A pathogen-inducible endogenous siRNA in plant immunity

doi:10.1073/pnas.0608258103

A pathogen-inducible endogenous siRNA in plant immunity

Departments of *Plant Pathology and
^‡Botany and Plant Sciences, Center for Plant Cell Biology and Institute for Integrative Genome Biology, University of California, Riverside, CA 92521; and
^†Department of Plant and Microbial Biology, University of California, Berkeley, CA 94720

Contributed by Brian J. Staskawicz, September 19, 2006

Abstract

RNA interference, mediated by small interfering RNAs (siRNAs), is a conserved regulatory process that has evolved as an antiviral defense mechanism in plants and animals. It is not known whether host cells also use siRNAs as an antibacterial defense mechanism in eukaryotes. Here, we report the discovery of an endogenous siRNA, nat-siRNAATGB2, that is specifically induced by the bacterial pathogen Pseudomonas syringae carrying effector avrRpt2. We demonstrate that the biogenesis of this siRNA requires DCL1, HYL1, HEN1, RDR6, NRPD1A, and SGS3. Its induction also depends on the cognate host disease resistance gene RPS2 and the NDR1 gene that is required for RPS2-specified resistance. This siRNA contributes to RPS2-mediated race-specific disease resistance by repressing PPRL, a putative negative regulator of the RPS2 resistance pathway.

Footnotes

^§To whom correspondence may be addressed. E-mail: hailingj{at}ucr.edu or stask{at}nature.berkeley.edu
Author contributions: H.J. designed research; S.K.-A., R.M., D.D., O.B., A.V., and H.J. performed research; J.-K.Z., B.J.S., and H.J. analyzed data; and S.K.-A. and H.J. wrote the paper.
The authors declare no conflict of interest.
Abbreviations:

miRNA,

microRNA;

ta-siRNA,

transacting siRNA;

NAT,

natural antisense transcript;

Ps,

Pseudomonas syringae;

Pst,

Ps pathovar tomato;

avr,

avirulence;

DCL,

DICER-like;

RDR,

RNA-dependent RNA polymerase;

Dex,

dexamethasone;

hpi,

h postinoculation;

dpi,

days postinoculation;

PPR,

pentatricopeptide repeat;

PPRL,

PPR protein-like;

HR,

hypersensitive responses.