植物小RNA荧光原位杂交实验方法

小RNA是对植物生长发育十分重要的一类小分子核苷酸,在多种生命过程以及胁迫响应中发挥重要调控作用。对小RNA的定位研究有助于揭示它们的功能,而小RNA荧光原位杂交(sRNA-FISH)是一种通过荧光检测技术对生物体内小RNA进行定性或半定量分析的技术,目前该技术已经在动物体内被广泛应用,而在植物体内的应用还比较少。该文...     

在实验动物水平通过恢复和改善胰岛β细胞功能的糖尿病治疗新进展

糖尿病是一个世界性问题,在中国就有超过1.3亿人患有糖尿病.糖尿病主要分为1型糖尿病和2型糖尿病.遗憾的是,糖尿病至今尚未达成有效的预防和治愈手段.但是,近年来的一系列突破性的研究成果,让我们看到了治愈糖尿病的希望.在这里我们回顾了目前关于1型糖尿病和2型糖尿病可能的治愈途径的研究进展.这些途径包括胰岛移植和1型糖尿病...     

Identifying core habitats and corridors for giant pandas by combining multiscale random forest and connectivity analysis

Habitat loss and fragmentation are widely acknowledged as the main driver of the decline of giant panda populations. The Chinese government has made great efforts to protect this charming species and has made remarkable achievements, such as population growth and habitat expansion. However, habitat fragmentation has not been reversed. Protecting giant pandas in a large spatial extent needs to identify core habitat patches and corridors connecting them. This study used an equal‐sampling multiscale random forest habitat model to predict a habitat suitability map for the giant panda. Then, we applied the resistant kernel method and factorial least‐cost path analysis to identify core habitats connected by panda dispersal and corridors among panda occurrences, respectively. Finally, we evaluated the effectiveness of current protected areas in representing core habitats and corridors. Our results showed high scale dependence of giant panda habitat selection. Giant pandas strongly respond to bamboo percentage and elevation at a relatively fine scale (1 km), whereas they respond to anthropogenic factors at a coarse scale (≥2 km). Dispersal ability has significant effects on core habitats extent and population fragmentation evaluation. Under medium and high dispersal ability scenarios (12,000 and 20,000 cost units), most giant panda habitats in the Qionglai mountain are predicted to be well connected by dispersal. The proportion of core habitats covered by protected areas varied between 38% and 43% under different dispersal ability scenarios, highlighting significant gaps in the protected area network. Similarly, only 43% of corridors that connect giant panda occurrences were protected. Our results can provide crucial information for conservation managers to develop wise strategies to safeguard the long‐term viability of the giant panda population.     

A circular intronic RNA ciPVT1 delays endothelial cell senescence by regulating the miR‐24‐3p/CDK4/pRb axis

Circular RNAs (circRNAs) have been established to be involved in numerous processes in the human genome, but their function in vascular aging remains largely unknown. In this study, we aimed to characterize and analyze the function of a circular intronic RNA, ciPVT1, in endothelial cell senescence. We observed significant downregulation of ciPVT1 in senescent endothelial cells. In proliferating endothelial cells, ciPVT1 knockdown induced a premature senescence‐like phenotype, inhibited proliferation, and led to an impairment in angiogenesis. An in vivo angiogenic plug assay revealed that ciPVT1 silencing significantly inhibited endothelial tube formation and decreased hemoglobin content. Conversely, overexpression of ciPVT1 in old endothelial cells delayed senescence, promoted proliferation, and increased angiogenic activity. Mechanistic studies revealed that ciPVT1 can sponge miR‐24‐3p to upregulate the expression of CDK4, resulting in enhanced Rb phosphorylation. Moreover, enforced expression of ciPVT1 reversed the senescence induction effect of miR‐24‐3p in endothelial cells. In summary, the present study reveals a pivotal role for ciPVT1 in regulating endothelial cell senescence and may have important implications in the search of strategies to counteract the development of age‐associated vascular pathologies.     

LPS/Bcl3/YAP1 signaling promotes Sox9+HNF4α+ hepatocyte-mediated liver regeneration after hepatectomy

Recent reports have demonstrated that Sox9⁺HNF4α⁺ hepatocytes are involved in liver regeneration after chronic liver injury; however, little is known about the origin of Sox9⁺HNF4α⁺ hepatocytes and the regulatory mechanism. Employing a combination of chimeric lineage tracing, immunofluorescence, and immunohistochemistry, we demonstrate that Sox9⁺HNF4α⁺ hepatocytes, generated by transition from mature hepatocytes, play an important role in the initial phase after partial hepatectomy (PHx). Additionally, knocking down the expression of Sox9 suppresses hepatocyte proliferation and blocks the recovery of lost hepatic tissue. In vitro and in vivo assays demonstrated that Bcl3, activated by LPS, promotes hepatocyte conversion and liver regeneration. Mechanistically, Bcl3 forms a complex with and deubiquitinates YAP1 and further induces YAP1 to translocate into the nucleus, resulting in Sox9 upregulation and mature hepatocyte conversion. We demonstrate that Bcl3 promotes Sox9⁺HNF4α⁺ hepatocytes to participate in liver regeneration, and might therefore be a potential target for enhancing regeneration after liver injury.Subject terms: Ubiquitylation, Transdifferentiation, NF-kappaB, Regeneration, Stem-cell research