The Hengduan Mountains (HDM) biodiversity hotspot exhibits exceptional alpine plant diversity. Here, we investigate factors driving intraspecific divergence within a HDM alpine species Salix brachista (Cushion willow), a common component of subnival assemblages. We produce a high-quality genome assembly for this species and characterize its genetic diversity, population structure and pattern of evolution by resequencing individuals collected across its distribution. We detect population divergence that has been shaped by a landscape of isolated sky island-like habitats displaying strong environmental heterogeneity across elevational gradients, combined with population size fluctuations that have occurred since approximately the late Miocene. These factors are likely important drivers of intraspecific divergence within Cushion willow and possibly other alpine plants with a similar distribution. Since intraspecific divergence is often the first step toward speciation, the same factors can be important contributors to the high alpine species diversity in the HDM.

The ability of LBD29 to regulate lateral root initiation is associated with its maintenance of the cell division capacity of the pericycle in response to auxin and its involvement in the auxin signalling pathway.

SummaryThe overexpression of miR319 in plants results in delayed senescence, and high levels of miR319‐targeted TCP4 transcription factor cause premature onset of this process. However, the underlying mechanisms of this pathway remain elusive. Here, we found that miR319 overexpression results in a decrease in TCP4 abundance and secondary cell wall formation in the stem. Conversely, constitutive expression of miR319‐resistant TCP4 promotes secondary cell wall formation, indicating that miR319‐mediated TCP4 controls secondary cell wall formation during development. Further analysis revealed that TCP4 might directly bind the promoter of VND7 to activate its expression, which triggers the expression of a VND7 transcriptional network associated with secondary cell wall biosynthesis and programmed cell death and accelerates vessel formation. In addition, the development process gradually increased TCP4 expression. These results suggest that miR319 and its target TCP4 can act as switches that turn on secondary cell wall synthesis and programmed cell death.

Plantlets of Populus yunnanensis Dode were examined in a greenhouse for 48 h to analyze their physiological and proteomic responses to sustained heat, drought, and combined heat and drought. Compared with the application of a single stress, simultaneous treatment with both stresses damaged the plantlets more heavily. The plantlets experienced two apparent response stages under sustained heat and drought. During the first stage, malondialdehyde and reactive oxygen species (ROS) contents were induced by heat, but many protective substances, including antioxidant enzymes, proline, abscisic acid (ABA), dehydrin, and small heat shock proteins (sHSPs), were also stimulated. The plants thus actively defended themselves against stress and exhibited few pathological morphological features, most likely because a new cellular homeostasis was established through the collaborative operation of physiological and proteomic responses. During the second stage, ROS homeostasis was overwhelmed by substantial ROS production and a sharp decline in antioxidant enzyme activities, while the synthesis of some protective elements, such as proline and ABA, was suppressed. As a result, photosynthetic levels in P. yunnanensis decreased sharply and buds began to die, despite continued accumulation of sHSPs and dehydrin. This study supplies important information about the effects of extreme abiotic environments on woody plants.

The objective of this study was to evaluate the effects of specific NF-kappaB inhibitor pyrrolidine dithiocarbamate (PDTC) on inflammatory response and cardiac function in a rat model of coronary microembolization (CME). CME was developed by injecting a suspension of microthrombotic particles (MTPs) into the left ventricle when obstructing the ascending aorta. MTPs were generated from the rat clots sized by filtration through 38 microm screen. Thirty-two Sprague-Dawley rats served as sham group, 128 CME rats were randomized to untreated (CMEU) and PDTC-treated (CMEp) group. Rats in CMEp were administered intraperitoneally with 50, 100, 200 mg kg-1 day-1 PDTC, respectively, from 1 h before to 7 days after operation. The rats were sacrificed on day 1, 3, 7, 14 post-operationally and each subgroup consisted of eight rats. The general morphological characteristics were observed in sections with HE staining, and the severity of myocardial loss (SML) was determined by percent micro-necrotic area in sections with hematoxylin basic fuchsin picric (HBFP) staining 1 day or by percent micro-fibrotic area in sections with Masson's trichrome staining 14 days post-operationally. Left ventricular (LV) function was evaluated echocardiographically and hemodynamically. Activity of NF-kappaB/DNA-binding was analyzed by electrophoresis mobility shift assays (EMSA), and expressions of TNF-alpha, IL-6, and ICAM-1 genes and proteins were detected by Real-time PCR and western blots, respectively. CME rats exhibited pathological changes evidenced by multi-focal myocardial necrosis, inflammatory cell infiltration with remarkably increased SML and persistent reduction of LV function. Activity of NF-kappaB/DNA-binding was markedly increased, also TNF-alpha, IL-6 and ICAM-1 transcripts and their protein expressions were upregulated strongly in the myocardium following CME. PDTC in a dose-dependency significantly suppressed the myocardial inflammatory cytokine transcriptions, decreased SML and improved LV function. Thus, NF-kappaB is markedly activated in CME hearts, and inhibition of NF-kappaB by PDTC prevents the subsequent inflammatory activation and improves cardiac function. Patients with or at risk of CME may benefit from acute anti-inflammatory treatment with PDTC.

