The photosynthetic basis for increasing the yield of major field crops is examined in terms of improving the interception of seasonal solar radiation by crop foliage, the efficiency of conversion of intercepted light to photosynthetic assimilates, and the partitioning of photoassimilates to organs of economic interest. It is concluded that, in practice, genetic and chemical manipulation of light interception over the season and of partitioning offer the most potential for achieving further increases in yield. During the history of improvement of genetic yield potential of crops, increase in the partitioning of photoassimilates to harvested organs has been of primary importance.

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p-Chloromercuribenzenesulfonic acid markedly inhibited sucrose accumulation into sugar beet source leaves without inhibiting hexose accumulation. The site of inhibition is proposed to be the plasmalemma ATPase, since the ATPase-mediated H+ efflux was completely inhibited by p chloromercuribenzenesuffonic acid under conditions where intracellular metabolism, as measured by photosynthesis and hexose accumulation, was unaffected. Fusicoccin, a potent activator of active H+/K+ exchange, stimulated both active sucrose accumulation and proton efflux in the sugar beet leaf tissue. These data provide strong evidence for the phloem loading of sucrose being coupled to a proton transport mechanism driven by a vectorial plasmalemma ATPase. Inasmuch as the cellular events operating in exporting leaves govern translocation (3,7,8,12), their elucidation at the mechanistic level is of considerable importance in understanding assimilate transport. Phloem loading, the process by which photosynthate enters the sieve tubes prior to export, is one aspect of source leaf physiology that has recently received attention (8)(9)(10). These studies have dealt mainly with the cellular transport pathway and sugar selectivity of the loading process. There is compelling evidence that photosynthetically derived sucrose, synthesized in the mesophyll cytoplasm, enters the apoplast prior to its metabolic and selective accumulation into the phloem (8-10). The coupling mechanism between the sucrose transporter and metabolism remains unresolved. Based on the proton dependence of sucrose accumulation and translocation, and the characteristics of the sieve tubes, we have proposed that the phloem loading of sucrose is coupled to the co-transport of protons (9-1 1). The driving force was proposed to be the electrochemical potential gradient of protons generated by a vectorial plasmalemma ATPase (I 1). This hypothesis is attractive for phloem loading not only because of the sieve tube characteristics (low H+/K+ ratio, membrane ATPase) but also because sugar transport coupled to proton fluxes has been documented in bacteria, algae, fungi (10 and refs. therein), and most recently in higher plants (16)(17)(18)(19) 24). The sucrose/H+ model may also explain, in part, the observed ATP stimulation of phloem loading (8) and the acquisition of sieve tube ATPase activity during the onset of export (13).Several recent studies have substantiated the existence of a sucrose-specific/proton co-transport system in higher plants. Racusen and Galston (24) (21) have recently proposed such a mechanism for sugar uptake into Ricinus phloem.This study further investigates phloem loading of sucrose in sugar beet source leaves in relation to ATPase-mediated proton transport. Evidence is presented that PCMBS2 selectively inhibits sucrose transport by inhibiting plasmalemma ATPase-proton transport. FC, a stimulator of active H+/K+ exchange, stimulated both net proton efflux and sucrose accumulation. These data are discussed in terms of a sucrose/H+ co-transport invo...