4.6 Article

Rice Snl6, a Cinnamoyl-CoA Reductase-Like Gene Family Member, Is Required for NH1-Mediated Immunity to Xanthomonas oryzae pv. oryzae

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PLOS GENETICS
卷 6, 期 9, 页码 -

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PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pgen.1001123

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资金

  1. William G. and Kathleen Golden International Agriculture Fellowship
  2. UC Davis Consortium for Women
  3. D. Marlin Brandon Fellowship
  4. Henry A. Jastro and Peter J. Shields Graduate Research Scholarship
  5. NIH [2-R01-GM055962-09]
  6. DOE [DE-AC02-05CH11231]
  7. USDA [2004-63560416640]
  8. U. S. Department of Energy, Office of Science, Office of Biological and Environmental Research [DE-AC02-05CH11231]
  9. Lawrence Berkeley National Laboratory
  10. U. S. Department of Energy

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Rice NH1 (NPR1 homolog 1) is a key mediator of innate immunity. In both plants and animals, the innate immune response is often accompanied by rapid cell death at the site of pathogen infection. Over-expression of NH1 in rice results in resistance to the bacterial pathogen, Xanthomonas oryzae pv. oryzae (Xoo), constitutive expression of defense related genes and enhanced benzothiadiazole (BTH)- mediated cell death. Here we describe a forward genetic screen that identified a suppressor of NH1-mediated lesion formation and resistance, snl6. Comparative genome hybridization and fine mapping rapidly identified the genomic location of the Snl6 gene. Snl6 is a member of the cinnamoyl-CoA reductase (CCR)-like gene family. We show that Snl6 is required for NH1-mediated resistance to Xoo. Further, we show that Snl6 is required for pathogenesis-related gene expression. In contrast to previously described CCR family members, disruption of Snl6 does not result in an obvious morphologic phenotype. Snl6 mutants have reduced lignin content and increased sugar extractability, an important trait for the production of cellulosic biofuels. These results suggest the existence of a conserved group of CCR-like genes involved in the defense response, and with the potential to alter lignin content without affecting development.

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