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Published March 15, 2007 | Published
Journal Article Open

Redundancy and specialization among plant microRNAs : role of the MIR164 family in developmental robustness

Abstract

In plants, members of microRNA (miRNA) families are often predicted to target the same or overlapping sets of genes. It has thus been hypothesized that these miRNAs may act in a functionally redundant manner. This hypothesis is tested here by studying the effects of elimination of all three members of the MIR164 family from Arabidopsis. It was found that a loss of miR164 activity leads to a severe disruption of shoot development, in contrast to the effect of mutation in any single MIR164 gene. This indicates that these miRNAs are indeed functionally redundant. Differences in the expression patterns of the individual MIR164 genes imply, however, that redundancy among them is not complete, and that these miRNAs show functional specialization. Furthermore, the results of molecular and genetic analyses of miR164-mediated target regulation indicate that miR164 miRNAs function to control the transcript levels, as well as the expression patterns, of their targets, suggesting that they might contribute to developmental robustness. For two of the miR164 targets, namely CUP-SHAPED COTYLEDON1 (CUC1) and CUC2, we provide evidence for their involvement in the regulation of growth and show that their derepression in miR164 loss-of-function mutants is likely to account for most of the mutant phenotype.

Additional Information

© 2007 Company of Biologists Ltd. Accepted 22 January 2007; first published online 7 February 2007. We thank Drs J. Fletcher, L. Williams and A. Mallory for protocols; Drs J. Long and P. Das for plasmids; A. Garda for technical assistance; and Drs A. Roeder, M. Heisler, C. Ohno and Z. Nimchuk for comments on the manuscript. We are indebted to members of the Meyerowitz laboratory, especially Dr C. Baker, for stimulating discussions, and to Prof. Dr U. Grossniklaus for his support of P.S. This work was supported by National Science Foundation grant MCB-0520193 to J.L.R. and E.M.M., by the Millard and Muriel Jacobs Genetics and Genomics Laboratory at the California Institute of Technology, and by a European Molecular Biology Organization long-term fellowship (ALTF 460-2003) and a Forschungskredit from the University of Zurich to P.S. J.G. was supported by a grant from the Swiss National Science Foundation to Ueli Grossniklaus.

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