Abstract
The establishment of polarity is a critical process in pathogenic fungi, mediating infection-related morphogenesis and host tissue invasion. Here, we report the identification of TPC1 (Transcription factor for Polarity Control 1), which regulates invasive polarized growth in the rice blast fungus Magnaporthe oryzae. TPC1 encodes a putative transcription factor of the fungal Zn(II)2Cys6 family, exclusive to filamentous fungi. Tpc1-deficient mutants show severe defects in conidiogenesis, infection-associated autophagy, glycogen and lipid metabolism, and plant tissue colonisation. By tracking actin-binding proteins, septin-5 and autophagosome components, we show that Tpc1 regulates cytoskeletal dynamics and infection-associated autophagy during appressorium-mediated plant penetration. We found that Tpc1 interacts with Mst12 and modulates its DNA-binding activity, while Tpc1 nuclear localisation also depends on the MAP kinase Pmk1, consistent with the involvement of Tpc1 in this signalling pathway, which is critical for appressorium development. Importantly, Tpc1 directly regulates NOXD expression, the p22phox subunit of the fungal NADPH oxidase complex via an interaction with Mst12. Tpc1 therefore controls spatial and temporal regulation of cortical F-actin through regulation of the NADPH oxidase complex during appressorium re-polarisation. Consequently, Tpc1 is a core developmental regulator in filamentous fungi, linking the regulated synthesis of reactive oxygen species and the Pmk1 pathway, with polarity control during host invasion.
Highlights
Rice blast disease is one of the most serious diseases of cultivated rice worldwide and is caused by the filamentous, ascomycete fungus Magnaporthe oryzae[1,2]
We identified a gene required for fungal polar growth and virulence in the rice blast fungus Magnaporthe oryzae
The M. oryzae Δtpc1 mutant shows a delay in glycogen and lipid metabolism, and infection-associated autophagy–processes that regulate appressorium-mediated M. oryzae plant infection
Summary
Rice blast disease is one of the most serious diseases of cultivated rice worldwide and is caused by the filamentous, ascomycete fungus Magnaporthe oryzae[1,2]. The disease is initiated when a conidium lands on the rice leaf surface. It germinates to produce a single germ tube that differentiates at its tip to develop a specialised infection structure called an appressorium [3]. A penetration peg emerges from the base of the appressorium and ruptures the leaf cuticle. A toroidal filamentous actin network forms at the base of the appressorium pore, scaffolded by septin GTPases[5]. F-actin ring formation is necessary for penetration peg emergence and re-establishment of polarized growth at the point of plant penetration. Disease symptoms appear between 72h and 96h after initial infection and coalesce into large spreading necrotic lesions from which the fungus sporulates. M. oryzae has the capacity to penetrate roots by means of hyphopodia and can colonize root tissue and spread systemically throughout the plant under laboratory conditions [11,12]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
