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Plant Cell Advance Online Publication
Published on April 13, 2005; 10.1105/tpc.105.031716

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Received February 9, 2005
Accepted March 20, 2005

microRNA-Directed Regulation of Arabidopsis AUXIN RESPONSE FACTOR17 Is Essential for Proper Development and Modulates Expression of Early Auxin Response Genes

Allison C. Mallory 1, David P. Bartel 2, and Bonnie Bartel 3*

1 Whitehead Institute for Biomedical Research, Cambridge, Massachusetts 02142
2 Whitehead Institute for Biomedical Research, Cambridge, Massachusetts 02142; Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139
3 Department of Biochemistry and Cell Biology, Rice University, Houston, Texas 77005

* To whom correspondence should be addressed. E-mail: bartel{at}rice.edu.

The phytohormone auxin plays critical roles during plant growth, many of which are mediated by the auxin response transcription factor (ARF) family. microRNAs (miRNAs), endogenous 21-nucleotide riboregulators, target several mRNAs implicated in auxin responses. miR160 targets ARF10, ARF16, and ARF17, three of the 23 Arabidopsis thaliana ARF genes. Here, we describe roles of miR160-directed ARF17 posttranscriptional regulation. Plants expressing a miRNA-resistant version of ARF17 have increased ARF17 mRNA levels and altered accumulation of auxin-inducible GH3-like mRNAs, YDK1/GH3.2, GH3.3, GH3.5, and DFL1/GH3.6, which encode auxin-conjugating proteins. These expression changes correlate with dramatic developmental defects, including embryo and emerging leaf symmetry anomalies, leaf shape defects, premature inflorescence development, altered phyllotaxy along the stem, reduced petal size, abnormal stamens, sterility, and root growth defects. These defects demonstrate the importance of miR160-directed ARF17 regulation and implicate ARF17 as a regulator of GH3-like early auxin response genes. Many of these defects resemble phenotypes previously observed in plants expressing viral suppressors of RNA silencing and plants with mutations in genes important for miRNA biogenesis or function, providing a molecular rationale for phenotypes previously associated with more general disruptions of miRNA function.




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