影响因子:
5.6
通讯作者:
Masuda T
Masuda T
中科院分区:
生物学2区
文献类型:
--
作者:
Espinas NA;Kobayashi K;Sato Y;Mochizuki N;Takahashi K;Tanaka R;Masuda T

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血红素作为多种细胞器中血红素蛋白的辅因子参与多种生物学过程。在植物细胞中,血红素由两种位于质体的亚铁螯合酶同工型FC 1和FC2合成。在这项研究中,通过表征拟南芥T-DNA插入突变体,我们表明,亚铁螯合酶异构体在植物细胞中的血红素的分配差异调节。弱(FC 1 -1)和无效(FC 1 -2)突变体的分析表明,FC 1生产血红素是必需的幼苗发育的初始生长。相反,FC 2的弱突变体(fc2-1)和无效突变体(fc2-2)显示淡绿色叶片和生长迟缓,表明FC 2产生血红素是叶绿体发育所必需的。在生长初期,FC 2缺乏引起质体细胞色素减少。此外,FC 2的缺乏虽然对光合反应中心复合体的组装影响不大,但会导致反应中心捕光天线相对较大但数量不足,导致光合效率降低。然而,在后期的营养生长中,fc 2 -2恢复了光合生长,表明产生FC 1的血红素可以补充FC 2的不足。另一方面,在微粒体组分中的细胞色素的水平降低,发现在FC 1 -1,表明FC 1产生血红素主要分配到质体外细胞器。此外,诱导子flg 22的处理诱导了FC 1的表达,而FC 2的表达减少,并且fc 1 -1消除了FC 1表达和过氧化物酶活性的flg 22依赖性诱导。因此,我们的研究结果澄清,FC2产生血红素的光合作用机制在叶绿体中,而FC 1是管家酶提供血红素辅因子到整个细胞。此外,FC 1可以部分补充FC2的不足,也参与了对应激条件的防御。
Heme is involved in various biological processes as a cofactor of hemoproteins located in various organelles. In plant cells, heme is synthesized by two isoforms of plastid-localized ferrochelatase, FC1 and FC2. In this study, by characterizing Arabidopsis T-DNA insertional mutants, we showed that the allocation of heme is differentially regulated by ferrochelatase isoforms in plant cells. Analyses of weak (fc1-1) and null (fc1-2) mutants suggest that FC1-producing heme is required for initial growth of seedling development. In contrast, weak (fc2-1) and null (fc2-2) mutants of FC2 showed pale green leaves and retarded growth, indicating that FC2-producing heme is necessary for chloroplast development. During the initial growth stage, FC2 deficiency caused reduction of plastid cytochromes. In addition, although FC2 deficiency marginally affected the assembly of photosynthetic reaction center complexes, it caused relatively larger but insufficient light-harvesting antenna to reaction centers, resulting in lower efficiency of photosynthesis. In the later vegetative growth, however, fc2-2 recovered photosynthetic growth, showing that FC1-producing heme may complement the FC2 deficiency. On the other hand, reduced level of cytochromes in microsomal fraction was discovered in fc1-1, suggesting that FC1-producing heme is mainly allocated to extraplastidic organelles. Furthermore, the expression of FC1 is induced by the treatment of an elicitor flg22 while that of FC2 was reduced, and fc1-1 abolished the flg22-dependent induction of FC1 expression and peroxidase activity. Consequently, our results clarified that FC2 produces heme for the photosynthetic machinery in the chloroplast, while FC1 is the housekeeping enzyme providing heme cofactor to the entire cell. In addition, FC1 can partly complement FC2 deficiency and is also involved in defense against stressful conditions.
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