1.12.7
GENETIC SEPARATION OF NECROSIS AND RESISTANCE PRESENT IN THE HYPERSENSITIVE RESPONSE OF NICOTIANA EDWARDSONII TO CAULIFLOWER MOSAIC VIRUS

J SCHOELZ, L KIRALY, A COLE and J BOURQUE

University of Missouri, Columbia, USA

Background and objectives
The hypersensitive response (HR) to plant pathogens, including plant viruses, is defined as a resistance response in which the plant pathogen remains localized in necrotic lesions on the inoculated leaf. In general, necrosis and the resistance are closely associated, and considered physiologically and genetically linked phenomena. Here we present evidence which suggests that the HR of Nicotiana edwardsonii to CaMV strain W260 can be genetically separated into resistance and necrosis traits that are derived from two different plant species. N. edwardsonii is a solanaceous plant that originated from a cross between Nicotiana glutinosa and Nicotiana clevelandii [1]. N. glutinosa is resistant to W260, but reacts with localized chlorotic lesions rather than necrotic lesions. In contrast, N. clevelandii can be systemically infected by W260. A mixture of necrotic and chlorotic lesions appear in N. clevelandii leaves inoculated with W260, while a systemic necrosis symptom develops in upper, non-inoculated leaves. In this paper, we have identified which gene of W260 is responsible for elicitation of HR in N. edwardsonii and systemic necrosis in N. clevelandii. In addition, we present evidence that the resistance and necrosis that comprise the HR of N. edwardsonii to W260 infection can be genetically separated; resistance to W260 is derived from N. glutinosa, while the necrosis trait may be contributed by N. clevelandii.

Results and discussion
To identify the viral genes that elicit HR in N. edwardsonii and systemic necrosis in N. clevelandii, chimaeric viruses were constructed using CaMV strains W260 and D4. The D4 virus was chosen because it does not induce necrosis in either host. Instead, both N. edwardsonii and N. clevelandii develop a systemic mosaic in response to D4 infection. The chimaeric viruses constructed between D4 and W260 revealed that W260 gene VI was responsible for eliciting both HR and the systemic necrosis symptom.

To determine whether the HR of N. edwardsonii could be separated into resistance and necrosis components, two types of experiments were conducted. First, we reconstituted N. edwardsonii by crossing N. glutinosa with N. clevelandii and then determined the reaction of F1 progeny to infection with CaMV strain W260. The F1 plants developed lesions that were similar to those of N. clevelandii, indicating that N. clevelandii had contributed a necrosis trait in the cross.

In the second type of experiments, we crossed N. edwardsonii with N. bigelovii and N. clevelandii to see if the HR of N. edwardsonii could be modified. N. bigelovii was chosen because it reacts to W260 infection with chlorotic local lesions and a systemic mosaic. The F1 plants derived from a cross between N. edwardsonii and N. clevelandii reacted to W260 infection with a hypersensitive response. This might be predicted if both N. edwardsonii and N. clevelandii are homozygous for the necrosis trait. In contrast, the F1 plants derived from a cross between N. edwardsonii and N. bigelovii developed local chlorotic lesions in response to W260, but the plants remained resistant to systemic infection by W260. This experiment indicated that the development of necrosis present in the HR of N. edwardsonii can be suppressed, although the plants can still resist infection by CaMV strain W260.

References
1. Christie SR, 1969. Plant Disease Reporter 53, 939-941.