Necrotic Lesion Resistance Induced by Peronospora tabacina on Leaves of Nicotiana obtusifolia

Abstract

Infection of Nicotiana obtusifolia plant introduction (PI) #555573 by the downy mildew pathogen Peronospora tabacina resulted in a compatible interaction, in which P. tabacina penetrated and freely colonized host leaf tissue. This interaction became incompatible 5 to 6 days later, with the appearance of necrotic lesions (NLs) and inhibition of pathogen growth and subsequent sporulation. NL development depended upon the presence of P. tabacina in host tissue, was not due to the effects of other microbes, and occurred co-incident in time with the pathogen's ability to produce asexual sporangia on a susceptible N. obtusifolia genotype. Inhibition of the necrotic response by CoCl(2) (a calcium channel blocker) and pathogen-induced transcription of a defense-related gene (PR-1a) suggested that necrosis was due to hypersensitive cell death in the host. In contrast, N. obtusifolia PI#555543 did not exhibit hypersensitivity upon infection by P. tabacina, but rather developed characteristic symptoms of tobacco blue mold disease: chlorotic lesions accompanied by abundant pathogen sporulation. Disease reactions scored on PI#555573 x PI#555543 F(2) progeny inoculated with P. tabacina sporangia indicated that the resistance phenotype was due to the action of a single gene from N. obtusifolia PI#555573, which we have named Rpt1. To date, Rpt1 is the only gene known to confer a hypersensitive response (HR) to P. tabacina infection in any species of Nicotiana. A survey of wild N. obtusifolia revealed that the HR to P. tabacina was expressed in the progeny of 7 of 21 (33%) plants collected in southern Arizona, but not in the progeny of plants originating from Death Valley National Park in California and the Big Bend National Park in west Texas.

Expression of the tobacco β-1,3-glucanase gene, PR-2d, following induction of SAR with Peronospora tabacina

“…Cultivated tobacco is highly susceptible to P. tabacina and no known R-gene resistance is available in commercially desirable cultivars [14]. The leaf is a natural site of infection by air-borne sporangia (asexual spores) of the pathogen, resulting in the production of chlorotic lesions from which emerge huge numbers of sporangia [2,29].…”

Genetic Dissection of Disease Resistance to the Blue Mold Pathogen, Peronospora tabacina, in Tobacco

“…This resistance is conferred by a single, dominant gene named NlRPT [36,37]. Incompatible interactions with P. tabacina have also been identified in N. obtusifolia genotypes expressing HR caused by a single, partially dominant gene known as Rpt1 [38]. Although several sources of genetic resistance to P. tabacina are available, we cannot predict whether the genetic effects mediated by these genes will be intact after transfer to tobacco by hybridization.…”

Overexpression of the Synthetic Chimeric Native-T-phylloplanin-GFP Genes Optimized for Monocot and Dicot Plants Renders Enhanced Resistance to Blue Mold Disease in Tobacco (N. tabacumL.)

“…The pathogen was maintained by weekly serial passage on N. tabacum cv. KY 14 plants (7–12-week-old) as described earlier [33]. A water suspension containing fresh sporangiospores of KY79 (10 5 sporangiospores/mL) was used for challenge inoculations by drop inoculation as described earlier [1].…”