A comparison between virus replication and abiotic stress (heat) as modifiers of host gene expression in pea.

Abstract Pea embryonic tissues respond to active replication of pea seed-borne mosaic potyvirus (PSbMV) by the down-regulation of a range of genes and the induction of others. Both of these responses can be seen when tissues are subjected to abiotic stress, particularly heat. We have compared the effects of the two inducers to assess whether the host alterations following virus replication represent generic responses to stress, or more specific effects. Five classes of response were identified: (i) genes induced by both stresses (e.g. heat shock protein 70, hsp70); (ii) genes induced by virus replication but unaffected by heat (e.g. glutathione reductase 2, gor2); (iii) genes induced by heat but unaffected by virus replication (e.g. heat shock factor, hsf); (iv) genes down-regulated by virus replication and unaffected by heat (e.g. vicilin, vic); and (v) genes unaffected by both inducers (e.g. actin, act and beta-tubulin, tub). A change in the appearance and organization of the endoplasmic reticulum (ER) was also seen in cells actively replicating PSbMV RNA. Heat treatment of pea embryonic tissues also produced altered ER, although the changes were different from those seen following virus infection. Collectively, these data show that, while there are some common features of the responses to virus infection and heat, there are also substantial differences. Hence, it appears that the host response to virus replication is not a general stress response.