Fig. 8

A hypothesis about the regulation of stability of sterility in CMS-S. Sterility in CMS-S is the consequence of inability of mitochondrial function to counteract the deleterious effect of orf355. Mitochondrial activity increases in anther tissue to meet the large amount energy required for pollen development, which is a representative example of mitochondrial robustness (indicated by blue arrows). However, mitochondrial activity varies among tissues and even among different cells of the same tissue. In anthers of CMS-Sa, microspores with moderate mitochondrial activity that higher enough to reach the threshold (dotted line) for normal pollen development can revert to being fertile. In CMS-Sb, the loss of one copy of nad1-exon1 reduces the mitochondrial robustness. The mitochondrial activity of all microspores could not reach the threshold required for normal pollen development. This defect may be sufficient to sustain the normal vegetative growth, but is manifested in specific situations such as sterility reversion