4.7 Article

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

Journal

PLANT CELL REPORTS
Volume 41, Issue 2, Pages 347-363

Publisher

SPRINGER
DOI: 10.1007/s00299-021-02812-3

Keywords

Inositol polyphosphates; Arabidopsis thaliana; Basal immunity; PstDC3000; Salicylic acid; Phosphate-starvation response

Categories

Funding

  1. Regional Centre for Biotechnology (RCB), Faridabad
  2. Regional Centre for Biotechnology (RCB) core Grants
  3. DBT-Ramalingaswami Re-Entry Fellowship [BT/PR23666/AGIII/103/1039/2018]
  4. Deutsche Forschungsgemeinschaft [SCHA 1274/5-1, EXC-2070-390732324, HE 8362/1-1]
  5. Department of Science & Technology for Improvement of S&T Infrastructure (DST-FIST)
  6. Indian Institute of Science, India

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Selective Arabidopsis thaliana inositol phosphate kinase functions modulate response amplitudes in innate immunity by balancing signaling adjustments with phosphate homeostasis networks. Pyrophosphorylation of InsP(6) generates high-energy metabolites InsP(7) and InsP(8) that play crucial roles in plant development and stress responses. Plants are able to regulate immune responses and phosphate homeostasis under phosphate deprivation conditions.
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.

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