1The S. Tolkowsky Laboratory, ARO, The Volcani Center, Israel
2Department of Plant Pathology, CREC, Lake Alfred, Florida, USA.
Abstracts of the papers presented at the International Conference of Indian Virological Society on “Emerging and Re-emerging viral Diseases of the Tropics and Subtropics” at Indian Agricultural Research Institute, New Delhi, India, December 11–14, 2007.
Citrus tristeza virus (CTV) is the causal agent of at least two serious diseases of citrus trees, quick decline (QD) affecting different Citrus sp. scion varieties grafted on the sour orange rootstock and stem pitting decline (SPD) of grapefruit and orange trees regardless of the rootstock combination. Grafting on CTV tolerant rootstocks and mild strain cross protection were the main practices for controlling QD and SPD epidemics, respectively. Since most of the previous efforts to extend QD and SPD tolerance of citrus trees through conventional breeding methods were inadequate the adaptation of novel transgenic technologies for obtaining CTV tolerance was inevitable. The considerable economic importance of CTV naturally attracted the interest of different laboratories to develop and apply pathogen derived resistance (PDR) for citrus rootstocks sensitive to QD and for varieties sensitive to SPD. The lecture will discuss results suggesting that unlike many other virus host systems where PDR was achieved by expressing viral coat protein, truncated replicase or viral dsRNAs, none of the above methodologies resulted in durable CTV resistance. Thus, while the introduction of the CTV p23 (ORF11) and 3′UTR sequences (p23U) engineered to fold into a double-stranded (ds) RNA structure into Nicotiana benthamiana resulted in transgenic resistance to infection by a viral vector made of Grapevine virus A (GVA) containing an insert of the corresponding CTV sequences (GVA-p23U). Similarly transformed Alemow (C. macrophylla) plants did not show sufficient resistance to infection by CTV. Although some transgenic p23UI-Alemow line challenged with CTV showed short delay in symptom development, there was no difference in viral accumulation between the transgenic and non-transgenic citrus plants. These contrasting results with two different virus systems follow several previous failures of transgenic citrus harboring other CTV sequences. Possible mechanisms that provide CTV, and probably also other Closteroviridae members, the ability to override transgenic PDR will be discussed.
