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Annexin 1 regulates the H2O2-induced calcium signature in Arabidopsis thaliana roots
journal contribution
posted on 2023-05-18, 01:59 authored by Richards, SL, Laohavisit, A, Mortimer, JC, Svetlana ShabalaSvetlana Shabala, Swarbreck, SM, Sergey ShabalaSergey Shabala, Davies, JMHydrogen peroxide is the most stable of the reactive oxygen species (ROS) and is a regulator of development, immunity and adaptation to stress. It frequently acts by elevating cytosolic free Ca2+ ([Ca2+]cyt) as a second messenger, with activation of plasma membrane Ca2+-permeable influx channels as a fundamental part of this process. At the genetic level, to date only the Ca2+-permeable Stelar K+ Outward Rectifier (SKOR) channel has been identified as being responsive to hydrogen peroxide. We show here that the ROS-regulated Ca2+ transport protein Annexin 1 in Arabidopsis thaliana (AtANN1) is involved in regulating the root epidermal [Ca2+]cyt response to stress levels of extracellular hydrogen peroxide. Peroxide-stimulated [Ca2+]cyt elevation (determined using aequorin luminometry) was aberrant in roots and root epidermal protoplasts of the Atann1 knockout mutant. Similarly, peroxide-stimulated net Ca2+ influx and K+ efflux were aberrant in Atann1 root mature epidermis, determined using extracellular vibrating ion-selective microelectrodes. Peroxide induction of GSTU1 (Glutathione-S-Transferase1 Tau 1), which is known to be [Ca2+]cyt-dependent was impaired in mutant roots, consistent with a lesion in signalling. Expression of AtANN1 in roots was suppressed by peroxide, consistent with the need to restrict further Ca2+ influx. Differential regulation of annexin expression was evident, with AtANN2 down-regulation but up-regulation of AtANN3 and AtANN4. Overall the results point to involvement of AtANN1 in shaping the root peroxide-induced [Ca2+]cyt signature and downstream signalling.
History
Publication title
The Plant JournalVolume
77Pagination
136-145ISSN
0960-7412Department/School
Tasmanian Institute of Agriculture (TIA)Publisher
Blackwell Publishing LtdPlace of publication
9600 Garsington Rd, Oxford, England, Oxon, Ox4 2DgRights statement
Copyright 2013 The AuthorsRepository Status
- Restricted