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The DNA damage response signaling cascade regulates proliferation of the phytopathogenic fungus Ustilago maydis in planta.

TitleThe DNA damage response signaling cascade regulates proliferation of the phytopathogenic fungus Ustilago maydis in planta.
Publication TypeJournal Article
Year of Publication2011
Authorsde Sena-Tomás C, Fernández-Álvarez A, Holloman WK, Pérez-Martín J
JournalPlant Cell
Volume23
Issue4
Pagination1654-65
Date Published2011 Apr
ISSN1532-298X
KeywordsCell Cycle, Cell Nucleus, DNA Damage, Enzyme Activation, Fungal Proteins, Models, Biological, Phosphorylation, Protein Kinases, Signal Transduction, Ustilago, Virulence, Zea mays
Abstract

In the phytopathogenic fungus Ustilago maydis, the dikaryotic state dominates the period of growth occurring during the infectious phase. Dikaryons are cells in which two nuclei, one from each parent cell, share a single cytoplasm for a period of time without undergoing nuclear fusion. In fungal cells, maintenance of the dikaryotic state requires an intricate cell division process that often involves the formation of a structure known as the clamp connection as well as the sorting of one of the nuclei to this structure to ensure that each daughter dikaryon inherits a balance of each parental genome. Here, we describe an atypical role of the DNA damage checkpoint kinases Chk1 and Atr1 during pathogenic growth of U. maydis. We found that Chk1 and Atr1 collaborate to control cell cycle arrest during the induction of the virulence program in U. maydis and that Chk1 and Atr1 work together to control the dikaryon formation. These findings uncover a link between a widely conserved signaling cascade and the virulence program in a phytopathogen. We propose a model in which adjustment of the cell cycle by the Atr1-Chk1 axis controls fidelity in dikaryon formation. Therefore, Chk1 and Atr1 emerge as critical cell type regulators in addition to their roles in the DNA damage response.

DOI10.1105/tpc.110.082552
Alternate JournalPlant Cell
PubMed ID21478441
PubMed Central IDPMC3101559
Grant ListGM042482 / GM / NIGMS NIH HHS / United States
R01 GM042482 / GM / NIGMS NIH HHS / United States

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