Many fungi that cause diseases in plants need specialized structures to penetrate the plant’s tissues. To form these structures, the fungus must carefully control when and where its cells divide. As in other organisms, the sequence of events that lead to a fungal cell dividing in two are known as the cell cycle. Progress through the distinct steps in the cell cycle is regulated by enzymes including many that add or remove phosphate groups on other proteins. It remains unclear which regulatory enzymes allow any plant-infecting fungus to control its cell cycle when it forms an infection structure, but one fungus that could help answer this question is Ustilago maydis, the cause of a disease known as corn smut.
The corn smut fungus forms infection structures after two different mating strains meet on the surface of the plant, stop dividing and then fuse. This implies that the cell cycles of both strains need to be coordinated to allow the fungus to infect the plant. The two strains recognize each other via chemical signals known as pheromones, and Bardetti et al. now show that pheromone recognition in the corn smut fungus results in an enzyme called Cdc25 being disabled, which in turn causes cell division to stop. Cdc25 is a phosphatase, meaning it removes phosphate groups from cell cycle regulators that are found in the nucleus of the cell. Specifically, Cdc25 targets phosphate groups that would otherwise inhibit the activity of these proteins. Further experiments showed that, following pheromone recognition, Cdc25 is disabled via a two-step process: first it is prevented from entering the nucleus which keeps it away from its targets, and then it is degraded. Bardetti et al. went on to show that this last step was required for the fungus to infect corn plants, since interfering with the breakdown of Cdc25 impairs its ability to stop the cell cycle and form an infection structure.
Entry into plant tissue is a critical step for any parasites looking to invade a plant. Since it is difficult to reach the interior of plants with pesticides, most antimicrobial treatments in plants aim at prevention rather than cure. This means that increasing the delay between a fungus recognizing the surface of a plant and penetrating its tissues could give more time to prevent infections. These new findings represent a step towards achieving that goal, though more research is needed to better understand the molecular mechanisms required for the formation of infection structures in plant-infecting fungi.