Arabidopsis inositol polyphosphate kinases IPK1 and ITPK1 modulate crosstalk between SA-dependent immunity and phosphate-starvation responses

Arabidopsis inositol polyphosphate kinases IPK1 and ITPK1 modulate crosstalk between SA-dependent immunity and phosphate-starvation responses
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拟南芥肌醇多磷酸激酶IPK1和ITPK1调节sa依赖性免疫和磷酸盐饥饿反应之间的串音

DOI:
10.1007/s00299-021-02812-3
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发表时间:
2021-11-19
期刊:
影响因子:
6.2
通讯作者:
Bhattacharjee, Saikat
Bhattacharjee, Saikat
中科院分区:
生物学2区
文献类型:
--
作者:
Gulabani, Hitika;Goswami, Krishnendu;Bhattacharjee, Saikat

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关键信息选择拟南芥酪氨酸肌醇磷酸激酶功能通过平衡信号调节和磷酸稳态网络来调节先天免疫的反应幅度。InSP(6)的焦磷酸化生成InSP(7)和/或InSP(8),该InSP(7)和/或InSP(8)包含在电池能量需求期间被利用的高能磷酸酸酐键。作为几个植物激素网络的真正辅助因子,Insp(7)/Insp(8)调控着关键的发育过程。由于需要转导茉莉酸(JA)和磷酸饥饿反应(PSR),Insp(8)是一种多功能的代谢物,用于在不同的应激暴露下不同细胞通路之间的串扰。在这里,我们发现了与InSP(8)生物合成有关的拟南芥肌醇五磷酸磷酸肌醇2-激酶1(IPK1)、肌醇1,3,4-三磷酸5/6-激酶1(ITPK1)和二磷醇五磷酸激酶2(VIH2),它们抑制了水杨酸(SA)依赖的免疫。在ipk1、itpk1或vih2突变体中,结构性的防御激活导致了对番茄假单胞菌Sringae PV DC3000(PstDC3000)菌株的抗性增强。我们的数据显示,上调的SA信号区段增强了几个磷酸饥饿诱导(PSI)基因的表达,这些基因以前在这些突变体中已知。在相互作用中,上调的PSI基因适度表达防御相关标记的幅度。我们证明,SA在缺磷植物中被诱导,但其促进防御的功能可能被转移到PSR支持作用上。总体而言,我们的研究揭示了选择性Insps在防御-磷酸盐动态平衡和重新编程胁迫适当的反应强度中作为串扰介体。
Key message SelectiveArabidopsis thalianainositol phosphate kinase functions modulate response amplitudes in innate immunity by balancing signalling adjustments with phosphate homeostasis networks. Pyrophosphorylation of InsP(6) generates InsP(7) and/or InsP(8) containing high-energy phosphoanhydride bonds that are harnessed during energy requirements of a cell. As bona fide co-factors for several phytohormone networks, InsP(7)/InsP(8) modulate key developmental processes. With requirements in transducing jasmonic acid (JA) and phosphate-starvation responses (PSR), InsP(8) exemplifies a versatile metabolite for crosstalks between different cellular pathways during diverse stress exposures. Here we show that Arabidopsis thaliana INOSITOL PENTAKISPHOSPHATE 2-KINASE 1 (IPK1), INOSITOL 1,3,4-TRISPHOSPHATE 5/6-KINASE 1 (ITPK1), and DIPHOSPHOINOSITOL PENTAKISPHOSPHATE KINASE 2 (VIH2) implicated in InsP(8) biosynthesis, suppress salicylic acid (SA)-dependent immunity. In ipk1, itpk1 or vih2 mutants, constitutive activation of defenses lead to enhanced resistance against the Pseudomonas syringae pv tomato DC3000 (PstDC3000) strain. Our data reveal that upregulated SA-signaling sectors potentiate increased expression of several phosphate-starvation inducible (PSI)-genes, previously known in these mutants. In reciprocation, upregulated PSI-genes moderate expression amplitudes of defense-associated markers. We demonstrate that SA is induced in phosphate-deprived plants, however its defense-promoting functions are likely diverted to PSR-supportive roles. Overall, our investigations reveal selective InsPs as crosstalk mediators in defense-phosphate homeostasis and in reprogramming stress-appropriate response intensities.