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Based on our findings, we suggest that during early embryogenesis, specific miRNAs down-regulate one or more miRNA targets
to both promote the repressors and repress the inducers of maturation. Later in embryonic development, a reduction in those
miRNAs leads to the induction of maturation. We cannot deduce from our data whether this is a linear pathway (i.e. miRNA targets
repress the repressors, which in turn silence the activators) or whether miRNA targets act at more than one level.
In a report published while this article was in preparation, Nodine and Bartel (2010) demonstrated that globular stage dcl1-5 embryos show heterochronic gene expression. Their genetic data also suggest that the increased expression of the miR156 targets
SQUAMOSA PROMOTER-BINDING PROTEIN-LIKE10 (SPL10) and SPL11 is partly responsible for the early onset of the maturation program in the mutant, despite the fact that the RNA levels of
these genes do not change significantly during embryogenesis, according to the Goldberg-Harada data set. Another SPL gene,
SPL5, does significantly increase in expression during embryogenesis in this data set, however. Thus, it might be possible that
multiple miR156-targetted SPL genes redundantly regulate the same targets, with the developmental increase in SPL5 expression allowing for the threshold for maturation to be crossed.
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