Methylation is involved in the Ustilago maydis mating response.
Methionine auxotrophs of Ustilago maydis were deficient in mating; unlike wild-type cells, they neither induced nor produced normal mating filaments in the presence of compatible cells. The deficiency was most severe when cells were located some distance apart, but when in direct contact with compatible cells methionine auxotrophs mated and infected plants fairly normally. The mating deficiency was genetically linked to the methionine auxotrophy, segregating with it through in planta crosses. Wild-type cells exposed to the methyltransferase inhibitors ethionine and homocysteine thiolactone were similarly impaired in mating. Exogenous methionine, S-adenosylmethionine (SAM), synthetic mating pheromone, or cAMP all compensated for the mating impairment of the auxotrophs to some extent. Although SAM-dependent methylation could influence activities of various molecules in diverse pathways, these observations indicate that the most likely cause of the mating deficiency in met(-) cells is failure to methylate a component of the U. maydis pheromone signal transduction pathway.