Seeds are highly resilient to the external environment, which allows plants to persist in unpredictable and unfavorable conditions. Some plant species have adopted a bet-hedging strategy to germinate a variable fraction of seeds in any given condition, and this could be explained by population-based threshold models. Here, in the model plant Arabidopsis (Arabidopsis thaliana), we induced secondary dormancy (SD) to address the transcriptional heterogeneity among seeds that leads to binary germination/nongermination outcomes. We developed a single-seed RNA-seq strategy that allowed us to observe a reduction in seed transcriptional heterogeneity as seeds enter stress conditions, followed by an increase during recovery. We identified groups of genes whose expression showed a specific pattern through a time course and used these groups to position the individual seeds along the transcriptional gradient of germination competence. In agreement, transcriptomes of dormancy-deficient seeds (mutant of DELAY OF GERMINATION 1) showed a shift toward higher values of the germination competence index. Interestingly, a significant fraction of genes with variable expression encoded translation-related factors. In summary, interrogating hundreds of single-seed transcriptomes during SD-inducing treatment revealed variability among the transcriptomes that could result from the distribution of population-based sensitivity thresholds. Our results also showed that single-seed RNA-seq is the method of choice for analyzing seed bet-hedging-related phenomena.

Background. Elevated concentrations of airborne pollutants are correlated with an enlarged rate of obstructive lung disease morbidity as well as acute disease exacerbations. This study aimed to analyze the epithelium mRNA profile in response to airborne particulate matter in the control, asthma, and COPD groups. Results. A triple co-culture of nasal epithelium, monocyte-derived macrophages, and monocyte-derived dendritic cells obtained from the controls, asthma, and COPD were exposed to urban particulate matter (UPM) for 24 h. RNA-Seq analysis found differences in seven (CYP1B1, CYP1B1-AS1, NCF1, ME1, LINC02029, BPIFA2, EEF1A2), five (CYP1B1, ARC, ENPEP, RASD1, CYP1B1-AS1), and six (CYP1B1, CYP1B1-AS1, IRF4, ATP1B2, TIPARP, CCL22) differentially expressed genes between UPM exposed and unexposed triple co-cultured epithelium in the control, asthma, and COPD groups, respectively. PCR analysis showed that mRNA expression of BPIFA2 and ENPEP was upregulated in both asthma and COPD, while the expression of CYP1B1-AS1 and TIPARP was increased in the epithelium from COPD patients only. Biological processes changed in UPM exposed triple co-cultured epithelium were associated with epidermis development and epidermal cell differentiation in asthma and with response to toxic substances in COPD. Conclusions. The biochemical processes associated with pathophysiology of asthma and COPD impairs the airway epithelial response to UPM.

The red microalga Cyanidioschyzon merolae inhabits extreme environments with high temperatures (40–56 °C), high acidity (pH 0.05–4), and high concentrations of heavy metals that are lethal to most forms of life. However, information is scarce on the precise adaptation mechanisms of this extremophile to such hostile conditions. Gaining such knowledge is important for understanding the evolution of microorganisms in the early stages of life on Earth characterized by such extreme environments. Through an analysis of the re-programming of the global transcriptome upon the long-term (up to 15 days) exposure of C. merolae to extremely high concentrations of nickel (1 and 3 mM), the key adaptive metabolic pathways and associated molecular components were identified. Our work shows that the long-term Ni exposure of C. merolae leads to the lagged metabolic switch demonstrated via the transcriptional upregulation of the metabolic pathways critical for cell survival. DNA replication, cell cycle, and protein quality control processes were upregulated, while downregulation occurred with energetically costly processes, including the assembly of the photosynthetic apparatus and lipid biosynthesis. This study paves the way for future multi-omic studies of the molecular mechanisms of abiotic stress adaptation in phototrophs, as well as the future development of rational approaches to the bioremediation of contaminated aquatic environments.

