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Compromising early salicylic acid accumulation delays the hypersensitive response and increases viral dispersal during lesion establishment in TMV‐infected tobacco
Author(s) -
Mur Luis A.J.,
Bi YongMei,
Darby Robert M.,
Firek Simon,
Draper John
Publication year - 1997
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1046/j.1365-313x.1997.12051113.x
Subject(s) - tobacco mosaic virus , lesion , salicylic acid , biology , hypersensitive response , microbiology and biotechnology , phenotype , gene , virus , virology , programmed cell death , apoptosis , biochemistry , medicine , pathology
Summary To investigate the role of salicylic acid (SA) in the hypersensitive response (HR) its accumulation was compromised during different phases of lesion development by differential expression of a salicylate hydroxylase gene (SH‐L). Constitutive suppression of SA accumulation was achieved by expression of a gene fusion between the CaMV35S promoter (35S) and SH‐L. Using the H 2 O 2 ‐responsive AoPR1 promoter to drive SH‐L SA accumulation could be compromised at an early stage, on lesion formation and possibly prior to visible necrosis, whilst use of the salicylate‐responsive PR1a promoter reduced SA accumulation at a later stage as lesions expand. TMV infection of 35S‐SH‐L and AoPR1‐SH‐L, but not PR1a‐SH‐L, tobacco resulted in significantly greater rates of lesion growth than in wild‐type tobacco. TMV was detected in asymptomatic tissue surrounding lesions only in 35S‐SH‐L and AoPR1‐SH‐L lines; subsequently these transgenic lines exhibited a ‘spreading‐necrosis’ originating from the lesion which entered the stem and eventually other leaves, a phenotype which could be correlated with the presence of TMV particles. Analysis of TMV‐infected and ‘temperature‐shifted’ tobacco indicated that both 35S‐SH‐L and AoPR1‐SH‐L, but not PR1a‐SH‐L, transgenics exhibited delayed cell‐death compared to wild‐type infections. We propose that the SH‐L phenotypes indicate that early SA accumulation is a major factor in preventing viral escape, via mechanism(s) which may include influencing the rate of host‐cell death and, possibly, an effect on viral function.