IDENTIFICATION AND CHARACTERIZATION OF A LOCUS (RTM1) THAT RESTRICTS LONG-DISTANCE MOVEMENT OF TOBACCO ETCH VIRUS IN ARABIDOPSIS-THALIANA

Citation
Sk. Mahajan et al., IDENTIFICATION AND CHARACTERIZATION OF A LOCUS (RTM1) THAT RESTRICTS LONG-DISTANCE MOVEMENT OF TOBACCO ETCH VIRUS IN ARABIDOPSIS-THALIANA, Plant journal, 14(2), 1998, pp. 177-186
Citations number
48
Categorie Soggetti
Plant Sciences",Biology
Journal title
ISSN journal
09607412
Volume
14
Issue
2
Year of publication
1998
Pages
177 - 186
Database
ISI
SICI code
0960-7412(1998)14:2<177:IACOAL>2.0.ZU;2-V
Abstract
Screens of Arabidopsis thaliana for susceptibility to tobacco etch vir us (TEV) revealed that each of 10 ecotypes were able to support genome replication and cell-to-cell movement in inoculated leaves. However, only four ecotypes, including C24 and La-er, supported complete infect ions in which TEV was able to replicate and move from cell to cell and long distances through the vasculature. The rates of cell-to-cell mov ement of a reporter-tagged TEV strain (TEV-GUS) in inoculated leaves o f C24 and Columbia (Col-3) were similar, and infection foci continued to expand in both ecotypes through 10 days post inoculation. No visibl e or microscopic hypersensitive or cell death responses were evident i n inoculated leaves of Col-3 plants. Infection of neither C24 nor Col- 3 plants with TEV-GUS resulted in induction of PR-1a gene expression, which is normally associated with active defence responses and systemi c acquired resistance. The genetic basis for the restriction of long-d istance movement of TEV-GUS in Columbia was investigated using C24 x C ol-3 crosses and backcrosses and using La-er x Col-0 recombinant inbre d lines. A dominant locus conditioning the restricted TEV infection ph enotype was identified on chromosome 1 between markers ATEAT1 and NCC1 at approximately 14 cM in both genetic analyses. This locus was desig nated RTM1 (restricted TEV movement 1). It is proposed that RTM1 media tes a restriction of long-distance movement through a mechanism that d iffers substantially from those conditioned by the dominant resistance genes normally associated with gene-for-gene interactions.