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The present study evaluated the size and germination characteristics of seeds of seven species of Syngonanthus (distributed among four sections) that occur in different microhabitats in campos rupestres vegetation in Minas Gerais State, to determine if (1) the germination responses of the various species characterize a single germination pattern for the genus; and (2) there is a correlation between the germination characteristics and the geographic distribution as well as the microhabitat of the different species. The experiments were undertaken with recently collected seeds exposed to a 12-h photoperiod and continuous darkness, at constant temperatures of 10-408C (at intervals of 58C) in germination chambers. The results indicated the existence of a pattern of reduced seed size and light requirements for germination within the genus. The geographic distribution of different species of the genus cannot be explained by the responses of seed germination to different temperatures, but suggests some relationship to their edaphic microhabitats. Therefore, germination characteristics of the populations studied may have been selected to colonize specific environments at different soil water conditions.

Seeds can synchronize their germination and dormancy cycles to regular seasonal environmental changes. The present work sought to evaluate thein-situlongevity of the buried seeds of two species ofSyngonanthusand two species ofComanthera(Eriocaulaceae) in the region of natural occurrence (Serra do Cipó Range, south-eastern Brazil), and to relate their germination responses to seasonal climatic changes. Samples were exhumed bimonthly and germination was tested under a 12-h photoperiod (30 μmol m− 2s− 1) at optimal germination temperature. The seeds ofComantherashowed high deterioration after the first year of burial, especiallyC. elegans, which reflects their incapacity to form viable soil seed banks. The buried seeds ofC. bisulcata, S. anthemidiflorusandS. verticillatusacquired secondary dormancy during the rainy season (spring/summer, higher temperatures) which was alleviated during the subsequent dry season (autumn/winter, lower temperatures). It is concluded thatC. bisulcata, S. anthemidiflorus, andS. verticillatusform seed banks of the persistent type and demonstrate consecutive cycles of germination/dormancy, accompanying annual seasonal changes for at least 2 years.

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BackgroundGlucose metabolism, specifically, hexokinase 2 (HK2), has a critical role in rheumatoid arthritis (RA) fibroblast-like synoviocyte (FLS) phenotype. HK2 localizes not only in the cytosol but also in the mitochondria, where it protects mitochondria against stress. We hypothesize that mitochondria-bound HK2 is a key regulator of RA FLS phenotype.MethodsHK2 localization was evaluated by confocal microscopy after FLS stimulation. RA FLSs were infected with Green fluorescent protein (GFP), full-length (FL)–HK2, or HK2 lacking its mitochondrial binding motif (HK2ΔN) expressing adenovirus (Ad). RA FLS was also incubated with methyl jasmonate (MJ; 2.5 mM), tofacitinib (1 µM), or methotrexate (1 µM). RA FLS was tested for migration and invasion and gene expression. Gene associations with HK2 expression were identified by examining single-cell RNA sequencing (scRNA-seq) data from murine models of arthritis. Mice were injected with K/BxN serum and given MJ. Ad-FLHK2 or Ad-HK2ΔN was injected into the knee of wild-type mice.ResultsCobalt chloride (CoCl2) and platelet-derived growth factor (PDGF) stimulation induced HK2 mitochondrial translocation. Overexpression of the HK2 mutant and MJ incubation reversed the invasive and migrative phenotype induced by FL-HK2 after PDGF stimulation, and MJ also decreased the expression of C-X-C Motif Chemokine Ligand 1 (CXCL1) and Collagen Type I Alpha 1 Chain (COL1A1). Of interest, tofacitinib but not methotrexate had an effect on HK2 dissociation from the mitochondria. In murine models, MJ treatment significantly decreased arthritis severity, whereas HK2FL was able to induce synovial hypertrophy as opposed to HK2ΔN.ConclusionOur results suggest that mitochondrial HK2 regulates the aggressive phenotype of RA FLS. New therapeutic approaches to dissociate HK2 from mitochondria offer a safer approach than global glycolysis inhibition.