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沉默 ATG6 和 PI3K 可加速花瓣衰老,减少矮牵牛的花数和茎生物量。

Silencing ATG6 and PI3K accelerates petal senescence and reduces flower number and shoot biomass in petunia.

机构信息

Department of Horticulture and Crop Science, The Ohio State University, Ohio Agricultural Research and Development Center (OARDC), 1680 Madison Avenue, Wooster, OH, 44691, USA.

Department of Horticulture and Crop Science, The Ohio State University, Ohio Agricultural Research and Development Center (OARDC), 1680 Madison Avenue, Wooster, OH, 44691, USA.

出版信息

Plant Sci. 2021 Jan;302:110713. doi: 10.1016/j.plantsci.2020.110713. Epub 2020 Oct 10.

DOI:10.1016/j.plantsci.2020.110713
PMID:33288020
Abstract

Petal senescence is a form of developmental programmed cell death (PCD) that is regulated by internal and environmental signals. Autophagy, a metabolic pathway that regulates intercellular nutrient recycling, is thought to play an important role in the regulation of petal senescence-associated PCD. To characterize the function of two central autophagy genes in petal senescence, we down-regulated Autophagy Gene 6 (PhATG6) and Phosphoinositide 3-Kinase (PhPI3K) using Virus-Induced Gene Silencing (VIGS) in Petunia × hybrida. The silencing of PhATG6 and PhPI3K accelerated petal senescence, thereby reducing flower longevity. Both PhATG6- and PhPI3K-silenced petunias had reduced flower numbers, flower biomass, and vegetative shoot biomass. These phenotypes were intensified when plants were grown under low nutrient conditions. Additionally, two important regulators of senescence, an ethylene biosynthesis gene (PhACS) and a type I metacaspase gene (PhMC1), were suppressed in senescing petals of PhATG6- and PhPI3K-silenced plants. In conclusion, our study identified PhATG6 and PhPI3K as negative regulators of flower senescence and demonstrated the influence of nutrient limitation on the function of autophagy during petal senescence. Our study also found that autophagy genes potentially influence the transcriptional regulation of metacaspases and ethylene biosynthetic genes during petal senescence. The results of this project will be fundamental for future studies of petal senescence and will provide genetic information for future crop improvement.

摘要

花瓣衰老(Petal senescence)是一种受内部和环境信号调控的发育程序性细胞死亡(PCD)形式。自噬(Autophagy)是一种调节细胞间营养物质回收的代谢途径,被认为在调控花瓣衰老相关 PCD 中发挥着重要作用。为了研究两个核心自噬基因在花瓣衰老中的功能,我们利用病毒诱导的基因沉默(VIGS)技术在矮牵牛(Petunia × hybrida)中下调了自噬基因 6(PhATG6)和磷酸肌醇 3-激酶(PhPI3K)。PhATG6 和 PhPI3K 的沉默加速了花瓣衰老,从而缩短了花朵的寿命。PhATG6 和 PhPI3K 沉默的矮牵牛花朵数量、花生物量和营养枝生物量均减少。在低营养条件下,这些表型更为明显。此外,衰老的花瓣中两个重要的衰老调控因子,乙烯生物合成基因(PhACS)和 I 型半胱天冬酶基因(PhMC1)在 PhATG6 和 PhPI3K 沉默的植株中也受到抑制。综上所述,本研究鉴定了 PhATG6 和 PhPI3K 是花朵衰老的负调控因子,并证明了营养限制对花瓣衰老过程中自噬功能的影响。我们的研究还发现,自噬基因可能影响花瓣衰老过程中半胱天冬酶和乙烯生物合成基因的转录调控。本研究的结果将为未来的花瓣衰老研究提供基础,并为未来的作物改良提供遗传信息。

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