Journal
PLOS ONE
Volume 13, Issue 3, Pages -Publisher
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0193458
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Funding
- National Natural Science Foundation of China [31600986]
- Li Dak Sum Yip Yio Chin Kenneth Li Marine Biopharmaceutical Development Fund
- National 111 Project of China
- K. C. Wong Magna Fund in Ningbo University
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The Mediator complex is at the core of transcriptional regulation and plays a central role in plant immunity. The MEDIATOR25 (MED25) subunit of Arabidopsis thaliana regulates jasmonate-dependent resistance to Botrytis cinerea through interacting with the basic helixloop-helix (bHLH) transcription factor of jasmonate signaling, MYC2. Another Mediator subunit, MED8, acts independently or together with MED25 in plant immunity. However, unlike MED25, the underlying action mechanisms of MED8 in regulating B. cinerea resistance are still unknown. Here, we demonstrated that MED8 regulated plant immunity to B. cinerea through interacting with another bHLH transcription factor, FAMA, which was previously shown to control the final proliferation/differentiation switch during stomatal development. Our research demonstrates that FAMA is also an essential component of B. cinerea resistance. The fama loss-of-function mutants (fama-1 and fama-2) increased susceptibility to B. cinerea infection and reduced defense-gene expression. On the contrary, transgenic lines constitutively overexpressing FAMA showed opposite B. cinerea responses compared with the fama loss-of-function mutants. FAMA-overexpressed plants displayed enhanced resistance to B. cinerea infection and increased expression levels of defensin genes following B. cinerea treatment. Genetic analysis of MED8 and FAMA suggested that FAMA-regulated pathogen resistance was dependent on MED8. In addition, MED8 and FAMA were both associated with the G-box region in the promoter of ORA59. Our findings indicate that the MED8 subunit of the A. thaliana Mediator regulates plant immunity to B. cinerea through interacting with the transcription factor FAMA, which was discovered to be a key component in B. cinerea resistance.
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