Among numerous enzymes involved in RNA decay, processive exoribonucleases are the most prominent group responsible for the degradation of the entire RNA molecules. The role of mammalian cytoplasmic 3’-5’ exonuclease DIS3L at the organismal level remained unknown. Herein, we established knock-in and knock-out mouse models to study DIS3L functions in mice. DIS3L in mice is indeed a subunit of the cytoplasmic exosome complex, the disruption of which leads to severe embryo degeneration and death in mice soon after implantation. These changes could not be prevented by supplementing extraembryonic tissue with functional DIS3L through the construction of chimeric embryos. Preimplantation Dis3l-/- embryos were unaffected in their morphology and ability to produce functional embryonic stem cells, showing that DIS3L is not essential for cell viability. There were also no major changes at the transcriptome level for both embryonic stem cells and blastocysts, as revealed by RNA sequencing experiments. Notably, however, Dis3l knock-out led to inhibition of the global protein synthesis. These results point to the essential role of DIS3L in mRNA metabolism, which is crucial for proper protein synthesis during embryo development.

Astrocytes differentiate and mature during postnatal development, but the molecular mechanisms linking their maturation to neuronal function remain unclear. We investigated the role of Wnt/β‐catenin signaling and its effector, the transcription factor TCF7L2, in postnatal astrocytes using single‐nucleus RNA sequencing, imaging, morphometric analysis, microdialysis, and electrophysiology in Tcf7l2 conditional knockout (cKO) mice. Loss of Tcf7l2 caused widespread transcriptional dysregulation in astrocytes, particularly in genes related to amino acid and ion transport, as well as membrane potential regulation. These mice showed disrupted amino acid homeostasis, astrocyte swelling, and impaired extracellular potassium clearance in the somatosensory cortex. These astrocytic changes were accompanied by altered gene expression in cortical pyramidal neurons, reduced excitability, and a hyperpolarized resting membrane potential. Our results suggest that astrocytic TCF7L2 is crucial in coordinating ion and amino acid transport in adulthood, thereby contributing to maintaining extracellular homeostasis and supporting neuronal function. This study identifies TCF7L2 as a key regulator of astrocyte‐mediated neurophysiological support and underscores the importance of its role in astrocyte maturation during postnatal development.

The study describes the whole-genome sequencing of two antibiotic-resistant representative Escherichia coli strains, isolated from poultry manure in 2020. The samples were obtained from a commercial chicken meat production facility in Poland. The antibiotic resistance profile was characterized by co-resistance to β-lactam antibiotics, aminoglycosides, and fluoroquinolones. The three identified resistance plasmids (R-plasmids), pECmdr13.2, pECmdr13.3 and pECmdr14.1, harbored various genes conferring resistance to tetracyclines ( tetR[A] ) for, aminoglycoside ( aph, aac and aad families), β-lactam ( bla _CMY-2 , bla _TEM-176 ), sulfonamide ( sul1, sul2 ), fluoroquinolone ( qnrS1 ), and phenicol ( floR ). These plasmids, which have not been previously reported in Poland, were found to carry IS26 insertion elements, the intI1-integrase gene, as well as conjugal transfer genes, facilitating horizontal gene transfer. Plasmids pECmdr13.2 and pECmdr14.1 also possessed a mercury resistance gene operon related to transposon Tn1696; this promotes plasmid persistence even without antibiotic selection pressure due to co-selection mechanisms such as co-resistance. The chicken manure-derived plasmids belonged to the IncX1 (narrow host range) and IncC (broad host range) incompatibility groups. Similar plasmids have been identified in various environments, clinical isolates, and farm animals, including cattle, swine, and poultry. This study holds significant importance for the One Health approach, as it highlights the potential for antimicrobial-resistant bacteria from livestock and food sources, particularly E. coli , to transfer through the food chain to humans and vice versa. This underscores the need for vigilant monitoring of R-plasmids prevalence in the human, animal and natural environments, and to implement strategies to mitigate the spread of antibiotic resistance.