Characterization of temperature and light effects on the defense response phenotypes associated with the maize Rp1-D21autoactive resistance gene

Abstract

BackgroundRp1 is a complex locus of maize, which carries a set of genes controlling race-specific resistance to the common rust fungus, Puccinia sorghi. The resistance response includes the “Hypersensitive response” (HR), a rapid response triggered by a pathogen recognition event that includes localized cell death at the point of pathogen penetration and the induction of pathogenesis associated genes. The Rp1-D21gene is an autoactive allelic variant at the Rp1 locus, causing spontaneous activation of the HR response, in the absence of pathogenesis. Previously we have shown that the severity of the phenotype conferred by Rp1-D21 is highly dependent on genetic background.ResultsIn this study we show that the phenotype conferred by Rp1-D21 is highly dependent on temperature, with lower temperatures favoring the expression of the HR lesion phenotype. This temperature effect was observed in all the 14 genetic backgrounds tested. Significant interactions between the temperature effects and genetic background were observed. When plants were grown at temperatures above 30°C, the spontaneous HR phenotype conferred by Rp1-D21 was entirely suppressed. Furthermore, this phenotype could be restored or suppressed by alternately reducing and increasing the temperature appropriately. Light was also required for the expression of this phenotype. By examining the expression of genes associated with the defense response we showed that, at temperatures above 30°C, the Rp1-D21 phenotype was suppressed at both the phenotypic and molecular level.ConclusionsWe have shown that the lesion phenotype conferred by maize autoactive resistance gene Rp1-D21 is temperature sensitive in a reversible manner, that the temperature-sensitivity phenotype interacts with genetic background and that the phenotype is light sensitive. This is the first detailed demonstration of this phenomenon in monocots and also the first demonstration of the interaction of this effect with genetic background. The use of temperature shifts to induce a massive and synchronous HR in plants carrying the Rp1-D21 genes will be valuable in identifying components of the defense response pathway.

The Genetics of Leaf Flecking in Maize and Its Relationship to Plant Defense and Disease Resistance

“…Les mutants in several species require light for the initiation and/or propagation of lesions (Buckner et al, 2000;Negeri et al, 2013). We show here that flecking, at least in some lines, also is light responsive (Fig.…”

“…Light modulates the severity of various Les mutants (Gray et al, 2002;Penning et al, 2004;Negeri et al, 2013). To establish if variation in light intensity had an effect on the severity of flecking, moderately, mild, and nonflecking lines (Mo17, Ki11, and NC250, respectively) were grown under low light intensity (0.09-0.12 mE m 22 s 21 ) in the greenhouse until 4 weeks old (lowlight treatment).…”

The Chloroplastic Protein THF1 Interacts with the Coiled-Coil Domain of the Disease Resistance Protein N′ and Regulates Light-Dependent Cell Death

“…Taken together, these findings suggest that THF1 is a critical hub for the control of programmed cell death in leaves exposed to light. Although I2-like proteins are unique to Solanaceae, given that light is often required for the HR (Chandra-Shekara et al, 2006;Negeri et al, 2013), it will be interesting to determine if additional NB-LRR proteins can interfere with the stability of THF1 to promote light-dependent cell death.…”

Maize Homologs of CCoAOMT and HCT, Two Key Enzymes in Lignin Biosynthesis, Form Complexes with the NLR Rp1 Protein to Modulate the Defense Response

“…Several other hallmarks of the pathogen-induced defense response are also associated with Rp1-D21-mediated HR phenotype in maize, including high accumulation of H 2 O 2 and increased expression of defense-related genes (Chintamanani et al, 2010). The Rp1-D21 HR lesion phenotype is influenced by light, temperature, and genetic background (Chintamanani et al, 2010;Negeri et al, 2013).…”