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Convergence of mitochondrial and chloroplastic ANAC017/PAP-dependent retrograde signalling pathways and suppression of programmed cell death

机译:线粒体和叶片αAC017/ PAP依赖性逆行信号通路的收敛性和编程细胞死亡的抑制

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摘要

The energy-converting organelles mitochondria and chloroplasts are tightly embedded in cellular metabolism and stress response. To appropriately control organelle function, extensive regulatory mechanisms are at play that involve two-way exchange between the nucleus and mitochondria/chloroplasts. In recent years, our understanding of how mitochondria and chloroplasts provide â € retrograde' feedback to the nucleus, resulting in targeted transcriptional changes, has greatly increased. Nevertheless, mitochondrial and chloroplast retrograde signalling have largely been studied independently, and only few points of interaction have been found or proposed. Through reassessment of recent publications, this perspective proposes that two of the most well-studied retrograde signalling pathways in plants, those mediated by ANAC017 and those mediated by phosphoadenosine phosphate (PAP), are most likely convergent and can direct overlapping genes. Furthermore, at least part of this common retrograde response appears targeted towards suppression of programmed cell death (PCD) triggered by organellar defects. The identified target genes are discussed in light of their roles in PCD suppression and amplifying the signalling cascade via positive-feedback loops. Finally, a mechanism is proposed that may explain why the convergence of PAP/ANAC017-dependent signalling appears capable of suppressing some types of PCD lesions, but not others, based on the subcellular location of the initial PCD-inducing dysfunction.
机译:能量转换细胞器线粒体和叶绿体紧密地嵌入细胞代谢和应激反应中。为了适当控制细胞器功能,广泛的监管机制在游戏中涉及细胞核和线粒体/叶绿体之间的双向交换。近年来,我们对线粒体和叶绿体如何为核心提供的对核的反馈,导致有针对性转录变化的理解,大大增加。然而,线粒体和叶绿体逆行信号在很大程度上被独立研究,并且已经发现或提出了几点相互作用。通过重新评估最近的出版物,这种观点提出了植物中最良好研究的逆行信号传导途径,由Anac017介导的两种逆行信号传导途径和由磷甲酸磷酸磷酸磷酸磷酸磷酸磷酸磷酸酯(PAP)介导的那些,最可能会会聚,并且可以直接重叠基因。此外,该常见的逆行响应的至少一部分出现针对由细胞细胞缺陷引发的编程细胞死亡(PCD)的抑制。鉴于它们的角色在PCD抑制中讨论了所识别的靶基因,并通过正反馈回路放大信号级联。最后,提出了一种机制,其可以解释为什么基于初始PCD引起功能障碍的亚细胞位置抑制某些类型的PCD病变,而不是其他类型的PCD病变,可以解释为什么PAP / ANAC017依赖信子的收敛。

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