HOMOLOGY-DEPENDENT RESISTANCE - TRANSGENIC VIRUS-RESISTANCE IN PLANTSRELATED TO HOMOLOGY-DEPENDENT GENE SILENCING

Citation
E. Mueller et al., HOMOLOGY-DEPENDENT RESISTANCE - TRANSGENIC VIRUS-RESISTANCE IN PLANTSRELATED TO HOMOLOGY-DEPENDENT GENE SILENCING, Plant journal, 7(6), 1995, pp. 1001-1013
Citations number
53
Categorie Soggetti
Plant Sciences",Biology
Journal title
ISSN journal
09607412
Volume
7
Issue
6
Year of publication
1995
Pages
1001 - 1013
Database
ISI
SICI code
0960-7412(1995)7:6<1001:HR-TVI>2.0.ZU;2-4
Abstract
Tobacco plants transformed with the RNA polymerase (RdRp) gene of pota to virus X (PVX) that are extremely resistant to infection by potato v irus X have previously been described. The PVX-resistant plants accumu lated the RdRp protein at a lower level than fully susceptible plants transformed with the same RdRp construct. In this paper the difference between the PVX-resistant and susceptible transformed plants is inves tigated and it is demonstrated that there are three associated phenoty pes of the RdRp transgene that vary in parallel between transformed li nes. These phenotypes are: accumulation of the transgenic RdRp RNA at a low level; strain-specific resistance to PVX; and the ability of the transgene to trans-inactivate homologous transgenes. This gene-silenc ing potential of the transgenes conferring PVX resistance was illustra ted by analysis of progeny from a cross between a transformant that wa s extremely resistant to PVX and a second PVX-susceptible transformant . In other transformants, in which the resistance was less extreme, th e same three phenotypes were associated but in a transgene dosage-depe ndent manner. The same association of strain-specific resistance and l ow-level accumulation of the transgenic RdRp RNA was observed with pla nts that were transformed with mutant or wild-type versions of the RdR p gene. Strain-specific resistance was also produced in plants transfo rmed with untranslatable versions of the RdRp transgene. Based on thes e data it is proposed that homology-dependent gene silencing and trans genic resistance to PVX may be due to the same RNA-based mechanism. An undefined genomic feature is proposed to account for the variation in the resistance and trans-inactivation phenotypes of different transfo rmants. It is further proposed that this genome feature influences a c ytoplasmic mechanism that degrades RNA with sequence homology to the s ilencing transgene.