Abstract
BackgroundThe non conventional RTM (Restricted Tobacco etch virus Movement) resistance which restricts long distance movement of some plant viruses in Arabidopsis thaliana is still poorly understood. Though at least three RTM genes have been identified, their precise role(s) in the process as well as whether other genes are involved needs to be elucidated.Methodology/Principal FindingsIn this study, the natural variation of the RTM genes was analysed at the amino acid level in relation with their functionality to restrict the long distance movement of Lettuce mosaic potyvirus (LMV). We identified non-functional RTM alleles in LMV-susceptible Arabidopsis accessions as well as some of the mutations leading to the non-functionality of the RTM proteins. Our data also indicate that more than 40% of the resistant accessions to LMV are controlled by the RTM genes. In addition, two new RTM loci were genetically identified.Conclusions/SignificanceOur results show that the RTM resistance seems to be a complex biological process which would involves at least five different proteins. The next challenges will be to understand how the different RTM protein domains are involved in the resistance mechanism and to characterise the new RTM genes for a better understanding of the blocking of the long distance transport of plant viruses.
Highlights
Systemic infection of plants by viruses is the result of compatible interactions between plant and viral factors
The present study addresses two main questions: (i) what is the basis of the inactivation of the RTM resistance in LMVsusceptible Arabidopsis accessions? And (ii) are there other RTM genes involved in the resistance process?
Screening of a panel of Arabidopsis accessions with Lettuce mosaic potyvirus (LMV) showed that some are permissive to the long distance movement of LMV, indicating that the RTM resistance is not active in these accessions
Summary
Systemic infection of plants by viruses is the result of compatible interactions between plant and viral factors. These molecular interactions control translation and replication of the viral nucleic acid(s) and generalized invasion of the host through cell-to-cell and long distance movements of viral particles or ribonucleoprotein complexes [1,2]. Passive resistances generally result in incompatible interactions of plant and viral factors, blocking the viral cycle step(s) in which the particular interaction is involved, and are usually controlled by recessive resistance genes [3]. Active resistances are generally triggered by the recognition of viral factors by plant sensors and are controlled by at least two types of mechanisms. Though at least three RTM genes have been identified, their precise role(s) in the process as well as whether other genes are involved needs to be elucidated
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