Floral transition is a critical event in the life cycle of a flowering plant as it determines its reproductive success. Despite extensive studies of specific genes that regulate this process, the global changes in transcript expression profiles at the point when a vegetative meristem transitions into an inflorescence have not been reported. We analyzed gene expression during Arabidopsis thaliana meristem development under long day conditions from day 7 to 16 after germination in one-day increments. The dynamics of the expression of the main flowering regulators was consistent with previous reports: notably, the expression of FLOWERING LOCUS C (FLC) decreased over the course of the time series while expression of LEAFY (LFY) increased. This analysis revealed a developmental time point between 10 and 12 days after germination where FLC expression had decreased but LFY expression had not yet increased, which was characterized by a peak in the number of differentially expressed genes. Gene Ontology (GO) enrichment analysis of these genes identified an overrepresentation of genes related to the cell cycle. We discovered an unprecedented burst of differential expression of cell cycle related genes at one particular point during transition to flowering. We suggest that acceleration of rate of the divisions and partial cell cycling synchronization takes place at this point.

Populations of different species vary in the amounts of genetic diversity they possess. Nucleotide diversity π, the fraction of nucleotides that are different between two randomly chosen genotypes, has been known to range in eukaryotes between 0.0001 in Lynx lynx and 0.16 in Caenorhabditis brenneri. Here, we report the results of a comparative analysis of 24 haploid genotypes (12 from the United States and 12 from European Russia) of a split-gill fungus Schizophyllum commune. The diversity at synonymous sites is 0.20 in the American population of S. commune and 0.13 in the Russian population. This exceptionally high level of nucleotide diversity also leads to extreme amino acid diversity of protein-coding genes. Using whole-genome resequencing of 2 parental and 17 offspring haploid genotypes, we estimate that the mutation rate in S. commune is high, at 2.0 × 10⁻⁸ (95% CI: 1.1 × 10⁻⁸ to 4.1 × 10⁻⁸) per nucleotide per generation. Therefore, the high diversity of S. commune is primarily determined by its elevated mutation rate, although high effective population size likely also plays a role. Small genome size, ease of cultivation and completion of the life cycle in the laboratory, free-living haploid life stages and exceptionally high variability of S. commune make it a promising model organism for population, quantitative, and evolutionary genetics.

The generation of human macrophages from induced pluripotent stem cells (iMacs) is a rapidly developing approach used to create disease models, screen drugs, study macrophage–pathogen interactions and develop macrophage-based cell therapy. To generate iMacs, different types of protocols have been suggested, all thought to result in the generation of similar iMac populations. However, direct comparison of iMacs generated using different protocols has not been performed. We have compared the productivity, the differentiation trajectories and the characteristics of iMacs generated using two widely used protocols: one based on the formation of embryoid bodies and the induction of myeloid differentiation by only two cytokines, interleukin-3 and macrophage colony-stimulating factor, and the other utilizing multiple exogenous factors for iMac generation. We report inter-protocol differences in the following: (i) protocol productivity; (ii) dynamic changes in the expression of genes related to inflammation and lipid homeostasis following iMac differentiation and (iii) the transcriptomic profiles of terminally differentiated iMacs, including the expression of genes involved in inflammatory response, antigen presentation and lipid homeostasis. The results document the dependence of fine iMac characteristics on the type of differentiation protocol, which is important for further development of the field, including the development of iMac-based cell therapy.

Generation of energy in mitochondria is subjected to physiological regulation at many levels, and its malfunction may result in mitochondrial diseases. Mitochondrial dysfunction is associated with different environmental influences or certain genetic conditions, and can be artificially induced by inhibitors acting at different steps of the mitochondrial electron transport chain (ETC). We found that a short-term (5 h) inhibition of ETC complex III with myxothiazol results in the phosphorylation of translation initiation factor eIF2α and upregulation of mRNA for the activating transcription factor 4 (ATF4) and several ATF4-regulated genes. The changes are characteristic for the adaptive integrated stress response (ISR), which is known to be triggered by unfolded proteins, nutrient and metabolic deficiency, and mitochondrial dysfunctions. However, after a prolonged incubation with myxothiazol (13–17 h), levels of ATF4 mRNA and ATF4-regulated transcripts were found substantially suppressed. The suppression was dependent on the p53 response, which is triggered by the impairment of the complex III-dependent de novo biosynthesis of pyrimidines by mitochondrial dihydroorotate dehydrogenase. The initial adaptive induction of ATF4/ISR acted to promote viability of cells by attenuating apoptosis. In contrast, the induction of p53 upon a sustained inhibition of ETC complex III produced a pro-apoptotic effect, which was additionally stimulated by the p53-mediated abrogation of the pro-survival activities of the ISR. Interestingly, a sustained inhibition of ETC complex I by piericidine did not induce the p53 response and stably maintained the pro-survival activation of ATF4/ISR. We conclude that a downregulation of mitochondrial ETC generally induces adaptive pro-survival responses, which are specifically abrogated by the suicidal p53 response triggered by the genetic risks of the pyrimidine nucleotide deficiency.

For many years, progress in the identification of gene functions has been based on classical genetic approaches. However, considerable recent omics developments have brought to the fore indirect but high-resolution methods of gene function identification such as transcriptomics, proteomics, and metabolomics. A transcriptome map is a powerful source of functional information and the result of the genome-wide expression analysis of a broad sampling of tissues and/or organs from different developmental stages and/or environmental conditions. In plant science, the application of transcriptome maps extends from the inference of gene regulatory networks to evolutionary studies. However, only some of these data have been integrated into databases, thus enabling analyses to be conducted without raw data; without this integration, extensive data preprocessing is required, which limits data usability. In this review, we summarize the state of plant transcriptome maps, analyze the problems associated with the combined analysis of large-scale data from various studies, and outline possible solutions to these problems.