Score: 1.00 | Title: The tig1 histone deacetylase complex regulates infectious growth in the rice blast fungus Magnaporthe oryzae .
| Author: Ding SL Liu W Iliuk A Ribot C Vallet J Tao A Wang Y Lebrun MH Xu JR | Journal: Plant Cell Citation: V : 22 P : 2495-508 Year: 2010 Type: MEDLINE | Literature: oryza Field: abstract Doc ID: pub20675574 Accession (PMID): 20675574 | Abstract: Magnaporthe oryzae is the most damaging fungal pathogen of rice ( Oryza sativa ) .
In this study , we characterized the TIG1 transducin beta-like gene required for infectious growth and its interacting genes that are required for plant infection in this model phytopathogenic fungus .
Tig1 homologs in yeast and mammalian cells are part of a conserved histone deacetylase ( HDAC ) transcriptional corepressor complex The tig1 deletion mutant was nonpathogenic and defective in conidiogenesis .
It had an increased sensitivity to oxidative stress and failed to develop invasive hyphae in plant cells .
Using affinity purification and coimmunoprecipitation assays , we identified several Tig1-associated proteins , including two HDACs that are homologous to components of the yeast Set3 complex Functional analyses revealed that TIG1 , SET3 , SNT1 , and HOS2 were core components of the Tig1 complex in M oryzae .
The set3 , snt1 , and hos2 deletion mutants displayed similar defects as those observed in the tig1 mutant , but deletion of HST1 or HOS4 had no detectable phenotypes .
Deletion of any of these core components of the Tig1 complex resulted in a significant reduction in HDAC activities .
Our results showed that TIG1 , like its putative yeast and mammalian orthologs , is one component of a conserved HDAC complex that is required for infectious growth and conidiogenesis in M oryzae and highlighted that chromatin modification is an essential regulatory mechanism during plant infection .
| Matching Sentences: [ Sen. 6, subscore: 1.00 ]: The set3 , snt1 , and hos2 deletion mutants displayed similar defects as those observed in the tig1 mutant , but deletion of HST1 or HOS4 had no detectable phenotypes .
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