A novel class of bacteria-induced small RNAs in Arabidopsis

  1. Surekha Katiyar-Agarwal1,3,
  2. Shang Gao1,
  3. Adam Vivian-Smith2, and
  4. Hailing Jin1,4
  1. 1 Department of Plant Pathology and Microbiology, Center for Plant Cell Biology and Institute for Integrative Genome Biology, University of California at Riverside, Riverside, California 92521, USA;
  2. 2 Institute of Biology, Leiden University, 2332 AL Leiden, The Netherlands

Abstract

Small RNAs, including microRNAs (miRNAs) and small interfering RNAs (siRNAs), are essential regulatory molecules of many cellular processes. Arabidopsis has at least three classes of endogenous siRNAs—chromatin-associated siRNAs, trans-acting siRNAs (tasiRNAs), and natural antisense transcript (NAT)-associated siRNAs (nat-siRNAs)—all 20–25 nucleotides (nt) in length. Here, we identified a novel class of small RNAs, long siRNAs (lsiRNAs), which are 30–40 nt and share many common features with known siRNAs. The lsiRNAs identified so far are induced by pathogen infection or under specific growth conditions. One of the lsiRNAs, AtlsiRNA-1, is generated from SRRLK/AtRAP NAT pair and specifically induced by the bacterium Pseudomonas syringae carrying effector avrRpt2. Recently, 25- to 31-nt PIWI-interacting RNAs (piRNAs) and repeat-associated siRNAs (rasiRNAs) were identified in animal germline cells. In contrast to the biogenesis of piRNAs/rasiRNAs, which is dicer independent and requires PIWI subfamily proteins, generation of AtlsiRNA-1 requires DCL1, DCL4, and the ARGONAUTE subfamily protein AGO7. It also depends on HYL1, HEN1, HST1, RDR6, and Pol IV. Induction of AtlsiRNA-1 silences AtRAP, which encodes a RAP-domain protein involved in disease resistance. Our further analysis implies that AtlsiRNA-1 may destabilize target mRNA through decapping and XRN4-mediated 5′-to-3′ degradation.

Keywords

Footnotes

  • 3 Present address: Department of Plant Molecular Biology, University of Delhi South Campus, Benito Juarez Road, New Delhi 110021, India.

  • 4 Corresponding author.

    4 E-MAIL hailingj{at}ucr.edu; FAX (951) 827-4294.

  • Supplemental material is available at http://www.genesdev.org.

  • Article published online ahead of print. Article and publication date are online at http://www.genesdev.org/cgi/doi/10.1101/gad.1595107

    • Received July 20, 2007.
    • Accepted October 9, 2007.
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