Some plants can avoid shaded conditions via rapid shoot elongation, thus growing into better lit areas in a canopy. Cell wallmodifying mechanisms promoting this elongation response, therefore, are important regulatory points during shade avoidance. Two major cell wall-modifying protein families are expansins and xyloglucan endotransglucosylase/hydrolases (XTHs). The role of these proteins during shade avoidance was studied in Arabidopsis (Arabidopsis thaliana). In response to two shade cues, low red to far-red light (implying neighbor proximity) and green shade (mimicking dense canopy conditions), Arabidopsis showed classic shade avoidance features: petiole elongation and leaf hyponasty. Measurement of the apoplastic proton flux in green shade-treated petioles revealed a rapid efflux of protons into the apoplast within minutes, unlike white light controls. This apoplastic acidification probably provides the acidic pH required for the optimal activity of cell wallmodifying proteins like expansins and XTHs. Acid-induced extension, expansin susceptibility, and extractable expansin activity were similar in petioles from white light-and shade-treated plants. XTH activity, however, was high in petioles exposed to shade treatments. Five XTH genes (XTH9, were positively regulated by low red to far-red light conditions, while the latter four and XTH22 showed a significant up-regulation also in response to green shade. Consistently, knockout mutants for two of these XTH genes also had reduced or absent shade avoidance responses to these light signals. These results point toward the cell wall as a vital regulatory point during shade avoidance.

SummaryGuard cells are electrically isolated from other plant cells and therefore offer the unique possibility to conduct current-and voltage-clamp recordings on single cells in an intact plant. Guard cells in their natural environment were impaled with double-barreled electrodes and found to exhibit three physiological states. A minority of cells were classi®ed as far-depolarized cells. These cells exhibited positive membrane potentials and were dominated by the activity of voltage-dependent anion channels. All other cells displayed both outward and inward rectifying K + -channel activity. These cells were either depolarized or hyperpolarized, with average membrane potentials of ±41 mV (SD 16) and ±112 mV (SD 19), respectively. Depolarized guard cells extrude K + through outward rectifying channels, while K + is taken up via inward rectifying channels in hyperpolarized cells. Upon a light/dark transition, guard cells that were hyperpolarized in the light switched to the depolarized state. The depolarization was accompanied by a 35 pA decrease in pump current and an increase in the conductance of inward rectifying channels. Both an increase in pump current and a decrease in the conductance of the inward recti®er were triggered by blue light, while red light was ineffective. From these studies we conclude that light modulates plasma membrane transport through large membrane potential changes, reversing the K + -ef¯ux via outward rectifying channels to a K + -in¯ux via inward rectifying channels.