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Title: Characterization of temperature and light effects on the defense response phenotypes associated with the maize Rp1-D21 gene

item NEGERI, ADISU - North Carolina State University
item BENAVENTE, LARISSA - US Department Of Agriculture (USDA)
item KIBITI, CROMWELL - Purdue University
item WANG, GUAN-FENG - North Carolina State University
item CHAIKAM, VIJAY - Purdue University
item JOHAL, GURI - Purdue University
item Balint-Kurti, Peter

Submitted to: BMC Plant Biology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 6/1/2013
Publication Date: 7/1/2013
Citation: Negeri, A., Benavente, L., Kibiti, C.M., Wang, G., Chaikam, V., Johal, G., Balint Kurti, P.J. 2013. Characterization of temperature and light effects on the defense response phenotypes associated with the maize Rp1-D21 gene. Biomed Central (BMC) Plant Biology. 13:106.

Interpretive Summary: We are working with a maize autoimmune mutant which has a massive (and rather debilitating) defense response. In this paper we examine the effects of temperature and light on expression of this defense response. It turns out that the response is inhibited by darkness and high temperatures (above 30 ºC). This inhibition is reversible.

Technical Abstract: Rp1 is a complex locus of maize controlling race-specific resistance to the common rust fungus, Puccinia sorghi. The resistance response includes the “Hypersensitive response” (HR) – a rapid 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 the spontaneous activation of the defense response, including HR, 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. In this study we show that the phenotype is also highly dependent on temperature and light, identify significant interactions between the temperature effects and genetic background and outline a procedure for precisely quantifying the effect of genetic background by measuring the kinetics of lesion formation. We show that the inhibition of HR caused by both light and high temperature is entirely reversible. Finally we show that, at temperatures above 30 ºC, the Rp1-D21 phenotype is completely suppressed at both the phenotypic and molecular level.