A NAC Domain Protein Interacts with Tomato leaf curl virus Replication Accessory Protein and Enhances Viral Replication
Luke A. Selth, Satish C. Dogra, M. Saif Rasheed, Helen Healy, John W. Randles and M. Ali Rezaian
Plant Cell.2005; 17: 311-325.

Dr. Luke A. Selth, of Commonwealth Scientific and Industrial Research Organization (CSIRO) Australia, and colleagues have found that “A NAC Domain Protein Interacts with Tomato leaf curl virus Replication Accessory Protein and Enhances Viral Replication.” Their findings are published online in Plant Cell.

Tomato Leaf Curl or Leaf Roll is a disease which causes tomato plants to grow slowly, and for tomato fruits, if ever they are produced, to be small, dry, and unfit for the market. The causative agent is the Tomato Leaf Curl Virus (TLCV), which is dependent on host factors for multiplication, and which does so by hijacking host cell processes. Replication enhancer (REn) proteins are produced during an infection, dramatically increasing the accumulation of viral DNA species by a hitherto unknown mechanism.

Selth’s study presents evidence that the tomato itself contains a protein, called SINAC1, which enhances TLCV infection through binding with REn. When TLCV starts infecting a plant, they found, it produces REn, which, in turn, induces SINAC1 expression; and all of which result in a substantial increase in viral DNA accumulation. Through in-vitro experiments, researchers not only identified SINAC1, but found that in acts as a transcriptional activator in uninfected yeast cells.

ABSTRACT

Geminivirus replication enhancer (REn) proteins dramatically increase the accumulation of viral DNA species by an unknown mechanism. In this study, we present evidence implicating SlNAC1, a new member of the NAC domain protein family from tomato (Solanum lycopersicum), in Tomato leaf curl virus (TLCV) REn function. We isolated SlNAC1 using yeast (Saccharomyces cerevisiae) two-hybrid technology and TLCV REn as bait, and confirmed the interaction between these proteins in vitro. TLCV induces SlNAC1 expression specifically in infected cells, and this upregulation requires REn. In a transient TLCV replication system, overexpression of SlNAC1 resulted in a substantial increase in viral DNA accumulation. SlNAC1 colocalized with REn to the nucleus and activated transcription of a reporter gene in yeast, suggesting that in healthy cells it functions as a transcription factor. Together, these results imply that SlNAC1 plays an important role in the process by which REn enhances TLCV replication.

The paper can be accessed online at http://www.plantcell.org/cgi/reprint/17/1/311