<i>SGS3</i> and <i>SGS2/SDE1/RDR6</i> are required for juvenile development and the production of <i>trans</i>-acting siRNAs in <i>Arabidopsis</i>

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Abstract

<jats:p>Higher plants undergo a transition from a juvenile to an adult phase of vegetative development prior to flowering. Screens for mutants that undergo this transition precociously produced alleles of two genes required for posttranscriptional gene silencing (PTGS)—<jats:italic>SUPPRESSOR OF GENE SILENCING3</jats:italic> (<jats:italic>SGS3</jats:italic>) and <jats:italic>SUPPRESSOR OF GENE SILENCING2(SGS2)/SILENCING DEFECTIVE1 (SDE1)/RNA-DEPENDENT POLYMERASE6</jats:italic> (<jats:italic>RDR6</jats:italic>). Loss-of-function mutations in these genes have a phenotype similar to that of mutations in the Argonaute gene <jats:italic>ZIPPY</jats:italic> (<jats:italic>ZIP</jats:italic>). Epistasis analysis suggests that <jats:italic>ZIP, SGS3, SGS2/SDE1/RDR6</jats:italic>, and the putative miRNA export receptor, <jats:italic>HASTY</jats:italic> (<jats:italic>HST</jats:italic>), operate in the same pathway(s). Microarray analysis revealed a small number of genes whose mRNA is increased in <jats:italic>ZIP, SGS3</jats:italic>, and <jats:italic>SGS2/SDE1/RDR6</jats:italic> mutants, as well as genes that are up-regulated in <jats:italic>SGS3</jats:italic> and <jats:italic>SGS2/SDE1/RDR6</jats:italic> mutants, but not in <jats:italic>ZIP</jats:italic> mutants. One of these latter genes (At5g18040) is silenced posttranscriptionally in <jats:italic>trans</jats:italic> by the sRNA255 family of endogenous, noncoding, small interfering RNAs (siRNAs). The increase in At5g18040 mRNA in <jats:italic>SGS3</jats:italic> and <jats:italic>SGS2/SDE1/RDR6</jats:italic> mutants is attributable to the absence of sRNA255-like siRNAs in these mutants. These results demonstrate a role for endogenous siRNAs in the regulation of gene expression, and suggest that PTGS plays a central role in the temporal control of shoot development in plants.</jats:p>

Journal

  • Genes & Development

    Genes & Development 18 (19), 2368-2379, 2004-10-01

    Cold Spring Harbor Laboratory

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