A REEVALUATION OF THE ROLE OF THE INFECTED CELL IN THE CONTROL OF O-2DIFFUSION IN LEGUME NODULES

Two different simulation models were constructed to describe O-2 diffu sion into the bacteria-infected cells of legume nodules: one based on a central zone of uniform spherical cells and the other on a central z one of packed, uniform cubical cells with air spaces along the edges. The cubical model more closely approximated the geometry and gas diffu sion characteristics of infected cells than did the spherical model. T he models relied on set values for the innermost O-2 concentration in the infected cell (1-20 nM) and predicted values for the free O-2 and oxygenated leghemoglobin gradients toward the cell:space interface. Th e cubical model but not the spherical model predicted saturation of le ghemoglobin (Lb) oxygenation at or within a few micrometers of the gas -filled intercellular space and predicted that the space concentration could be as high as 1.3% O-2 when the fractional oxygenation of Lb an d respiration rate within the infected cell were typical of that which has been measured in vivo. In the model, the higher the space O-2 con centration, the greater the saturation of Lb by O-2 and the greater th e collapse of Lb-facilitated diffusion near the cell:space interface. This was predicted to result in a greater resistance to O-2 diffusion from the space to the bacteroids, thereby providing an intrinsic, home ostatic mechanism for controlling the rate of O-2 influx into infected cells. Changes in the physiological features of the simulated cubical infected cell, such as the proportion of the cell as cytosol, the sur face area of the cell exposed to a space, the maximum rate of cellular respiration, or the concentration of Lb in the cytoplasm, significant ly altered the extent to which the infected cell would be able to regu late its diffusive resistance. These results demonstrate the possibili ty of a Lb-based mechanism for controlling the O-2 concentration withi n the infected cells. If such a mechanism exists in legume nodules, it would give the infected cell an ability to exercise fine control over its internal environment, a process that could complement a physical diffusion barrier that may exist in the inner cortex or elsewhere in t he nodule and provide coarse control over O-2 diffusion.