Autophagy triggered by iron mediated ER stress is an important stress response to the early phase of Pi starvation in plants

Autophagy triggered by iron mediated ER stress is an important stress response to the early phase of Pi starvation in plants
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铁介导的内质网应激引发的自噬是植物对 Pi 饥饿早期的重要应激反应

DOI:
10.1111/tpj.15743
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发表时间:
2022
期刊:
The Plant Journal
影响因子:
--
通讯作者:
Kohki Yoshimoto
Kohki Yoshimoto
中科院分区:
--
文献类型:
--
作者:
Yushi Yoshitake;Daiki Shinozaki;Kohki Yoshimoto

文献摘要

相似文献

无机磷(Pi)是植物生长所必需的。然而,Pi在土壤中通常是有限的。因此,植物已经建立了几种对Pi饥饿的反应机制。其中一个重要的机制是Pi再循环,其包括通过分解代谢酶的膜脂质重塑和质体DNA降解。然而,其他降解系统参与Pi回收仍不清楚。自噬是一种细胞内成分的降解系统,在饥饿条件下有助于某些营养物质(如氮、碳和锌)的再循环。在本研究中,我们发现自噬缺陷突变体在Pi饥饿的情况下早期耗尽Pi并表现出严重的叶片生长缺陷。由早期Pi耗尽条件诱导的自噬的主要货物是内质网(ER),表明ER-吞噬(一种选择性降解ER的自噬类型)参与对Pi饥饿的早期阶段的响应以促进Pi再循环。这种ER-吞噬在肌醇需求酶1双突变体ire 1a ire 1b中受到抑制,其中ER应激反应有缺陷,这表明早期Pi饥饿诱导的ER-吞噬是由ER应激诱导的。此外,铁限制和脂质活性氧积累的抑制抑制了ER吞噬。有趣的是,膜脂重塑,对后期Pi饥饿的反应,在早期Pi耗尽的条件下加速。我们的研究结果揭示了对Pi饥饿的两个不同阶段的反应(即早期和晚期),并表明ER应激介导的ER吞噬参与了早期阶段的Pi再循环,以抑制晚期阶段的加速。
Inorganic phosphate (Pi) is essential for plant growth. However, Pi is often limiting in soil. Hence, plants have established several mechanisms of response to Pi starvation. One of the important mechanisms is Pi recycling, which includes membrane lipid remodeling and plastid DNA degradation via catabolic enzymes. However, the involvement of other degradation systems in Pi recycling remains unclear. Autophagy, a system for degradation of intracellular components, contributes to recycling of some nutrients, such as nitrogen, carbon, and zinc, under starvation. In the present study, we found that autophagy‐deficient mutants depleted Pi early and exhibited severe leaf growth defects under Pi starvation. The main cargo of autophagy induced by early Pi depleted conditions was the endoplasmic reticulum (ER), indicating that ER‐phagy, a type of autophagy that selectively degrades the ER, is involved in the response to the early phase of Pi starvation for contribution to Pi recycling. This ER‐phagy was suppressed in an INOSITOL‐REQUIRING ENZYME 1 double mutant,ire1a ire1b, in which ER stress responses are defective, suggesting that the early Pi starvation induced ER‐phagy is induced by ER stress. Furthermore, iron limitation and inhibition of lipid‐reactive oxygen species accumulation suppressed the ER‐phagy. Interestingly, membrane lipid remodeling, a response to late Pi starvation, was accelerated in theire1a ire1bunder early Pi‐depleted conditions. Our findings reveal the existence of two different phases of responses to Pi starvation (i.e. early and late) and indicate that ER stress‐mediated ER‐phagy is involved in Pi recycling in the early phase to suppress acceleration of the late phase.