While many introduced invasive species can increase genetic diversity through multiple introductions and/or hybridization to colonize successfully in new environments, others with low genetic diversity have to persist by alternative mechanisms such as epigenetic variation. Given that Phragmites australis is a cosmopolitan reed growing in a wide range of habitats and its invasion history, especially in North America, has been relatively well studied, it provides an ideal system for studying the role and relationship of genetic and epigenetic variation in biological invasions. We used amplified fragment length polymorphism (AFLP) and methylation‐sensitive (MS) AFLP methods to evaluate genetic and epigenetic diversity and structure in groups of the common reed across its range in the world. Evidence from analysis of molecular variance (AMOVA) based on AFLP and MS‐AFLP data supported the previous conclusion that the invasive introduced populations of P. australis in North America were from European and Mediterranean regions. In the Gulf Coast region, the introduced group harbored a high level of genetic variation relative to originating group from its native location, and it showed epigenetic diversity equal to that of the native group, if not higher, while the introduced group held lower genetic diversity than the native. In the Great Lakes region, the native group displayed very low genetic and epigenetic variation, and the introduced one showed slightly lower genetic and epigenetic diversity than the original one. Unexpectedly, AMOVA and principal component analysis did not demonstrate any epigenetic convergence between native and introduced groups before genetic convergence. Our results suggested that intertwined changes in genetic and epigenetic variation were involved in the invasion success in North America. Although our study did not provide strong evidence proving the importance of epigenetic variation prior to genetic, it implied the similar role of stable epigenetic diversity to genetic diversity in the adaptation of P. australis to local environment.

Environmentally induced phenotypic plasticity is thought to play an important role in the adaption of plant populations to heterogeneous habitat conditions, and yet the importance of epigenetic variation as a mechanism of adaptive plasticity in natural plant populations still merits further research. In this study, we investigated populations of Vitex negundo var. heterophylla (Chinese chastetree) from adjacent habitat types at seven sampling sites. Using several functional traits, we detected a significant differentiation between habitat types. With amplified fragment length polymorphisms (AFLP) and methylation‐sensitive AFLP (MSAP), we found relatively high levels of genetic and epigenetic diversity but very low genetic and epigenetic differences between habitats within sites. Bayesian clustering showed a remarkable habitat‐related differentiation and more genetic loci associated with the habitat type than epigenetic, suggesting that the adaptation to the habitat is genetically based. However, we did not find any significant correlation between genetic or epigenetic variation and habitat using simple and partial Mantel tests. Moreover, we found no correlation between genetic and ecologically relevant phenotypic variation and a significant correlation between epigenetic and phenotypic variation. Although we did not find any direct relationship between epigenetic variation and habitat environment, our findings suggest that epigenetic variation may complement genetic variation as a source of functional phenotypic diversity associated with adaptation to the heterogeneous habitat in natural plant populations.

Biological invasions pose a significant threat to ecosystems, disrupting local biodiversity and ecosystem functions. The genomic underpinnings of invasiveness, however, are still largely unknown, making it difficult to predict and manage invasive species effectively. The common reed (Phragmites australis) is a dominant grass species in wetland ecosystems and has become particularly invasive when transferred from Europe to North America. Here, we present a high-quality gap-free, telomere-to-telomere genome assembly of Phragmites australis consisting of 24 pseudochromosomes and a B chromosome. Fully phased subgenomes demonstrated considerable subgenome dominance and revealed the divergence of diploid progenitors approximately 30.9 million years ago. Comparative genomics using chromosome-level scaffolds for three other lineages and a previously published draft genome assembly of an invasive lineage revealed that gene family expansions in the form of tandem duplications may have contributed to the invasiveness of the lineage. This study sheds light on the genome evolution of Arundinoideae grasses and suggests that genetic drivers, such as gene family expansions and tandem duplications, may underly the processes of biological invasion in plants. These findings provide a crucial step toward understanding and managing the genetic basis of invasiveness in plant species.

The mortality of sepsis is increasing and conventional therapies for it have no better therapeutic effects. We investigated the effects of adiponectin (APN) on mortality and high mobility group box 1 (HMGB1) in polymicrobial sepsis mouse models. Sepsis models were established by cecal ligation and puncture (CLP) in BALB/c mice. Animals were randomly divided into four groups including control group (C group), model group (CLP group), early APN treatment group (APN + CLP group), and late APN treatment group (CLP + APN group). Mice in each group were killed at 6, 12, 24, and 48 hr after CLP, respectively, to collect samples for determining the levels of serum interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), high mobility group protein-1 (HMGB1), and the expression of lung tissue HMGB1 mRNA. The survival curves in the four groups were drawn. The mortality rates were significantly lower in APN + CLP (30%) and CLP + APN (40%) groups than in CLP group (80%) seven days after CLP. Serum levels of cytokines (IL-6 and TNF-α) and HMGB1 were significantly reduced (p < .05) in APN + CLP and CLP + APN groups compared with those of CLP group. There was a significant correlation between serum HMGB1 and lung HMGB1 mRNA (r = 0.891). The levels of HMGB1 and HMGB1 mRNA were higher in CLP, APN + CLP, and CLP + APN groups than in C group (p < .01), but were lower in APN + CLP and CLP + APN groups than in CLP group (p < .01). APN can reduce the mortality rate and plays an anti-inflammatory role in polymicrobial sepsis mouse models through inhibiting HMGB1.