Background/Aims: Subacute ruminal acidosis (SARA) is a common disease in highproducing lactating cows. Rumenitis is the initial insult of SARA and is associated with the high concentrations of histamine produced in the rumen of dairy cows during SARA. However, the exact mechanism remains unclear. The objective of the current study is to investigate whether histamine induces inflammation of rumen epithelial cells and the underlying mechanism of this process. Methods: Bovine rumen epithelial cells were cultured and treated with different concentrations of histamine and pyrrolidine dithiocarbamate (PDTC, an NF-κB inhibitor) cultured in different pH medium (pH 7.2 or 5.5). qRT-PCR, Western-blotting, ELISA and immunocytofluorescence were used to evaluate whether histamine activated the NF-κB pathway and inflammatory cytokines. Results: The results showed that histamine significantly increased the activity of IKK β and the phosphorylation levels of IκB α, as well as upregulated the mRNA and protein expression levels of NF-κB p65 in the rumen epithelial cells cultured in neutral (pH=7.2) and acidic (pH=5.5) medium. Furthermore, histamine treatment also significantly increased the transcriptional activity of NF-κB p65. High expression and transcriptional activity of NF-κB p65 significantly increased the mRNA expressions and concentrations of inflammatory cytokines, tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6) and interleukin 1 beta (IL-1β), thereby inducing the inflammatory response in bovine rumen epithelial cells. However, inhibition of NF-κB p65 by PDTC significantly decreased the expressions and concentrations of the inflammatory cytokines induced by histamine in the rumen epithelial cells cultured in the neutral and acidic medium. Conclusion: The present data indicate that histamine induces the inflammatory response of bovine rumen epithelial cells through the NF-κB pathway.X. Sun and X Yuan contributed equally to this study.

BackgroundQuercetin is a natural bioactive flavonoid that is present in a wide variety of vegetables and fruits and exhibits a promising anti-metastasis property in various human cancer cells. However, the effect of quercetin on human HCCLM3 cells is unclear.Material/MethodsIn the current study, a wound-healing assay was performed using quercetin-treated HCCLM3 cells to further explore whether quercetin affects the motility of human HCCLM3 cells. Transwell assay was used to explore the potential effect of quercetin in HCCLM3 cells on cell migration and cell invasion. Western blotting analysis was used to explore the expression of p-Akt1, MMP-2, and MMP-9 in quercetin-treated HCCLM3 cells.ResultsThe wound-healing time was delayed in quercetin-treated HCCLM3 cells, and the ability to migrate and invade was inhibited in quercetin-treated human HCCLM3 cells. Moreover, the protein levels of p-Akt1, MMP-2, and MMP-9 were down-regulated in quercetin-treated HCCLM3 cells, as detected by Western blotting.ConclusionsOur data show that quercetin attenuated cell migration and invasion by suppressing the protein levels of p-Akt1, MMP-2, and MMP-9 in HCCLM3 cells.

LYC against H2O2-induced oxidative damage in bMEC at least partly depended on activation of the NFE2L2 signaling pathway.