探討阿拉伯芥 GTR1/NPF2.10 於鹽逆境下調控根系結構之機制

Abstract

阿拉伯芥的芥子油苷轉運蛋白 (Glucosinolate Transporter 1, GTR1/ NPF2.10) 可以運輸茉莉酸-異亮氨酸複合物 (JA-Ile) 以及脂肪族芥子油苷。在過去的研究中，GTR1參與在鹽逆境下茉莉酸訊息傳導路徑以及側根發育，而鹽逆境下 GTR1 介導改變根系結構的詳細機制尚不清楚。在本研究中，我們分析gtr1突變株在鹽處理下的訊息傳導調節因子的表現模式、活性氧類 (ROS) 的累積和根系結構的改變。結果發現，在鹽逆境下，不僅gtr1突變株中的茉莉酸訊息傳導路徑受到抑制，而且根中JA-Ile生合成基因JAR1的表現也顯著低於野生型。除了茉莉酸訊息傳導路徑，GTR還正向調控植物激發物Pep3訊息傳導路徑。另一方面，本研究也發現在鹽逆境下，gtr1 突變株根尖的ROS累積減少，並且在過氧化氫處理下，gtr1 突變株主根生長抑制得到緩解，而側根發育受到抑制。這些結果表示GTR1可能透過促進ROS累積來調節根系結構以應對鹽逆境。值得注意的是，我們還觀察到缺乏脂肪族芥子油苷的突變株 (myb28myb29) 與gtr1突變體，有相似的鹽誘導茉莉酸訊息傳導、Pep3訊息傳導，以及ROS累積情形。這些結果顯示鹽逆境下GTR1介導的相關途徑可能與調節脂肪族芥子油苷運輸有關。然而，GTR1介導的訊息傳導路徑和ROS累積是如何受到鹽逆境下脂肪族芥子油苷的調節，還需要進一步研究。

The Arabidopsis Glucosinolate Transporter 1 (GTR1/ NPF2.10) is shown to transport JA-Ile and aliphatic glucosinolate. Recent studies showed that GTR1 is the molecular link between salt stress, JA signaling, and lateral root development. However, the detailed mechanisms of GTR1-mediated root architecture under salt stress are unclear. This study analyzed expression patterns of signaling regulators, ROS accumulation, and root architecture to elucidate the underlying regulations under salt treatment. We found that gtr1 mutants exhibit repressed salt-induced JA signaling and have diminished JAR1 expression in the root stele. In addition to affecting salt-induced JA signaling, GTR1 also positively regulates salt-induced Pep3-PEPR1 signaling. Furthermore, in the gtr1 mutant, less ROS was accumulated in the root tip, and the sensitivity to H2O2 treatment of roots growth was altered under salt stress. These results suggest that GTR1 modulates root architecture under salinity stress by promoting ROS accumulation. Interestingly, in the mutant without aliphatic glucosinolates (GSLs), we observed similar phenotypes in the gene expression patterns of salt-induced JA signaling and Pep3-PEPR1 signaling, as well as the salt-induced ROS accumulation to those in gtr1 mutants. These results suggest that GTR1-mediated JA signaling, Pep3-PEPR1 signaling, and ROS accumulation may be associated with regulating aliphatic GSLs transport under salinity stress. However, how GTR1-mediated aliphatic GSLs transport modulates the salt responses needs further investigation.