Higher Plant Respiration and Its Relationships to Photosynthesis
81
to the rate in the dark at the same temperature, although total mitochondrial
CO 2 release could increase due to photorespiration. Although enzymes of
glycolysis and the oxidative pentose phosphate network exist in chloroplasts
(ap Rees 1985), it is reasonable to assume that those pathways are inhibited
or reversed during photosynthesis.
A high cytosolic A TP: ADP can inhibit oxidative phosphorylation (Dry
and Wiskich 1982), and although the ratio may increase in the light under
physiological conditions (Gardestrom and Wigge 1988), it may not be high
enough to be inhibitory. The availability of free (unbound) ADP to respiratory reactions in the light and dark has not, apparently, been well characterized and is probably important, and dynamic, in vivo. Photosynthesis may
produce mostly NADPH in the cytosol, compared to ATP and NADH;
Kromer and Heldt (1991b) cite evidence that NADPH may exceed NADH
by 250 times in the cytosol of photosynthesizing Spinacia oleracea cells. This
suggests an inhibition of the cytosolic oxidative pentose phosphate network,
but not necessarily glycolysis or the TCA cycle unless the NADPH is
oxidized by the respiratory chain (see Fig. 4.3).
Because CO2 is assimilated in photosynthesis while being released in
respiration, and O2 is generated by photosynthesis while being consumed in
respiration, simple gas exchange techniques cannot be used to estimate rates
of respiration in leaves in the light. The use of labeled CO2 or O 2 will
not fully overcome this difficulty for several reasons. The photosynthetic
assimilation of respired CO2 - mitochondria and chloroplasts are generally
in close association in leaves - is of particular importance. A similar situation
has existed for the direct measurement of photorespiration, resulting in a
range of "unreliable" estimates of its rate (Sharkey 1988). Fortunately for
the study of photorespiration, the kinetics of a single enzyme (Rubisco)
determines the ratio of RuP2 carboxylation to RuP2 oxygenation, and it
is possible to calculate the ratio of photosynthesis to photorespiration if
chloroplast CO2 concentration is known (Sharkey 1988). Diversion of
photorespiratory glycine to processes other than serine synthesis, which
results in photorespiratory decarboxylation (Fig. 4.6), will alter the ratio
of photosynthetic carboxylation to photo respiratory decarboxylation for a
given chloroplast CO2 concentration, but nonetheless, accurate estimates
of the concurrent CO2 fluxes associated with photosynthesis and photorespiration are possible because of the central role of Rubisco in those
processes. When the chloroplast CO2 concentration is equal to the CO 2
compensation point in the absence of respiration (r *; Farquhar et al. 1980),
respiration rate in photosynthesizing leaves can be estimated from gas
exchange rate (see, e.g., Kirschbaum and Farquhar 1987). The value of r *
is a function of the CO2!02 specificity of Rubisco (see Laing et al. 1974;
Farquhar et al. 1980; Jordan and Ogren 1984). If respiration rate is affected
by CO2 concentration (e.g., Amthor et al. 1992), effects of CO 2 on respiration must be accounted for to estimate respiration rate at CO2 levels different
from r *.
81
to the rate in the dark at the same temperature, although total mitochondrial
CO 2 release could increase due to photorespiration. Although enzymes of
glycolysis and the oxidative pentose phosphate network exist in chloroplasts
(ap Rees 1985), it is reasonable to assume that those pathways are inhibited
or reversed during photosynthesis.
A high cytosolic A TP: ADP can inhibit oxidative phosphorylation (Dry
and Wiskich 1982), and although the ratio may increase in the light under
physiological conditions (Gardestrom and Wigge 1988), it may not be high
enough to be inhibitory. The availability of free (unbound) ADP to respiratory reactions in the light and dark has not, apparently, been well characterized and is probably important, and dynamic, in vivo. Photosynthesis may
produce mostly NADPH in the cytosol, compared to ATP and NADH;
Kromer and Heldt (1991b) cite evidence that NADPH may exceed NADH
by 250 times in the cytosol of photosynthesizing Spinacia oleracea cells. This
suggests an inhibition of the cytosolic oxidative pentose phosphate network,
but not necessarily glycolysis or the TCA cycle unless the NADPH is
oxidized by the respiratory chain (see Fig. 4.3).
Because CO2 is assimilated in photosynthesis while being released in
respiration, and O2 is generated by photosynthesis while being consumed in
respiration, simple gas exchange techniques cannot be used to estimate rates
of respiration in leaves in the light. The use of labeled CO2 or O 2 will
not fully overcome this difficulty for several reasons. The photosynthetic
assimilation of respired CO2 - mitochondria and chloroplasts are generally
in close association in leaves - is of particular importance. A similar situation
has existed for the direct measurement of photorespiration, resulting in a
range of "unreliable" estimates of its rate (Sharkey 1988). Fortunately for
the study of photorespiration, the kinetics of a single enzyme (Rubisco)
determines the ratio of RuP2 carboxylation to RuP2 oxygenation, and it
is possible to calculate the ratio of photosynthesis to photorespiration if
chloroplast CO2 concentration is known (Sharkey 1988). Diversion of
photorespiratory glycine to processes other than serine synthesis, which
results in photorespiratory decarboxylation (Fig. 4.6), will alter the ratio
of photosynthetic carboxylation to photo respiratory decarboxylation for a
given chloroplast CO2 concentration, but nonetheless, accurate estimates
of the concurrent CO2 fluxes associated with photosynthesis and photorespiration are possible because of the central role of Rubisco in those
processes. When the chloroplast CO2 concentration is equal to the CO 2
compensation point in the absence of respiration (r *; Farquhar et al. 1980),
respiration rate in photosynthesizing leaves can be estimated from gas
exchange rate (see, e.g., Kirschbaum and Farquhar 1987). The value of r *
is a function of the CO2!02 specificity of Rubisco (see Laing et al. 1974;
Farquhar et al. 1980; Jordan and Ogren 1984). If respiration rate is affected
by CO2 concentration (e.g., Amthor et al. 1992), effects of CO 2 on respiration must be accounted for to estimate respiration rate at CO2 levels different
from r *.