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BIOCHEMICAL PROCESSES AND MACROMOLECULAR STRUCTURES

Reduced Expression of Aconitase Results in an Enhanced Rate of Photosynthesis and Marked Shifts in Carbon Partitioning in Illuminated Leaves of Wild Species Tomato¹

Department Willmitzer, Max-Planck-Institut für Molekulare Pflanzenphysiologie, Am Mühlenberg 1, 14476 Golm, Germany (F.C., A.N.-N., Y.G., A.L., A.R.F.); and Departamento de Biologia Vegetal, Federal University of Vicosa, 36571–000 Viçosa-MG, Brazil (M.E.L.)

Wild species tomato (Lycopersicon pennellii) plants bearing a genetic lesion in the gene encoding aconitase (Aco-1; aconitate hydratase EC 4.2.1.3) were characterized at molecular and biochemical levels. The genetic basis of this lesion was revealed by cloning the wild-type and mutant alleles. The mutation resulted in lowered expression of the Aco-1 transcript and lowered levels of both cytosolic and mitochondrial aconitase protein and activity. After in silico analysis, we concluded that in the absence of a recognizable target sequence, the best explanation for the dual location of this protein is inefficient targeting. Biochemical analysis of leaves of the Aco-1 accession suggested that they exhibited a restricted flux through the Krebs cycle and reduced levels of Krebs cycle intermediates but were characterized by elevated adenylate levels and an enhanced rate of CO₂ assimilation. Furthermore, the analysis of both steady-state metabolite levels and metabolic fluxes revealed that this accession also exhibited elevated rates of photosynthetic Suc synthesis and a corresponding increase in fruit yield. Therefore, we conclude that the Krebs cycle normally competes with the Suc synthetic pathway for carbon but is not essential for the supply of energy to fuel the operation of this pathway.

¹ This work was supported by Max-Planck-Gesellschaft (to F.C. and A.N.-N.), by Conselho Nacional de Desenvolvimento Científìco e Technológico (Brazil; to A.N.-N. and A.R.F.), and by DIP (to A.N.-N. and A.R.F.).

^* Corresponding author; e-mail fernie{at}mpimp-golm.mpg.de; fax 49–0–331–5678408.

Received May 11, 2003; returned for revision May 27, 2003; accepted July 17, 2003.

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