AI Article Synopsis

  • Oxidative burst, particularly through hydrogen peroxide (H2O2), is crucial in plant defense against incompatible pathogens.
  • Transgenic rice plants were created to study whether higher H2O2 levels lead to cell death, activation of defense genes, and improved resistance to pathogens.
  • While both constant and induced expressions of a fungal gene (GOX) increased H2O2, the constant expression caused more negative effects on seed viability, suggesting that induced expression may be a better strategy for enhancing disease resistance.

Article Abstract

Oxidative burst, mediated by hydrogen peroxide (H2O2), has been recognized as a key component of plant defense response during an incompatible interaction. To determine if elevated levels of H2O2 lead to cell death, activation of defense genes and enhanced resistance to diverse pathogens, transgenic rice plants expressing a fungal glucose oxidase gene (GOX) were generated using both constitutive and inducible expression systems. Constitutive or wound/pathogen-induced expression of GOX also allowed us to determine the effectiveness of these systems in conferring long lasting resistance to various pathogens. Both constitutive and wound/pathogen-induced expression of GOX lead to increases in the endogenous levels of H2O2, which in turn caused cell death. Elevated levels of H2O2 also activated the expression of several defense genes and these transgenic plants showed enhanced resistance to both bacterial and fungal pathogens. In comparison to inducible expression, constitutive expression of GOX resulted in 3-10-fold higher levels of the GOX transcript and the corresponding enzymatic activity. Such increased levels of GOX, which would result in elevated levels of H2O2, caused improper seed set and decreased seed viability in transgenic plants constitutively expressing GOX. Our results suggest that pathogen inducible expression of heterologous genes may be a practical and robust way of generating broad spectrum disease resistance.

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Source
http://dx.doi.org/10.1023/a:1025896513472DOI Listing

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