JAZ repressors of metabolic defense promote growth and reproductive fitness in Arabidopsis.
JAZ repressors of metabolic defense promote growth and reproductive fitness in Arabidopsis.
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DOI：
10.1073/pnas.1811828115
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发表时间：
2018-11-06
影响因子：
11.1
通讯作者：
Howe GA
中科院分区：
文献类型：
--
作者：
Guo Q;Yoshida Y;Major IT;Wang K;Sugimoto K;Kapali G;Havko NE;Benning C;Howe GA
植物激素茉莉酸可增强对食植物生物（从病原微生物到哺乳动物）的抵抗力。茉莉酸重新编程代谢，以促进多种防御化合物的产生，同时抑制植物生长。了解生长如何在一系列防御水平上受到影响仍不清楚，但对优化作物生产力具有重要意义。使用遗传方法来“调整”茉莉酸响应，我们评估了整个植物生命周期的离散水平的防御的生理后果。茉莉酸响应的过度激活导致碳饥饿，种子生产的近损失，在极端条件下，致死。我们的研究结果解释了不同策略的出现，以保持茉莉酸反应，并提供了新的见解代谢过程的基础生长防御权衡。由激素茉莉酰基-l-异亮氨酸（JA-Ile）介导的植物免疫应答在代谢上是昂贵的，并且通常与生长减缓有关。虽然已知JA-Ile通过触发JAZ转录抑制蛋白的降解来激活防御反应，但JAZ基因家族在维管植物中的扩展阻碍了理解这种激素如何影响个体发育过程中的生长和其他生理任务的努力。在这里，我们结合突变的13个成员的拟南芥JAZ基因家族，研究慢性JAZ缺乏对生长，防御和生殖输出的影响。一个缺失10个JAZ基因（JAZ 1 -7、-9、-10和-13）的高阶突变体（jazdecuple，jazD）表现出对食草昆虫和真菌病原菌的强烈抗性，伴随着缓慢的营养生长和不良的繁殖性能。从全球转录本和蛋白质谱中识别的jazD代谢表型表明，由免疫的JA-Ile和乙烯分支控制的基于氨基酸、蛋白质和内质网体的防御的碳分配升高。资源分配到一个强大的防御库在jazD叶与呼吸增加和碳饥饿的标志，但没有明显的光合速率的变化。在jazD中剩余的JAZ阻遏物的耗尽进一步加剧了生长发育迟缓，几乎取消了种子生产，并且在极端条件下，引起了扩散性坏死病变和组织死亡。我们的研究结果表明，JAZ蛋白促进生长和生殖成功，至少部分是通过防止不受限制的免疫反应的灾难性代谢效应。
The plant hormone jasmonate promotes resistance to plant-eating organisms, ranging from pathogenic microbes to mammals. Jasmonate reprograms metabolism to fuel the production of diverse defense compounds and simultaneously inhibits plant growth. Understanding how growth is influenced across a range of defense levels remains unclear, but has important implications for optimizing crop productivity. Using a genetic approach to “tune” the jasmonate response, we assessed the physiological consequences of discrete levels of defense throughout the plant life cycle. Overactivation of jasmonate response led to carbon starvation, near loss of seed production and, under extreme conditions, lethality. Our findings explain the emergence of diverse strategies to keep jasmonate responses at bay and provide new insights into metabolic processes that underlie growth–defense trade-offs. Plant immune responses mediated by the hormone jasmonoyl-l-isoleucine (JA-Ile) are metabolically costly and often linked to reduced growth. Although it is known that JA-Ile activates defense responses by triggering the degradation of JASMONATE ZIM DOMAIN (JAZ) transcriptional repressor proteins, expansion of the JAZ gene family in vascular plants has hampered efforts to understand how this hormone impacts growth and other physiological tasks over the course of ontogeny. Here, we combined mutations within the 13-member Arabidopsis JAZ gene family to investigate the effects of chronic JAZ deficiency on growth, defense, and reproductive output. A higher-order mutant (jaz decuple, jazD) defective in 10 JAZ genes (JAZ1–7, -9, -10, and -13) exhibited robust resistance to insect herbivores and fungal pathogens, which was accompanied by slow vegetative growth and poor reproductive performance. Metabolic phenotypes of jazD discerned from global transcript and protein profiling were indicative of elevated carbon partitioning to amino acid-, protein-, and endoplasmic reticulum body-based defenses controlled by the JA-Ile and ethylene branches of immunity. Resource allocation to a strong defense sink in jazD leaves was associated with increased respiration and hallmarks of carbon starvation but no overt changes in photosynthetic rate. Depletion of the remaining JAZ repressors in jazD further exaggerated growth stunting, nearly abolished seed production and, under extreme conditions, caused spreading necrotic lesions and tissue death. Our results demonstrate that JAZ proteins promote growth and reproductive success at least in part by preventing catastrophic metabolic effects of an unrestrained immune response.
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影响因子：
11.6
作者：
Benstein, Ruben Maximilian;Ludewig, Katja;Krueger, Stephan
通讯作者：
Krueger, Stephan
影响因子：
7.4
作者：
Attaran, Elham;Major, Ian T.;Howe, Gregg A.
通讯作者：
Howe, Gregg A.
DOI：
10.1073/pnas.95.14.8113
发表时间：
1998-07-07
影响因子：
11.1
作者：
Baldwin, IT
通讯作者：
Baldwin, IT
影响因子：
7.2
作者：
Gigolashvili, Tamara;Berger, Bettina;Fluegge, Ulf-Ingo
通讯作者：
Fluegge, Ulf-Ingo
影响因子：
56.9
作者：
Agrawal, AA
通讯作者：
Agrawal, AA