Development · 2006 · 757 citations · 50 references
Life SciencesPlant BiologyPlant SciencesGametogenesisPlant Developmental BiologyPlant Molecular BiologyAuxin BiologyFlower DevelopmentPlant Small Rna BiologyPlant Transcriptional RegulationPollen DevelopmentPollen ProductionHaploid Phase DevelopmentPollen Developmental MutantsPollen Developmental RegulationPollen EmbryologyStamen AnatomyStamen DevelopmentStamen MorphologyTranscripts
In flowering plants, ovule and anther development are supported by diploid sporophytic tissues, and the Auxin Response Factors ARF6 and ARF8 are known to regulate gynoecium and stamen formation, suggesting shared mechanisms across these reproductive organs. miR167 targets ARF6 and ARF8 transcripts for cleavage, and its overexpression mimics the arf6 arf8 mutant phenotypes. Loss of miR167 function causes ectopic ARF6/8 expression, arrested ovule integument growth, abnormal anther development, and impaired pollen release, demonstrating that miR167 is essential for proper gene patterning and fertility in both ovules and anthers.
In flowering plants, diploid sporophytic tissues in ovules and anthers support meiosis and subsequent haploid gametophyte development. These analogous reproductive functions suggest that common mechanisms may regulate ovule and anther development. Two Arabidopsis Auxin Response Factors, ARF6 and ARF8, regulate gynoecium and stamen development in immature flowers. Wild-type pollen grew poorly in arf6 arf8 gynoecia, correlating with ARF6 and ARF8 expression in style and transmitting tract. ARF6 and ARF8 transcripts are cleavage targets of the microRNA miR167, and overexpressing miR167 mimicked arf6 arf8 phenotypes. Mutations in the miR167 target sites of ARF6 or ARF8 caused ectopic expression of these genes in domains of both ovules and anthers where miR167 was normally present. As a result, ovule integuments had arrested growth, and anthers grew abnormally and failed to release pollen. Thus, miR167 is essential for correct patterning of gene expression, and for fertility of both ovules and anthers. The essential patterning function of miR167 contrasts with cases from animals in which miRNAs reinforce or maintain transcriptionally established gene expression patterns.
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