Regulatory involvement of abscisic acid in potato tuber wound-healing

Abstract

Rapid wound-healing is crucial in protecting potato tubers from infection and dehydration. Wound-induced suberization and the accumulation of hydrophobic barriers to reduce water vapour conductance/loss are principal protective wound-healing processes. However, little is known about the cognate mechanisms that effect or regulate these processes. The objective of this research was to determine the involvement of abscisic acid (ABA) in the regulation of wound-induced suberization and tuber water vapour loss (dehydration). Analysis by liquid chromatography-mass spectrometry showed that ABA concentrations varied little throughout the tuber, but were slightly higher near the periderm and lowest in the pith. ABA concentrations increase then decrease during tuber storage. Tuber wounding induced changes in ABA content. ABA content in wound-healing tuber discs decreased after wounding, reached a minimum by 24 h, and then increased from the 3rd to the 7th day after wounding. Wound-induced ABA accumulations were reduced by fluridone (FLD); an inhibitor of de novo ABA biosynthesis. Wound-induced phenylalanine ammonia lyase activity was slightly reduced and the accumulation of suberin poly(phenolics) and poly(aliphatics) noticeably reduced in FLD-treated tissues. Addition of ABA to the FLD treatment restored phenylalanine ammonia lyase activity and suberization, unequivocally indicating that endogenous ABA is involved in the regulation of these wound-healing processes. Similar experiments showed that endogenous ABA is involved in the regulation of water vapour loss, a process linked to wax accumulation in wound-healing tubers. Rapid reduction of water vapour loss across the wound surface is essential in preventing desiccation and death of cells at the wound site; live cells are required for suberization. These results unequivocally show that endogenous ABA is involved in the regulation of wound-induced suberization and the processes that protect surface cells from water vapour loss and death by dehydration.

Biological differences that distinguish the 2 major stages of wound healing in potato tubers

“…The reduction in water vapor loss is measurable, hastened by the addition of ABA, and occurs within hours after wounding as a means of preventing desiccation and death of surface cells that ultimately must survive to be suberized as part of the closing layer process. 3,6 Based on examination of native periderm, a more tightly controlled process for reduction in water vapor loss likely occurs days later as suberin biopolymers are synthesized and assembled on cell walls. 8,9 This tighter control of water vapor loss appears to occur after initiation of WPF thereby suggesting that there may be different mechanisms operative in CLF vs WPF.…”

“…1). 3,14 However, ethylene and jasmonic acid are also wound-induced, but they are not required for suberization. 15 Nor does it appear that significant amounts of endogenous gibberellins or combinations of interacting auxin, indole acetic acid (IAA), and cytokinins are essential for CLF.…”

“…3,4 The effect of treatments with biologically active cytokinins (CK), dihydrozeatin and cis zeatin, on suberin polyphenolic (SPP) accumulation were conducted as previously outlined with the exception that the CKs were dissolved in MES buffer (pH 5.7, 10 mM).…”

Signals involved in tuber wound-healing

“…ABA content in tuber discs decreased dramatically to near non-detectable amounts one or two days after wounding then increased unless precursor biosynthesis was blocked by fluridone. 13 Here, we show additional data from determinations of ABA content in less traumatized WH half tubers (single wound surface) obtained at six months of storage, after the break of dormancy (Fig. 1A).…”

“…11 The involvement of two important regulatory compounds, ethylene 12 and ABA, 13 in potato tuber WH was determined in our laboratories by quantifying their content and using depletion and blocking tactics during the period of wound response. A third regulatory compound, JA, continues to be investigated in our laboratory.…”