By examining the front of virus invasion in immature pea embryos infected with pea seed-borne mosaic virus (PSbMV), the selective control of different host genes has been observed. From our observations, the early responses to PSbMV replication can be grouped into three classes, inhibited host gene expression, induced host gene expression, and no effect on a normal host function. The expression of two heat-inducible genes encoding HSP70 and polyubiquitin was induced coordinately with the onset of virus replication and the down-regulation of two other genes encoding lipoxygenase and heat shock cognate protein. The down-regulation was part of a general suppression of host gene expression that may be achieved through the degradation of host transcripts. We discuss the possibilities of whether the induction of HSP70 and polyubiquitin genes represents a requirement for the respective protein products by the virus or is merely a consequence of the depletion of other host transcripts. The former is feasible, as the induction of both genes does result in increased HSP70 and ubiquitin accumulation. This also indicates that, in contrast to some animal virus infections, there is not a general inhibition of translation of host mRNAs following PSbMV infection. This selective control of host gene expression was observed in all cell types of the embryo and identifies mechanisms of cellular disruption that could act as triggers for symptom expression.For maximum efficiency, a virus must balance the exploitation of host cellular processes against consequential cellular damage. How this is achieved is not well understood. However, examples from a wide range of animal viruses (reviewed in ref. 1) and our earlier work with the plant virus pea seed-borne mosaic virus (PSbMV; ref.2) suggest that a major component in the control exerted by the virus is the shutoff of transcription and͞or translation of host mRNAs. Because the virus must use the host machinery for polynucleotide and protein synthesis, either the control must be highly selective or virus replication must depend on long-lived host mRNAs and͞or proteins. A similar argument may also apply to the use of host processes for the correct folding and turnover of viral proteins.The host shutoff phenomenon has been studied in most detail for poliovirus in which viral proteins interfere with DNA polymerase I, II, and III transcription (3-5) and translation (6, 7) and for herpes simplex virus 1 in which host translation is inhibited and there is a rapid degradation of capped mRNAs by a viral protein with riboexonuclease activity (8). For PSbMV replicating in pea embryonic tissues, there is a transient host shutoff associated with a loss of host gene transcripts associated with diverse areas of metabolism (2).In common with all viruses, PSbMV replication is associated with the translation of viral RNA and the multifarious activities of virus-encoded proteins. Hence, the basic translational machinery and processes required to assist in the correct folding and turnover of prote...

The response of pea embryonic tissues to the replication of a range of different viruses was investigated using in situ hybridization to analyze changes in the expression of two host genes, heat shock protein 70 (hsp70) and lipoxygenase (lox1). Excised pea embryos were infected using microprojectile bombardment with a nonseed transmissible strain of Pea seed-borne mosaic potyvirus, or with Pea early browning tobravirus (PEBV), White Clover mosaic potexvirus, or Beet curly top geminivirus. Collectively, these examples represent families of viruses with differing genomic features, differing numbers of genomic components and differing replication strategies. In all cases, there was an induction of hsp70 associated with virus replication and, in most cases, a downregulation of lox1. Hence, either each virus has a direct inducer of these common responses or the induction is indirectly the result of a generic feature of virus infection. By exploiting the bipartite nature of the PEBV genome, the coat protein gene and genes involved in vector transmission were excluded as potential inducers.

Summary Since some heat‐inducible genes [heat shock (hs) genes] can be induced by virus infection in pea [e.g. Hsp70;Aranda et al. 1996, Proc. Natl Acad. Sci. USA 93, 15289–15293], we have investigated the effect that heat and virus replication may have on the expression of a heat‐shock transcription factor gene (Hsf). We have characterized what appears to be the only member of the Hsf family in pea, PsHsfA. Similar to Hsp70, PsHsfA is heat‐inducible in vegetative and embryonic tissues, which is concordant with the presence of heat shock elements (HSEs) and stress responsive elements (STREs) on its promoter sequence. The expression of PsHsfA during virus replication was studied in pea cotyledons and leaves, and compared to that of Hsp70. In situ hybridization experiments showed that whereas Hsp70 is induced, there is no detectable increased accumulation of PsHsfA RNA associated with the replication of pea seed‐borne mosaic potyvirus (PSbMV). These experiments indicate that there is a selective control of virus‐induced hs gene expression, and suggest that different regulatory pathways control hs gene expression during heat shock and virus replication.