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In plants, ferritin proteins play an important role in iron (Fe) storage which contributes to plant growth and development. However, the biological functions of ferritins in fruit trees are essentially unknown. In this study, three Ferritin genes were isolated from 'Zhentong No. 3' peach, which were named PpFer1-PpFer3. The expression levels of these genes were different in distinct tissues/organs. Notably, PpFer1 was the most abundantly expressed Ferritin family gene in all tested tissues of 'Zhentong No. 3' peach; its expression levels were significantly enhanced throughout the entire peach seedling under Fe toxicity and H2O2 stress, particularly in the leaves. In addition, over-expression of PpFer1 was effective in rescuing the retarded growth of Arabidopsis fer1-2 knockout mutant, embodied in enhanced fresh weight, primary root length, lateral root numbers, total root length, total leaf chlorophyll, stomatal conductance (Gs), net photosynthetic rate (Pn), transpiration rate, and tissue Fe concentration. This study provides insights into understanding the molecular mechanisms of Fe storage and sequestration in perennial fruit trees. [ABSTRACT FROM AUTHOR]

Summary: Damage can be signalled by extracellular ATP (eATP) using plasma membrane (PM) receptors to effect cytosolic free calcium ion ([Ca2+]cyt) increase as a second messenger. The downstream PM Ca2+ channels remain enigmatic. Here, the Arabidopsis thaliana Ca2+ channel subunit CYCLIC NUCLEOTIDE‐GATED CHANNEL2 (CNGC2) was identified as a critical component linking eATP receptors to downstream [Ca2+]cyt signalling in roots.Extracellular ATP‐induced changes in single epidermal cell PM voltage and conductance were measured electrophysiologically, changes in root [Ca2+]cyt were measured with aequorin, and root transcriptional changes were determined by quantitative real‐time PCR. Two cngc2 loss‐of‐function mutants were used: cngc2‐3 and defence not death1 (which expresses cytosolic aequorin).Extracellular ATP‐induced transient depolarization of Arabidopsis root elongation zone epidermal PM voltage was Ca2+ dependent, requiring CNGC2 but not CNGC4 (its channel co‐subunit in immunity signalling). Activation of PM Ca2+ influx currents also required CNGC2. The eATP‐induced [Ca2+]cyt increase and transcriptional response in cngc2 roots were significantly impaired.CYCLIC NUCLEOTIDE‐GATED CHANNEL2 is required for eATP‐induced epidermal Ca2+ influx, causing depolarization leading to [Ca2+]cyt increase and damage‐related transcriptional response. [ABSTRACT FROM AUTHOR]