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In vivo manipulation of cuticular water permeance and its effect on stomatal response to air humidity

Research output: Contribution to journalJournal article


Journal publication date11/1997
JournalNew Phytologist
Number of pages8
Original languageEnglish


Cuticular water permeance was manipulated in Corylus avellana L., Hypericum androsaemum L. and Populus tremula L. by (1) long-term application of low doses of various systemic herbicides inhibiting biosynthesis of cuticular waxes, (2) very short-term application of organic solvents to the leaf surface, and (3) exposure to natural strong winds. Treatment effects were very variable, but increased the natural range of permeances by a factor of 10 or so in undamaged leaves. All species had hypostomatous leaves. Relative change of leaf conductance (g) in response to stepwise increases of leaf-to-air water vapour pressure difference (VPD) was measured for individual leaves (Corylus) or groups of leaves at the shoot or branch tip. Adaxial cuticular water permeance (P) was determined for the same leaves after measurement of the VPD-response. A proportional measure of relative change of g with VPD, d(log(e)g)/dVPD, was then plotted against P. No increase in the strength of the closing response to increasing VPD was found with increasing P, as would have been expected if water loss through the cuticle was involved in stomatal response to changes in VPD via a direct effect on guard cell turgor. By contrast, high P coincided, most clearly in Corylus, with a reduced strength of the stomatal closing response to increasing VPD, i.e. less negative d(log(e)g)/dVPD. As the responses were non-linear, the value of d(log(e)g)/dI/PD changed with VPD. With rising VPD, all three species and a fourth one previously studied showed a decline in the value of d[d(log(e)g)/dVPD]/d(log P), reaching negative values in one species. This is interpreted in terms of two independent and antagonistic effects of increased cuticular water permeance on guard cell response to VPD, one acting by reducing the backpressure exerted on guard cells by the epidermis, and the other one possibly causing greater depression of guard cell turgor through delivery of more chemical messengers (such as abscisic acid) to the guard cells with the cuticular transpiration stream.