| dc.description.abstract | Magnaporthe oryzae infects grass-family plants, such as barley and rice, by applying a special structure called the appressorium. A strain lacking the transcription factor BIP1 does not form infectious hyphae from mature appressoria and loses pathogenicity. Four of the BIP1-regulated genes are predicted to encode G-proteincoupled-receptor (GPCR)-like products, which may have potential functions in transducing environmental signals. One of the four genes, plg1 (pth11-like gene 1) is crucial for appressorium differentiation and melanization in response to hydrophobic surface cues, while deletion mutants of plg2 or plg3, and plg4 do not affect pathogenicity or appressorium formation on hydrophobic surfaces. The predicted structure of PLG1 is a novel transmembrane protein with a predicted membrane topology similar to that predicted for PTH11. The different effects of exogenous cAMP and DAG on pathogenicity of ∆plg1 spores on plants indicate that the cAMP- and DAG-dependent signaling pathways have different functions during appressorium development. As with wild-type spores on a hydrophilic surface, treatment of ∆pth11 spores with cAMP induced appressorium development, although higher concentrations of cAMP were needed for induction of ∆pth11 spores than for wild-type spores. In contrast, treatment of ∆plg1 spores with cAMP did not induce appressorium development. DAG treatment of Δplg1 or Δpth11 spores inoculated on a hydrophilic surface did not induce appressorium development, while DAG treatment induced appressorium development by wild-type spores. When both cAMP and DAG were added to Δplg1 or Δpth11 spores, they all showed increased appressorium formation. The reason why melanized appressoria of Δbip1 did not infect plants was investigated through cytorrhysis assay. Δbip1 and wildtype appressoria collapsed in response to treatment with similar concentrations of glycerol indicating that Δbip1 appressoria have normal turgor pressure. The failure of plant infection may be caused by disruption of the pore ring in appressoria. The addition of exogenous cAMP was not able to restore the formation of penetration pegs, indicating that the cAMP signaling pathway was not related to BIP1 regulation. | en |
