Figure 1.

Infected cell with a differentiated bacteroid in an indeterminate nodule. Nitrogenase reduces di-nitrogen (N₂) into ammonia (NH₃) in the inner space of the bacteroid (high pH), which is then protonated into ammonium (NH₄⁺) in the symbiosome space (low pH). Leghemoglobin (Lb) transports O₂ to the bacteroid cytochrome (Cyt) of the electron transport chain (ETC). Sucrose is downloaded in the cytoplasm, where it is transformed by glycolysis pathways (PEPC-MDH) into malate, the main source of carbon skeletons for N transport out of the nodule and reductant power for driving N₂ fixation. Malate is transported by dicarboxylate transport (Dct and DctA), either placed in the peribacteroid membrane (PBM) or the bacteroid membrane. A cation channel permeable to NH₄⁺ has been proposed as exporting NH₄⁺ across the PBM [69]. NH₄⁺ is transformed into asparagine (Asn) through the GS-GOGAT pathway using oxaloacetate (OAA) as a substrate. Asn is most likely involved in a negative feedback regulation of N₂ fixation. Part of the CO₂ from the tricarboxylic acid (TCA) cycle is recycled by the phosphoenolpyruvate carboxylase (PEPC). Nodule-specific cysteine-rich (NCR) peptides drive the final transformation of bacteria into a bacteroid by a recognition protein system (BacA) located in the bacteroid membrane. Figure adapted from: Fischinger [70], Oldroyd et al. [67], Udvardi and Poole [63], and Sulieman and Tran [20].