Cauliflower mosaic virus (CaMV) falls under the family of Caulimoviridae. This pararetrovirus mainly infects plants of the Brassicaeae while some strains also infect plants in the Solanaceae. This is virus is a problem in certain parts of the world including in the US and in Canada and is one of the top 10 viruses wit respect to a plant molecular biology perspective. Replication of CaMV is done by reverse transcription of a circular dsDNA genome that is 8kb and encodes 7 different open reading frames (ORFs) that are necessary for host entry, replication and spread of virus particles. The CaMV genome encodes a 62 kDa polypeptide named P6, which participates in several activities of the virus life cycle including: suppression of RNA silencing; formation of inclusion bodies, which are necessary for viral replication, viral assembly; and translation of a polycistronic 35s RNA by its Translational Transactivation (TAV) activity. It has been reported that temperature dramatically affects the plant-virus interactions. Research in this area has shown that the outbreak of virus diseases are frequently associated with lower temperature, while at higher temperatures the viral symptoms are weakened. Our lab discovered that in 2 different plant hosts of the Brassicaeae, cooler temperatures seems to delay the formation of systemic symptoms in both a greenhouse and growth chamber setting. Cooler temperature seems to delay the symptom formation, which contradicts past research done on the affects of temperature on other host-viral interactions. We are examining 3 aspects that could be affecting the symptom formation in cooler temperature: 1) properties of infection, 2) host reaction to the virus and 3) how cooler temperature might be affecting the viral processes. To study the properties of infection we will examine if symptom formation is host-dependent or virus strain-dependent. The RNAi pathway is poorly active or inoperative at the cooler temperatures. Since it was observed that cooler temperatures still delay the virus, it could be possible that the viral suppression of other host defenses may not work as well in cooler temperatures. To assay this, we will look at P6 interactions with the Salicylic Acid (SA) response as well as its interaction with the PAMP pathway that is also mediated by SA. In order to determine how viral processes are being affected by cooler temperatures, we will also be examining the activity of the CaMV 35s promoter, the stability of P6 and how the formation of inclusion bodies might be impaired. Our preliminary data suggest that inclusion body formation is affected by cooler temperatures.