Download Novel Mechanism of Viral Interference of Host Plant

This article is a Plant Cell Advance Online Publication. The date of its first appearance online is the official date of publication. The article has been
edited and the authors have corrected proofs, but minor changes could be made before the final version is published. Posting this version online
reduces the time to publication by several weeks.
IN BRIEF
Novel Mechanism of Viral Interference of Host Plant Suppression
by BSCTV C2
Plant–pathogen interactions are often described as an arms race because of the
variety of measures employed by plants to
limit the extent of pathogen infection and
disease and countermeasures by pathogens to suppress host defenses. Such
measures include, for example, host plant
ability to activate gene silencing pathways
directed against the pathogen and the
ability of pathogens to launch counterattacks that suppress gene silencing by the
host. New work by Zhang et al. (pages
nnn) describes the molecular mechanism
of a geminivirus protein, Beet severe curly
top virus (BSCTV) C2, which disrupts host
plant defenses by inhibiting DNA methylation-mediated gene silencing.
Geminiviruses, which cause a significant
amount of crop damage throughout the
world, have a small, circular single-stranded
DNA genome that encodes only a few proteins. Among these are a series of proteins
known as C2/L2 and AC2/AL2 that suppress
host plant defenses and enhance viral infectivity by interfering with gene silencing
and metabolic defense responses. For example, Tomato golden mosaic virus AL2 and
Beet curly top virus L2 are known to interact
with and inactivate host plant adenosine
kinase, which is essential for gene silencing,
and SNF1-related kinase, a global regulator
of metabolism (Hao et al., 2003; Wang et al.,
2005; Buchmann et al., 2009).
Zhang et al. performed yeast two-hybrid
screening in Arabidopsis to search for
proteins interacting with the BSCTV C2
protein and identified S-adenosyl-methionine decarboxylase (SAMDC1) as a candidate. The interaction was confirmed in
planta using a firefly luciferase complementation imaging assay. SAMDC1 catalyzes the conversion of S-adenosylmethionine (SAM) to decarboxylated SAM
(dcSAM), which is a key step in polyamine
biosynthesis. The reaction also regulates
DNA methylation because SAM and
dcSAM are substrates for and competitive
inhibitors of transmethylation, respectively.
The authors then identified a narrow region
of SAMDC1 essential for the interaction.
Interestingly, this region contained a highly
conserved PEST sequence, which is associated with high protein turnover and is
essential for subsequent proteasomemediated degradation. A series of experiments indeed showed that degradation of
SAMDC1 is mediated by the 26S proteasome and that the interaction with C2
attenuates SAMDC1 degradation and increases stability of the protein (see figure).
Interaction with C2 enhances stability of SAMDC1 protein, shown by a degradation assay of SAMDC1
with BSCTV C2 (C2) or with luciferase (Luc) as a control (left panel), and C2 deficiency leads to
enhanced DNA methylation of the BSCTV viral genome in infected Arabidopsis plants (right panel).
(Figure reproduced from Zhang et al. [2011].)
The authors hypothesized that increasing the stability of SAMDC1 following viral
infection results in higher SAMDC activity,
increasing the dcSAM/SAM ratio enough to
inhibit DNA methylation-mediated silencing
of the viral genome. Through a series of
experiments, they show that C2 deficiency
indeed leads to enhanced DNA methylation
of the BSCTV genome and, similar to the
loss of function of SAMDC1, results in decreased viral infectivity in infected plants.
Conversely, overexpression of SAMDC1
was shown to mimic the silencing suppression function of C2. These results show
that BSCTV C2 interferes with the host
defense mechanism of DNA methylationmediated gene silencing by attenuating
the proteasome-mediated degradation of
SAMDC1.
Nancy A. Eckardt
Senior Features Editor
[email protected]
REFERENCES
Buchmann, R.C., Asad, S., Wolf, J.N., Mohannath,
G., and Bisaro, D.M. (2009). Geminivirus AL2
and L2 proteins suppress transcriptional gene
silencing and cause genome-wide reductions in cytosine methylation. J. Virol. 83:
5005–5013.
Hao, L., Wang, H., Sunter, G., and Bisaro,
D.M. (2003). Geminivirus AL2 and L2 proteins
interact with and inactivate SNF1 kinase. Plant
Cell 15: 1034–1048.
Wang, H., Buckley, K.J., Yang, X., Buchmann,
R.C., and Bisaro, D.M. (2005). Adenosine
kinase inhibition and suppression of RNA
silencing by geminivirus AL2 and L2 proteins.
J. Virol. 79: 7410–7418.
Zhang, Z., et al. (2011). BSCTV C2 attenuates
the degradation of SAMDC1 to suppress DNA
methylation-mediated gene silencing in Arabidopsis. Plant Cell 23: xxx–xxx.
www.plantcell.org/cgi/doi/10.1105/tpc.111.230110
The Plant Cell Preview, www.aspb.org ã 2011 American Society of Plant Biologists
1 of 1