Description
In susceptible hosts, plant viruses typically induce a number of morphological and physiological modifications in combination with an altered expression pattern of host genes. Some of these alterations do not necessarily provide an advantage to the virus but nevertheless may have adverse effects on the host. To elucidate factors and processes contributing to disease response to pathogenic viruses, plant-virus interactions are studied under a functional genomic perspective.
Viruses develop an intimate intracellular relationship with their plant hosts. The symptom expression represents the sum of virus-induced molecular, cellular, and physiological changes that at least in part involve a host transcriptome response. These processes are being studied in our group using molecular, genomic and genetic tools. Currently, one approach to understanding the effects of viral infection on plant growth and development at the molecular level is to define the different ways in which viral infection affects the expression of plant genes. Host genes with altered expression profiles provide insight into the signaling pathways and biochemical changes that are modulated by viral infection, which are ultimately manifested as symptoms. Using cDNA microarrays, we have recently identified several sets of genes that change in expression in response to virus infection (Fig. 1).
Fig 1: Hierarchical cluster analysis of differential expression profiles in Nicotiana benthamiana plants infected with PVX, PVY or PVX+PVY.
Altered genes appear to be scattered among several metabolic pathways, confirming that the host response to compatible virus infection includes a coordinated rearrangement of a wide array of cellular processes, rather than a simple induction of genes involved in stress responses (Fig. 2).
Fig. 2: Transcription changes induced in Nicotiana benthamiana by PVX+PVY double infection
Moreover, we have just begun to understand the molecular events involved in systemic necrosis, one of the most severe symptoms elicited by virus in susceptible plants that eventually results in plant death. Recent findings suggest that the genetic basis for the systemic necrosis induced by compatible plant-virus interactions resembles in some aspects the programmed cell death induced by incompatible pathogens in resistance gene-mediated defense responses. We are using Agrobacterium-mediated plant transformation and reverse genetic approaches based on virus-induced gene silencing (VIGS) to identify plant genes and cellular circuits involved in symptom expression.
Our group maintains, over the last years, other research projects focused on the development of virus control strategies, i.e.: l) the analysis of pathogen-derived, transgenic resistance to viruses and the elucidation of the cellular and molecular mechanisms controlling resistance; 2) the analysis of dsRNA-induced interference with plant virus infections.
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