Plant Viruses Reprogram the Expression of Plant Genes - Whitham Laboratory
The vast majority of plant viruses are very simple entities comprising a nucleic acid genome encoding from 4 to 10 proteins needed for multiplication, systemic spread within the host plant, and transmission to a new plant. Since the late 1800’s viruses have been recognized as significant pathogens on plants, and they lead to numerous diseases that cause significant yield losses in a variety of crops. Despite the simple nature of these pathogens, there is still much to be learned about how they interact with their hosts and cause disease.
Viruses have a variety of obvious effects on their plant hosts, including stunted growth as shown here. To investigate the molecular mechanisms responsible for these symptoms, our lab uses a model plant, Arabidopsis thaliana, which is a host to a variety of different plant viruses that are relevant to crop plants. Arabidopsis plants suffer from many of the same symptoms as crop plants, and they allow many of the most recent tools of genomics and reverse genetics to be applied to this problem of virus-induced plant diseases. These tools allow us to decipher the effects of viral infection on plant growth and development at the molecular level.
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. Those genes that have altered patterns of expression in diseased tissues will provide insight into the cellular and biochemical changes that the viruses cause, which are ultimately manifested as symptoms. Using DNA microarrays, we have recently identified several sets of genes that change in expression in response to plant-virus infection.
The plant genes that are affected by viral infection maybe be expressed to higher levels or their levels of expression may be reduced. Frequently, we observe classes of genes with related function that are induced or decreased during viral infection suggesting that these distinct classes of genes may be coordinately regulated. The up or down-regulation of genes with related functions also suggests potential biochemical mechanisms that benefit the virus and/or lead to disease symptoms. The genetic pathways that control the expression of these genes as well as the roles of these genes in viral infection are currently under investigation in our lab.