While the role of proteins in determining cell identity has been extensively studied, the contribution of small noncoding RNA molecules such as miRNAs and siRNAs has been also recognised. miRNAs bind to complementary sites in target mRNA molecules to trigger the degradation or translational inhibition of those targets. Recent studies have revealed that miRNAs play pivotal roles in key developmental processes such as patterning of the embryo, meristem, leaf, and flower. Furthermore, these miRNAs have been recruited throughout plant evolution into pathways that create diverse plant organ forms and shapes. This review focuses on the roles of miRNAs in establishing plant cell identity during key plant development processes and creating morphological diversity during plant evolution.

A neuroprotective effect of fingolimod in vivo may result from its inhibitory action on key astrocyte activation steps.

How eukaryotic cells assess and maintain sizes specific for their species and cell type remains unclear. We show that in the Arabidopsis shoot stem cell niche, cell size variability caused by asymmetric divisions is corrected by adjusting the growth period before DNA synthesis. KIP-related protein 4 (KRP4) inhibits progression to DNA synthesis and associates with mitotic chromosomes. The F BOX-LIKE 17 (FBL17) protein removes excess KRP4. Consequently, daughter cells are born with comparable amounts of KRP4. Inhibitor dilution models predicted that KRP4 inherited through chromatin would robustly regulate size, whereas inheritance of excess free KRP4 would disrupt size homeostasis, as confirmed by mutant analyses. We propose that a cell cycle regulator, stabilized by association with mitotic chromosomes, reads DNA content as a cell size–independent scale.

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Objective:To perform systematic transcriptomic analysis of multiple sclerosis (MS) risk genes in peripheral blood mononuclear cells (PBMCs) of subjects with distinct MS stages and describe the pathways characterized by dysregulated gene expressions.Methods:We monitored gene expression levels in PBMCs from 3 independent cohorts for a total of 297 cases (including clinically isolated syndromes (CIS), relapsing-remitting MS, primary and secondary progressive MS) and 96 healthy controls by distinct microarray platforms and quantitative PCR. Differential expression and pathway analyses for distinct MS stages were defined and validated by literature mining.Results:Genes located in the vicinity of MS risk variants displayed altered expression in peripheral blood at distinct stages of MS compared with the healthy population. The frequency of dysregulation was significantly higher than expected in CIS and progressive forms of MS. Pathway analysis for each MS stage–specific gene list showed that dysregulated genes contributed to pathogenic processes with scientific evidence in MS.Conclusions:Systematic gene expression analysis in PBMCs highlighted selective dysregulation of MS susceptibility genes playing a role in novel and well-known pathogenic pathways.