264
GEORGE G. LATIES
tion imposed by the phosphorylative reactions within the cell. Dinitrophenol uncouples the phosphorylative from the oxidative reactions, and
thereby relieves the restraint; and auxin-induced growth apparently
causes a more rapid turnover of phosphate acceptor because of the
utilization of phosphorylated intermediates in the growth process. The
respiratory increment attending aging may be the consequence of ATP
utilization in protein synthesis (see Steward et al., 1940) or may simply
reflect the onset of a variety of cellular processes which convert ATP
to ADP.
The manner in which salt absorption may be thought to stimulate
respiration has been sketched by Rosenberg (1948). Assuming that a
substance is taken into the cell by means of combination with a carrier,
and that the carrier is a metabolic intermediate, Rosenberg says, "If this
movement has the direction from the outer phase into a single cell, the
carrier must be transformed in the latter by a chemical reaction in order
that the diffusion tendency should continue to be maintained." He continues, "if the outer concentration [of the substance being absorbed]
is increased, there is a possibility of an increased transport of the carrier
and thereby an acceleration of metabolism." To fit the present thesis,
one may consider the carrier complex to be a phosphorylated metabolic
intermediate associated with an ion. The complex may be formed
at the plasma membrane if the latter is considered the permeability
barrier, or in the cytoplasm if the vacuolar membrane is considered the
major resistance to ion passage. Upon migration through the permeability barrier the complex is hydrolyzed or otherwise dissociated, releasing
both the ion and inorganic phosphate. The potential carrier is thereupon
rephosphorylated by metabolically produced ATP, a phosphate acceptor
and the carrier both being produced anew in the process. The production of phosphate acceptor is thought to be the cause for the
increase in respiration, and the accumulation of salt is believed to
affect respiration in the same way as the auxin-induced uptake of water.
It is of particular significance that dinitrophenol completely abolishes
salt accumulation (Lundegárdh, 1953a; Robertson et al., 1951). The
hypothesis that the energy for metabolic water uptake and for salt
accumulation stems from the same source has been tested by Hanson
and Bonner (1954), using disks of Jerusalem artichoke. They have shown
that the rate of salt uptake can be diminished by the onset of auxininduced absorption of water. Conversely, the uptake of water was
shown to be lessened by active salt accumulation: the absorption of
1 mole of phosphate precluded the absorption of 900 moles of water.
Both salt accumulation and water absorption stimulated respiration.
However, when the stimulation of respiration was once achieved in
GEORGE G. LATIES
tion imposed by the phosphorylative reactions within the cell. Dinitrophenol uncouples the phosphorylative from the oxidative reactions, and
thereby relieves the restraint; and auxin-induced growth apparently
causes a more rapid turnover of phosphate acceptor because of the
utilization of phosphorylated intermediates in the growth process. The
respiratory increment attending aging may be the consequence of ATP
utilization in protein synthesis (see Steward et al., 1940) or may simply
reflect the onset of a variety of cellular processes which convert ATP
to ADP.
The manner in which salt absorption may be thought to stimulate
respiration has been sketched by Rosenberg (1948). Assuming that a
substance is taken into the cell by means of combination with a carrier,
and that the carrier is a metabolic intermediate, Rosenberg says, "If this
movement has the direction from the outer phase into a single cell, the
carrier must be transformed in the latter by a chemical reaction in order
that the diffusion tendency should continue to be maintained." He continues, "if the outer concentration [of the substance being absorbed]
is increased, there is a possibility of an increased transport of the carrier
and thereby an acceleration of metabolism." To fit the present thesis,
one may consider the carrier complex to be a phosphorylated metabolic
intermediate associated with an ion. The complex may be formed
at the plasma membrane if the latter is considered the permeability
barrier, or in the cytoplasm if the vacuolar membrane is considered the
major resistance to ion passage. Upon migration through the permeability barrier the complex is hydrolyzed or otherwise dissociated, releasing
both the ion and inorganic phosphate. The potential carrier is thereupon
rephosphorylated by metabolically produced ATP, a phosphate acceptor
and the carrier both being produced anew in the process. The production of phosphate acceptor is thought to be the cause for the
increase in respiration, and the accumulation of salt is believed to
affect respiration in the same way as the auxin-induced uptake of water.
It is of particular significance that dinitrophenol completely abolishes
salt accumulation (Lundegárdh, 1953a; Robertson et al., 1951). The
hypothesis that the energy for metabolic water uptake and for salt
accumulation stems from the same source has been tested by Hanson
and Bonner (1954), using disks of Jerusalem artichoke. They have shown
that the rate of salt uptake can be diminished by the onset of auxininduced absorption of water. Conversely, the uptake of water was
shown to be lessened by active salt accumulation: the absorption of
1 mole of phosphate precluded the absorption of 900 moles of water.
Both salt accumulation and water absorption stimulated respiration.
However, when the stimulation of respiration was once achieved in