Abstract

<jats:p>
Respiration (R, non-photorespiratory mitochondrial
CO2 release) in leaves is inhibited by light. However,
exposure to darkness after a period of illumination can also result in
R being temporarily stimulated (termed ‘light
enhanced dark respiration’, LEDR). We used a fast-response
CO2 exchange system to investigate these observations in
tobacco leaves. After switching off the light, there were two peaks of
CO2 release, the first at 15–20 s (the
photorespiratory post-illumination burst) and the second at 180–250 s
(LEDR). LEDR occurred in all post-illumination experiments, independent of
O2 or CO2 concentration. However,
LEDR increased with increasing irradiance during the pre-dark period,
suggesting some dependency on prior photosynthesis. We investigated the
inhibition of R by light at low
CO2 concentrations (?*):
?* is the intercellular CO2
concentration at which net CO2 release represents R in
the light. The inhibition of R in the light took about 50 s and was even
evident at 3 mmol photons m-2 s-1,
regardless of the light quality (red, blue or white). The inhibition of
R by light showed similar dependency on irradiance as
LEDR, such that the degree of inhibition was positively correlated with the
level of LEDR. In the light, switching from 350 ppm to a low
CO2 concentration that resulted in the intercellular
CO2 concentration being at ?*,
resulted in R initially increasing and then stabilising.
Maintaining the leaf at ?* did not, therefore, lead
to an underestimation of R. Our data suggest that a
common mechanism may be responsible for both the inhibition of
R by light and LEDR.</jats:p>