The concept of pathogen-derived resistance (PDR) strategy is based on the insertion of resistant genes that are derived from the pathogen (virus) into the host plant. Roger N. Beachy (1997) suggested two mechanisms through which PDR can confirm resistance in plants against virus infection. These mechanisms are:
1- Expression of genes that encode certain viral proteins in the host plant can protect these plants against certain viruses. In 1991, Namba et al. showed that the expression of the gene encoding the coat protein of cucumber mosaic virus (CMV) strain WL protected tobacco plants from the infection caused by several CMV strains.
2- The second strategy is through the nucleic acid mediated resistance. The first report that a transgene introduced into plants would lead to silencing (co-suppression) of both the transgene and its homologous endogenous gene were made by Powell et al. (1989). Transgene-induced gene silencing has since been demonstrated in several other organisms. Based on the known features, transgene-induced silencing effects have been divided into transcriptional and post transcriptional gene silencing (TGS and PTGS, respectively). Shou Wei Ding in 2000 suggested that gene silencing was mediated via the increased degradation of mRNA and that this appears to represent a novel cellular pathway that is functional in broad range of organisms. Recent work has established a role for RNA silencing in host antiviral defense and transposon silencing. Genes silenced transcriptionally are homologous in promoter regions, whereas genes targeted for PTGS share homology in transcribed regions. Furthermore, TGS silences genes at the level of transcription in the nucleus. In contrast, PTGS has no apparent effect on transcription of the target gene but promotes a rapid and specific turnover of RNA transcripts in the cytoplasm. It is perhaps more accurate to refer to these phenomena collectively as 'RNA Silencing' because the inactivation of genes in each example is achieved through targeted degradation of RNA. In 1992, Namba et al. studied the protection action of the transgenic plants expressing the coat protein gene of Watermelon mosaic virus II or Zucchini yellow mosaic virus against six potyviruses, which by then was described as a phenomenon related to the post transcriptional level for gene expression.
Post transcriptional gene silencing (PTGS) is a universal mechanism by which plants are able to systemically switch off expression of targeted genes via the reduction of steady state levels of specific RNAs. It is believed that PTGS is thought to have evolved as a mechanism by which plants protect themselves from viral infection by targeting viral transgenes. Ratcliff and his associates (1999) demonstrated that the virus infection of non-transgenic plants triggers RNA silencing directed against the invading viral RNAs and confirmed earlier findings that induction of RNA silencing dose not require homologous nuclear DNA sequences. So they showed for the first time that host recovery is not essential for silencing induction. Plant DNA viruses, both the ssDNA geminiviruses and the reverse-transcribing pararetroviruses, have properties with the potential to initiate gene silencing in the nucleus and in the cytoplasm. Characteristics include production of multiple copies of viral DNA genomes in the nucleus, illegitimate integration of viral DNA into host chromosomes mimicking transgene transformation for pararetroviruses, and generation of abundant viral RNAs in the cytoplasm.
Besides these two mechanisms described above, other PDR strategies have been studied. The trans-dominant lethal strategy has been explored as a mechanism for engineering plants with resistance to geminiviruses (Hanson and Maxwell, 1999). In this case, a mutated viral Rep gene, which is non-functional, would interfere with the action of the wild-type Rep protein and thus, inhibit viral replication.
· Namba, S, Ling, KH, Gonsalves, C, Gonsalves, D, Slightom, JL. 1991. Expression of the gene encoding the coat protein of cucumber mosaic virus (CMV) strain WL appears to provide protection to tobacco plants against infection by several different CMV strains. Gene 107: 181-188.
· Ferreira, S, Pitz, KY, Mau, RFL, Sugiyama, L, Gonsalves, D. 1992. Using mild strain cross protection to manage papaya ringspot virus in Hawaii. Phytopathology 82: 1156.
· Fitch, MMM, Manshardt, RM, Gonsalves, D, Slightom, JL, Sanford, JC. 1992. Virus resistant papaya derived from tissues bombarded with the coat protein gene of papaya ringspot virus. Bio/Technology 10: 1466-1472.
· Fuchs M, Tricoli D, Carney DM, Schesser KJ, McFerson JR, Gonsalves D. 1998. Comparative virus resistance and fruit yield of transgenic squash with single and multiple coat protein genes. Plant Dis 82:1350-1356.
· Fuchs, M, Xue, B, Gonsalves, CV, Provvidenti, R, Seem, RC, Slightom, JL, Gonsalves, D. 1993. Greenhouse and field resistance to cucumber mosaic virus (CMV) in transgenic tomatoes, squash, and melons expressing the coat protein gene of CMV-white leaf. Abstracts of 6th International congress of Plant Pathology, Montreal, Canada, July 28-August 6, 1993. p. 191.
· Gonsalves, D, Chee, P, Provvidenti, R, Seem, R, Slightom, JL. 1992. Comparison of coat protein-mediated and gentically-derived resistance in cucumbers to infection by cucumber mosaic virus under field conditions with natural challenge inoculations by vectors. Bio/Technology 10: 1562-1570.
· Gonsalves, C, Xue, B, Yepes, M, Fuchs, M, Ling, K, Namba, S, Chee, P, Slightom, JL, Gonsalves, D. 1994. Transferring cucumber mosaic virus-white leaf strain coat protein gene into Cucumis melo L. and evaluating transgenic plants for protection against infections. Journal of the American Society for Horticultural Science. 119: 345-355.
· Namba, S, Ling, K, Gonsalves, C, Slightom, JL, Gonsalves, D. 1992. Protection of transgenic plants expressing the coat protein gene of watermelon mosaic virus ii or zucchini yellow mosaic virus against six potyviruses. Phytopathology 82: 940-946.
Hanson, SF, Maxwell, DP. 1999. trans-Dominant inhibition of geminiviral DNA replication by bean golden mosaic geminivirus rep gene mutant. Phytopathology 89:480-486.
· Pang, S-Z, Nagpala, P, Wang, M, Slightom, JL, Gonsalves, D. 1992. Resistance to heterologous isolates of tomato spotted wilt virus in transgenic plants expressing its nucleocapsid protein gene. Phytopathology 82: 1223-1229.
· Pang, SZ, Bock, JH, Gonsalves, C, Slightom, JL, Gonsalves, D. 1994. Resistance of transgenic Nicotiana benthamiana plants to tomato spotted wilt and impatiens necrotic spot tospoviruses: Evidence of involvement of the N protein and N gene RNA in resistance. Phytopathology. 84: 243-249.
· Pang, S-Z, Jan, F-J, Gonsalves, D. 1997. Nontarget DNA sequences reduce the transgene length necessary for RNA-mediated topsovirus resistance in transgenic plants. Proc National Acad Sci, USA 94:8261-8266.
· Yang, H, Singsit, C, Wang, A, Gonsalves, D, Ozias-Akins, P. 1998. Transgenic peanut plants containing a nucleocapsid protein gene of tomato spotted wilt virus show divergent levels of gene expression. Plant Cell Rep 17:693-699.
Prepared by M. Abhary (email@example.com)
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