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A novel gene, phcA from Pseudomonas syringae induces programmed cell death in the filamentous fungus Neurospora crassa
Author(s) -
Wichmann Gale,
Sun Jianping,
Dementhon Karine,
Glass N. Louise,
Lindow Steven E.
Publication year - 2008
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/j.1365-2958.2008.06175.x
Subject(s) - pseudomonas syringae , biology , neurospora crassa , crassa , microbiology and biotechnology , fungal protein , hypha , botany , gene , genetics , peptide sequence , pathogen , mutant
Summary The phytopathogen Pseudomonas syringae competes with other epiphytic organisms, such as filamentous fungi, for resources. Here we characterize a gene in P. syringae pv. syringae B728a and P. syringae pv. tomato DC3000, termed phcA , that has homology to a filamentous fungal gene called het‐c . phcA is conserved in many P. syringae strains, but is absent in one of the major clades, which includes the P. syringae pathovar phaseolicola. In the filamentous fungus Neurospora crassa , HET‐C regulates a conserved programmed cell death pathway called heterokaryon incompatibility (HI). Ectopic expression of phcA in N. crassa induced HI and cell death that was dependent on the presence of a functional het‐c pin‐c haplotype. Further, by co‐immunoprecipitation experiments, a heterocomplex between N. crassa HET‐C1 and PhcA was associated with phcA‐ induced HI . P. syringae was able to attach and extensively colonize N. crassa hyphae, while an Escherichia coli control showed no association with the fungus. We further show that the P. syringae is able to use N. crassa as a sole nutrient source. Our results suggest that P. syringae has the potential to utilize phcA to acquire nutrients from fungi in nutrient‐limited environments like the phyllosphere by the novel mechanism of HI induction.