期刊
NEW PHYTOLOGIST
卷 236, 期 4, 页码 1455-1470出版社
WILEY
DOI: 10.1111/nph.18315
关键词
auxin; biotrophic interaction; effector; gall; maize; smut fungi; Topless; Ustilago maydis
资金
- European Research Council [335691]
- Austrian Science Fund [P27818-B22, I 3033-B22]
- Austrian Academy of Sciences
- Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) [EXC-2070-390732324]
- DFG [DJ 64/5-1]
- Projekt DEAL
- European Research Council (ERC) [335691] Funding Source: European Research Council (ERC)
Plant biotrophic pathogens suppress the host immune system and manipulate the host's metabolism and development by secreting effectors. In this study, a set of effectors from the pathogenic fungus Ustilago maydis were found to induce auxin signaling in plants, and their interaction with corepressors of the TPL family was elucidated.
Plant biotrophic pathogens employ secreted molecules, called effectors, to suppress the host immune system and redirect the host's metabolism and development in their favour. Putative effectors of the gall-inducing maize pathogenic fungus Ustilago maydis were analysed for their ability to induce auxin signalling in plants. Using genetic, biochemical, cell-biological, and bioinformatic approaches we functionally elucidate a set of five, genetically linked effectors, called Topless (TPL) interacting protein (Tips) effectors that induce auxin signalling. We show that Tips induce auxin signalling by interfering with central corepressors of the TPL family. CRISPR-Cas9 mutants and deletion strain analysis indicate that the auxin signalling inducing subcluster effectors plays a redundant role in virulence. Although none of the Tips seem to have a conserved interaction motif, four of them bind solely to the N-terminal TPL domain and, for Tip1 and Tip4, we demonstrate direct competition with auxin/indole-3-acetic acid transcriptional repressors for their binding to TPL class of corepressors. Our findings reveal that TPL proteins, key regulators of growth-defence antagonism, are a major target of the U. maydis effectome.
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