Department of Biology, Technische Universität Dresden Dresden, Germany.
Instituto de Agrobiotecnología del Litoral (CONICET-UNL), Universidad Nacional del Litoral Santa Fe, Argentina.
Front Plant Sci. 2014 Mar 25;5:87. doi: 10.3389/fpls.2014.00087. eCollection 2014.
The two related putative cytochrome c oxidase (COX) assembly factors HCC1 and HCC2 from Arabidopsis thaliana are Homologs of the yeast Copper Chaperones Sco1p and Sco2p. The hcc1 null mutation was previously shown to be embryo lethal while the disruption of the HCC2 gene function had no obvious effect on plant development, but increased the expression of stress-responsive genes. Both HCC1 and HCC2 contain a thioredoxin domain, but only HCC1 carries a Cu-binding motif also found in Sco1p and Sco2p. In order to investigate the physiological implications suggested by this difference, various hcc1 and hcc2 mutants were generated and analyzed. The lethality of the hcc1 knockout mutation was rescued by complementation with the HCC1 gene under the control of the embryo-specific promoter ABSCISIC ACID INSENSITIVE 3. However, the complemented seedlings did not grow into mature plants, underscoring the general importance of HCC1 for plant growth. The HCC2 homolog was shown to localize to mitochondria like HCC1, yet the function of HCC2 is evidently different, because two hcc2 knockout lines developed normally and exhibited only mild growth suppression compared with the wild type (WT). However, hcc2 knockouts were more sensitive to UV-B treatment than the WT. Complementation of the hcc2 knockout with HCC2 rescued the UV-B-sensitive phenotype. In agreement with this, exposure of wild-type plants to UV-B led to an increase of HCC2 transcripts. In order to corroborate a function of HCC1 and HCC2 in COX biogenesis, COX activity of hcc1 and hcc2 mutants was compared. While the loss of HCC2 function had no significant effect on COX activity, the disruption of one HCC1 gene copy was enough to suppress respiration by more than half compared with the WT. Therefore, we conclude that HCC1 is essential for COX function, most likely by delivering Cu to the catalytic center. HCC2, on the other hand, seems to be involved directly or indirectly in UV-B-stress responses.
拟南芥中与两个相关的细胞色素 c 氧化酶(COX)组装因子 HCC1 和 HCC2 是酵母铜伴侣 Sco1p 和 Sco2p 的同源物。先前的研究表明,hcc1 缺失突变是胚胎致死的,而 HCC2 基因功能的中断对植物发育没有明显影响,但增加了应激反应基因的表达。HCC1 和 HCC2 都含有一个硫氧还蛋白结构域,但只有 HCC1 携带一个在 Sco1p 和 Sco2p 中也发现的 Cu 结合基序。为了研究这种差异所暗示的生理意义,生成并分析了各种 hcc1 和 hcc2 突变体。通过在胚胎特异性启动子 ABSCISIC ACID INSENSITIVE 3 控制下用 HCC1 基因进行互补,挽救了 hcc1 敲除突变的致死性。然而,互补的幼苗并没有长成成熟的植物,这突显了 HCC1 对植物生长的重要性。HCC2 同源物被证明像 HCC1 一样定位于线粒体,但 HCC2 的功能显然不同,因为两个 hcc2 敲除系与野生型(WT)相比正常发育且仅表现出轻微的生长抑制。然而,hcc2 敲除系对 UV-B 处理更敏感。用 HCC2 互补 hcc2 敲除体挽救了对 UV-B 敏感的表型。这与以下结果一致:在 WT 植物中暴露于 UV-B 会导致 HCC2 转录物的增加。为了证实 HCC1 和 HCC2 在 COX 生物发生中的功能,比较了 hcc1 和 hcc2 突变体的 COX 活性。虽然 HCC2 功能的丧失对 COX 活性没有显著影响,但与 WT 相比,一个 HCC1 基因拷贝的缺失足以使呼吸作用降低一半以上。因此,我们得出结论,HCC1 对 COX 功能至关重要,可能是通过将 Cu 递送到催化中心。另一方面,HCC2 似乎直接或间接地参与了 UV-B 应激反应。