TY - JOUR
T1 - Appressorium-mediated plant infection by Magnaporthe oryzae is regulated by a Pmk1-dependent hierarchical transcriptional network
AU - Osés-Ruiz, Míriam
AU - Cruz Mireles, Neftaly
AU - Martin-Urdiroz, Magdalena
AU - Soanes, Darren M.
AU - Bisola Eseola, Alice
AU - Tang, Bozeng
AU - Derbyshire, Paul
AU - Nielsen, Mathias
AU - Cheema, Jitender
AU - Were, Vincent
AU - Eisermann, Iris
AU - Kershaw, Michael J.
AU - Yan, Xia
AU - Valdovinos-Ponce, Guadalupe
AU - Molinari, Camilla
AU - Littlejohn, George R.
AU - Valent, Barbara
AU - Menke, Frank L. H.
AU - Talbot, Nicholas J.
N1 - Acknowledgements:
This project was supported by a European Research Council Advanced Investigator award (to N.J.T.) under the European Union’s Seventh Framework Programme FP7/2007-2013/ERC Grant Agreement 294702 GENBLAST, BBSRC grant BB/N009959/1, and by the Gatsby Charitable Foundation.
We thank D. MacLean for help with statistical analysis and C. Dean (John Innes Centre) for her group’s guidance with the ChIP–seq analysis.
PY - 2021/11
Y1 - 2021/11
N2 - Rice blast is a devastating disease caused by the fungal pathogen Magnaporthe oryzae that threatens rice production around the world. The fungus produces a specialized infection cell, called the appressorium, that enables penetration through the plant cell wall in response to surface signals from the rice leaf. The underlying biology of plant infection, including the regulation of appressorium formation, is not completely understood. Here we report the identification of a network of temporally coregulated transcription factors that act downstream of the Pmk1 mitogen-activated protein kinase pathway to regulate gene expression during appressorium-mediated plant infection. We show that this tiered regulatory mechanism involves Pmk1-dependent phosphorylation of the Hox7 homeobox transcription factor, which regulates genes associated with induction of major physiological changes required for appressorium development—including cell-cycle control, autophagic cell death, turgor generation and melanin biosynthesis—as well as controlling a additional set of virulence-associated transcription factor–encoding genes. Pmk1-dependent phosphorylation of Mst12 then regulates gene functions involved in septin-dependent cytoskeletal re-organization, polarized exocytosis and effector gene expression, which are necessary for plant tissue invasion. Identification of this regulatory cascade provides new potential targets for disease intervention.
AB - Rice blast is a devastating disease caused by the fungal pathogen Magnaporthe oryzae that threatens rice production around the world. The fungus produces a specialized infection cell, called the appressorium, that enables penetration through the plant cell wall in response to surface signals from the rice leaf. The underlying biology of plant infection, including the regulation of appressorium formation, is not completely understood. Here we report the identification of a network of temporally coregulated transcription factors that act downstream of the Pmk1 mitogen-activated protein kinase pathway to regulate gene expression during appressorium-mediated plant infection. We show that this tiered regulatory mechanism involves Pmk1-dependent phosphorylation of the Hox7 homeobox transcription factor, which regulates genes associated with induction of major physiological changes required for appressorium development—including cell-cycle control, autophagic cell death, turgor generation and melanin biosynthesis—as well as controlling a additional set of virulence-associated transcription factor–encoding genes. Pmk1-dependent phosphorylation of Mst12 then regulates gene functions involved in septin-dependent cytoskeletal re-organization, polarized exocytosis and effector gene expression, which are necessary for plant tissue invasion. Identification of this regulatory cascade provides new potential targets for disease intervention.
UR - http://www.scopus.com/inward/record.url?scp=85117921614&partnerID=8YFLogxK
U2 - 10.1038/s41564-021-00978-w
DO - 10.1038/s41564-021-00978-w
M3 - Article
VL - 6
SP - 1383
EP - 1397
JO - Nature Microbiology
JF - Nature Microbiology
SN - 2058-5276
IS - 11
ER -