Plant Cell Advance Online Publication Published on March 4, 2003; 10.1105/tpc.009530
Received December 4, 2002
Accepted January 24, 2003
Geminivirus AL2 and L2 Proteins Interact with and Inactivate SNF1 Kinase
Linhui Hao 1, Hui Wang 1, Garry Sunter 1, and David M. Bisaro 1*
1
Department of Molecular Genetics, Plant Biotechnology Center, and Program in Molecular,
Cellular, and Developmental Biology, The Ohio State University, Columbus, Ohio 43210
* To whom correspondence should be addressed. E-mail: bisaro.1{at}osu.edu.
Geminivirus AL2 and L2 proteins cause enhanced susceptibility, characterized primarily
by an increase in viral infectivity, when expressed in transgenic plants. Here, we
present genetic and biochemical evidence that enhanced susceptibility is attributable
to the interaction of AL2 and L2 with SNF1 kinase, a global regulator of metabolism.
Specifically, we show that AL2 and L2 inactivate SNF1 in vitro and in vivo. We further
demonstrate that expression of an antisense SNF1 transgene in Nicotiana
benthamiana plants causes enhanced susceptibility similar to that conditioned
by the AL2 and L2 transgenes, whereas SNF1 overexpression leads
to enhanced resistance. Transgenic plants expressing an AL2 protein that lacks a
significant portion of the SNF1 interaction domain do not display enhanced susceptibility.
Together, these observations suggest that the metabolic alterations mediated by SNF1
are a component of innate antiviral defenses and that SNF1 inactivation by AL2 and
L2 is a counterdefensive measure. They also indicate that geminiviruses are able
to modify host metabolism to their own advantage, and they provide a molecular link
between metabolic status and inherent susceptibility to viral pathogens.
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