A connection between leaf tumor formation and nuclear status

The infectious form of U. maydis are dikaryotic hyphae that arise after mating of compatible haploid strains. At late stages of colonization, plant tumor are induced and dikaryotic nuclei fuse, followed by massive proliferation, hyphal aggregation and spore production. We have now demonstrated that mutants lacking the nlt1 transcription factor which is required for leaf tumor induction colonize plants efficiently but fail to undergo karyogamy and are attenuated in late proliferation. qRT-PCR revealed that Nlt1 either directly or indirectly represses see1, encoding an effector previously shown to contribute to leaf tumor induction and at the same time activates transcription of the ros1gene which encodes a transcription factor controlling karyogamy. In actively dividing maize organs nlt1 mutants undergo karyogamy and induce tumor formation. Surprisingly, when nlt1 is deleted in mononuclate solopathogenic strains, such mutants are able to induce leaf tumor formation, albeit less efficiently than respective wild type strains. We also show that Sporisorium reilianum, a smut fungus unable to induce leaf tumors, possesses an ortholog of nlt1 that controls the fusion of dikaryotic nuclei late in infection during cob colonization. These results have established a regulatory connection between nlt1, ros1 and see1 and suggest the existence of two stages contributing to leaf tumor formation, one prior to nuclear fusion and involving nlt1 and one post karyogamy that is nlt1 independent.

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