Unlike core histones, the linker histone H1 family is more evolutionarily diverse and many organisms have multiple H1 variants or subtypes. In mammals, the H1 family includes seven somatic H1 variants, H1.1 to H1.5 being expressed in a replication-dependent manner, whereas H1.0 and H1X are replication-independent. Using ChIP-seq data and cell fractionation, we have compared the genomic distribution of H1.0 and H1X in human breast cancer cells, in which we previously observed differential distribution of H1.2 compared to the other subtypes. We have found H1.0 to be enriched at nucleolus-associated DNA repeats and chromatin domains, whereas H1X is associated with coding regions, RNA polymerase II-enriched regions and hypomethylated CpG islands. Further, H1X accumulates within constitutive or included exons and retained introns, and towards the 3' end of expressed genes. Inducible H1X knock-down does not affect cell proliferation but dysregulates a subset of genes related to cell movement and transport. In H1X-depleted cells, the promoters of up-regulated genes are not occupied specifically by this variant, have a lower than average H1 content and, unexpectedly, do not form an H1 valley upon induction. We conclude that H1 variants are not distributed evenly across the genome and may participate with some specificity in chromatin domain organization or gene regulation.

Histone H1 has seven variants in human somatic cells and contributes to chromatin compaction and transcriptional regulation. Knock-down (KD) of each H1 variant in breast cancer cells results in altered gene expression and proliferation differently in a variant specific manner with H1.2 and H1.4 KDs being most deleterious. Here we show combined depletion of H1.2 and H1.4 has a strong deleterious effect resulting in a strong interferon (IFN) response, as evidenced by an up-regulation of many IFN-stimulated genes (ISGs) not seen in individual nor in other combinations of H1 variant KDs. Although H1 participates to repress ISG promoters, IFN activation upon H1.2 and H1.4 KD is mainly generated through the activation of the IFN response by cytosolic nucleic acid receptors and IFN synthesis, and without changes in histone modifications at induced ISG promoters. H1.2 and H1.4 co-KD also promotes the appearance of accessibility sites genome wide and, particularly, at satellites and other repeats. The IFN response may be triggered by the expression of noncoding RNA generated from heterochromatic repeats or endogenous retroviruses upon H1 KD. In conclusion, redundant H1-mediated silencing of heterochromatin is important to maintain cell homeostasis and to avoid an unspecific IFN response.

Plant pathogenic fungi pose a persistent global threat to food security, causing severe yield losses in staple crops and increasing dependence on chemical fungicides. However, the ecological and toxicological drawbacks of synthetic fungicides have intensified the search for safer, plant-derived alternatives. This review synthesizes current advances on the antifungal mechanisms of plant essential oils (EOs) and their prospects for biofungicide development. The literature reveals that the antifungal activity of EOs arises from their diverse phytochemical composition, principally terpenes, phenolics, and aldehydes that target multiple fungal cellular sites. These compounds disrupt membrane integrity through ergosterol depletion, inhibit chitin and β-glucan synthesis, interfere with mitochondrial energy metabolism, and induce oxidative stress, leading to lipid peroxidation and cell death. Morphological and transcriptomic evidence confirms that EOs alter hyphal growth, spore germination, and key gene expression pathways associated with fungal virulence. Furthermore, emerging nanotechnological and encapsulation strategies enhance EO stability, bioavailability, and field persistence, addressing major barriers to their large-scale agricultural application. The integration of EO-based biofungicides within sustainable and precision agriculture frameworks offers a promising route to reduce chemical inputs, mitigate resistance development, and promote ecological balance. This review underscores the need for interdisciplinary research linking phytochemistry, nanotechnology, and agronomy to translate EO-based antifungal mechanisms into next-generation, environmentally compatible crop protection systems.

The formation and hydrogen sorption properties of the NaMgH₃ perovskite/type hydride have been examined. Samples were mechanically ball milled under argon for 2, 5 and 15 h; then characterized by X-ray diffraction (XRD), differential scanning calorimetry (DSC), and thermogravimetric analysis (TGA) coupled with a mass spectrometer (MS). Lattice parameters and cell volume of the main NaMgH₃ phase increase as a function of milling. Dehydrogenation proceeded in two-step reactions for the NaMgH₃. The maximum amount of released hydrogen was achieved for the 2 h milled NaMgH₃ hydride accounting for 5.8 wt.% of H₂ from 287 °C to 408 °C. Decomposed NaMgH₃ samples were reversibly hydrogenated under 10 bar H₂ at ~200 °C.

The antioxidant activity of food compounds is one of the properties generating the most interest, due to its health benefits and correlation with the prevention of chronic disease. This activity is usually measured using in vitro assays, which cannot predict in vivo effects or mechanisms of action. The objective of this study was to evaluate the in vivo protective effects of six phenolic compounds (naringenin, apigenin, rutin, oleuropein, chlorogenic acid, and curcumin) and three carotenoids (lycopene B, β-carotene, and astaxanthin) naturally present in foods using a zebrafish embryo model. The zebrafish embryo was pretreated with each of the nine antioxidant compounds and then exposed to tert-butyl hydroperoxide (tBOOH), a known inducer of oxidative stress in zebrafish. Significant differences were determined by comparing the concentration-response of the tBOOH induced lethality and dysmorphogenesis against the pretreated embryos with the antioxidant compounds. A protective effect of each compound, except β-carotene, against oxidative-stress-induced lethality was found. Furthermore, apigenin, rutin, and curcumin also showed protective effects against dysmorphogenesis. On the other hand, β-carotene exhibited increased lethality and dysmorphogenesis compared to the tBOOH treatment alone.