Contemporary Understanding of miRNA-Based Regulation of Secondary Metabolites Biosynthesis in Plants

MicroRNAs (miRNAs) are short RNAs that direct messenger RNA degradation or disrupt mRNA translation in a sequence-dependent manner. For more than a decade, attempts to study the interaction of miRNAs with their targets were confined to the 3' untranslated regions of mRNAs, fuelling an underlying assumption that these regions are the principal recipients of miRNA activity. Here we focus on the mouse Nanog, Oct4 (also known as Pou5f1) and Sox2 genes and demonstrate the existence of many naturally occurring miRNA targets in their amino acid coding sequence (CDS). Some of the mouse targets analysed do not contain the miRNA seed, whereas others span exon-exon junctions or are not conserved in the human and rhesus genomes. miR-134, miR-296 and miR-470, upregulated on retinoic-acid-induced differentiation of mouse embryonic stem cells, target the CDS of each transcription factor in various combinations, leading to transcriptional and morphological changes characteristic of differentiating mouse embryonic stem cells, and resulting in a new phenotype. Silent mutations at the predicted targets abolish miRNA activity, prevent the downregulation of the corresponding genes and delay the induced phenotype. Our findings demonstrate the abundance of CDS-located miRNA targets, some of which can be species-specific, and support an augmented model whereby animal miRNAs exercise their control on mRNAs through targets that can reside beyond the 3' untranslated region. Show more

Several hypotheses, mainly Optimal Defense (OD), Carbon: Nutrient Balance (CNB), Growth Rate (GR), and Growth-Differentiation Balance (GDB), have individually served as frameworks for investigating the patterns of plant defense against herbivores, in particular the pattern of constitutive defense. The predictions and tests of these hypotheses have been problematic for a variety of reasons and have led to considerable confusion about the state of the "theory of plant defense." The primary contribution of the OD hypothesis is that it has served as the main framework for investigation of genotypic expression of plant defense, with the emphasis on allocation cost of defense. The primary contribution of the CNB hypothesis is that it has served as the main framework for investigation of how resources affect phenotypic expression of plant defense, often with studies concerned about allocation cost of defense. The primary contribution of the GR hypothesis is that it explains how intrinsic growth rate of plants shaped evolutionarily by resource availability affects defensive patterns. The primary contribution of the expanded GDB hypothesis is that it recognizes the constant physiological tradeoff between growth and differentiation at the cellular and tissue levels relative to the selective pressures of resource availability, including explicitly taking into account plant tolerance of damage by enemies. A clearer understanding of these hypotheses and what we have learned from investigations that use them can facilitate development of well-designed experiments that address the gaps in our knowledge of plant defense. Show more

Flavonoids are ubiquitous in the plant kingdom and have many diverse functions including defense, UV protection, auxin transport inhibition, allelopathy, and flower coloring. Interestingly, these compounds also have considerable biological activity in plant, animal and bacterial systems - such broad activity is accomplished by few compounds. Yet, for all the research over the last three decades, many of the cellular targets of these secondary metabolites are unknown. The many mutants available in model plant species such as Arabidopsis thaliana and Medicago truncatula are enabling the intricacies of the physiology of these compounds to be deduced. In the present review, we cover recent advances in flavonoid research, discuss deficiencies in our understanding of the physiological processes, and suggest approaches to identify the cellular targets of flavonoids. Show more