Stomatal closure induced by high vapor pressure deficit limited midday photosynthesis at the canopy top of Fagus crenata Blume on Naeba mountain in Japan

Diurnal changes in gas exchange, chlorophyll fluorescence and leaf water potential (psi(leaf)) were measured to determine the environmental and physiological factors that limit carbon gain in the horizontal leaves of Fagus crenata Blume at the canopy top. Although midday depression of the net CO2 assimilation rate (A(n)) and stomatal conductance (gH(2)O) were clearly evident on a fine day, the potential quantum yield of PS II (F-v/F-m) was fairly constant around 0.83 throughout the day. This result indicates that the leaves at the canopy top do not suffer from chronic photoinhibition, and the excess energy is dissipated safely. Large reversible increases in non-photochemical quenching (NPQ) were evident on fine days. Therefore, the non-radiative energy dissipation of excess light energy contributed to avoid chronic photoinhibition. The electron transfer rate (ETR) reached maximum during the midday depression, and thus there was no positive relation between ETR and A(n) under high light conditions, indicating a high rate of photorespiration and the absence of non-stomatal effect during midday. The protective mechanisms such as non-radiative energy dissipation and photorespiration play an important role in preventing photoinhibitory damage, and stomatal limitation is the main factor of midday depression of A(n). To separate the effect of air to leaf vapor pressure deficit (ALVPD) and leaf temperature (T-leaf) on gas exchange, the dependencies of An and gH(2)O on ALVPD and T-leaf were measured using detached branches under controlled conditions. A(n) and gH(2)O were insensitive to an increase in T-leaf. With the increase in ALVPD, An and gH(2)O exhibited more than a 50% decrease even though water supply was optimum, suggesting the dominant role of high ALVPD in the midday depression of gH(2)O. We conclude that midday depression of A(n) results from the midday stomatal closure caused by high ALVPD.