We have recently shown that transgenic expression of the truncated replication-associated protein (T-Rep) of TYLCSV-Sardinia confers resistance to the homologous virus by tightly repressing TYLCSV C1 gene transcription and viral replication (Brunetti et al., J. Virol. 75: 10573, 2001). In the course of the infection assays, some T-Rep expressing plants, initially resistant to virus invasion, developed a delayed infection (12-16 weeks post inoculation - wpi-). In the infected tissue the transgenic T-Rep was no longer detectable and its mRNA was strongly reduced. On the contrary, the expression of the nptII gene, also present in the transgenic plants, was not affected by the viral infection. Moreover, in plants that did not develop virus infection, the T-Rep was expressed for the entire duration of the experiment (up to 28 wpi). The transgenic T-Rep plants, unable to efficiently inhibit C1 gene transcription of TYLCSV-ES[1], were susceptible to this virus isolate and showed an early silencing of T-Rep. In conclusion, the chance for a plant expressing transgenic T-Rep to be infected by the virus relays on a fine balance between the inhibition of viral C1 gene transcription by T-Rep and the counter defense viral strategy of silencing the T-Rep gene. Interestingly, in contrast to commonly described virus-induced gene silencing events, TYLCSV is able to escape the silencing of its own Rep gene.
TYLCSV resistance in transgenic T-Rep expressing plants: a battle between transgene and virus-mediated regulation of gene transcription.
Noris E;Accotto GP;
2002
Abstract
We have recently shown that transgenic expression of the truncated replication-associated protein (T-Rep) of TYLCSV-Sardinia confers resistance to the homologous virus by tightly repressing TYLCSV C1 gene transcription and viral replication (Brunetti et al., J. Virol. 75: 10573, 2001). In the course of the infection assays, some T-Rep expressing plants, initially resistant to virus invasion, developed a delayed infection (12-16 weeks post inoculation - wpi-). In the infected tissue the transgenic T-Rep was no longer detectable and its mRNA was strongly reduced. On the contrary, the expression of the nptII gene, also present in the transgenic plants, was not affected by the viral infection. Moreover, in plants that did not develop virus infection, the T-Rep was expressed for the entire duration of the experiment (up to 28 wpi). The transgenic T-Rep plants, unable to efficiently inhibit C1 gene transcription of TYLCSV-ES[1], were susceptible to this virus isolate and showed an early silencing of T-Rep. In conclusion, the chance for a plant expressing transgenic T-Rep to be infected by the virus relays on a fine balance between the inhibition of viral C1 gene transcription by T-Rep and the counter defense viral strategy of silencing the T-Rep gene. Interestingly, in contrast to commonly described virus-induced gene silencing events, TYLCSV is able to escape the silencing of its own Rep gene.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.