Biology subjects

Qu, X.-J.

Publications and source records attributed to Qu, X.-J..

3 recordsLinked to original sources

bioRxiv2025

PlastidHub: an integrated analysis platform for plastid phylogenomics and comparative genomics

The plastome (plastid genome) represents an indispensable molecular data source for studying plant phylogeny and evolution. Although plastome size is much smaller than that of nuclear genome, accurate and efficient annotation and of use plastome sequences are not simple tasks. Therefore, a streamlined phylogenomic pipeline from plastome annotation to phylogenetic reconstruction and comparative genomics would greatly facilitate research using this important organellar genome. Here we develop PlastidHub, a new web application that primarily uses novel tools to analyze plastome sequences. In comparison with existing tools, new functionalities in PlastidHub include: (1) standardization of quadripartite structure; (2) improvement of annotation flexibility and consistency; (3) quantitative assessment of annotation completeness; (4) diverse extraction modes for canonical and specialized sequences; (5) intelligent screening of molecular markers for biodiversity studies; (6) visual comparison of structural variations and annotation completeness at the gene-level. PlastidHub has the following features: cloud-based web applications that do not require users to install, update, or maintain tools; detailed help documents including user guides, test examples, a static pop-up prompt box, and dynamic pop-up warning prompts when entering unreasonable parameter values; batch processing functionalities for all tools; intermediate result documents for secondary use; and easy-to-operate task flows between file upload and download. Interrelated task-based user interface design is the most important feature of PlastidHub. Give that PlastidHub is easy to use without specialized computational skills or resources, this new platform should become widely used among botanists and evolutionary biologists, improving and expediting research employing the plastome. PlastidHub is available at https://www.plastidhub.cn.

plant biology↗

bioRxiv2021

Gene duplications and genomic conflict underlie major pulses of phenotypic evolution in gymnosperms

Inferring the intrinsic and extrinsic drivers of species diversification and phenotypic disparity across the Tree of Life is a major challenge in evolutionary biology. In green plants, polyploidy (or whole-genome duplication, WGD) is known to play a major role in microevolution and speciation1, but the extent to which WGD has shaped macroevolutionary patterns of diversification and phenotypic innovation across plant phylogeny remains an open question. Here we examine the relationship of various facets of genomic evolution--including gene and genome duplication, genome size, and chromosome number--with macroevolutionary patterns of phenotypic innovation, species diversification, and climatic occupancy in gymnosperms. We show that genomic changes, such as WGD and genome-size shifts, underlie the origins of most major extant gymnosperm clades, and notably our results support an ancestral WGD in the gymnosperm lineage. Spikes of gene duplication typically coincide with major spikes of phenotypic innovation, while increased rates of phenotypic evolution are typically found at nodes with high gene-tree conflict, representing historic population-level dynamics during speciation. Most shifts in gymnosperm diversification since the rise of angiosperms are decoupled from putative WGDs and instead are associated with increased rates of climatic occupancy evolution, particularly in cooler and/or more arid climatic conditions, suggesting that ecological opportunity, especially in the later Cenozoic, and environmental heterogeneity have driven a resurgence of gymnosperm diversification. Our study provides critical insight on the processes underlying diversification and phenotypic evolution in gymnosperms, with important broader implications for the major drivers of both micro- and macroevolution in plants.

evolutionary biology↗

bioRxiv2018

Uric acid lowering treatment alleviates perivascular carotid collar placement induced neointimal lesions in Uricase knockout mice

Hyperuricemia (HU) is a cause of gout. Clinical studies show a link between HU and cardiovascular disease. However, the role of soluble serum urate on atherosclerosis development remains elusive. We aimed to use a new HU mouse model (Uricase/Uox knockout (KO)) to further investigate the relationship between HU and atherosclerosis. Mouse model of induced carotid atherosclerosis was established in the novel spontaneous HU Uox-KO mouse and their wild type littermates (C57BL/6J background). Mice were implanted with a perivascular collar placement around the right carotid artery in combination with a western-type diet. To investigate urate-lowering treatment (ULT) effects on intima, the mice were gavaged daily from the age of 6 weeks with allopurinol. Human umbilical vein endothelial cells (HUVECs) were co-incubated with soluble urate, with and without probenecid, to study the mechanism of urate-related atherosclerosis. The Uox-KO mice had significantly elevated serum urate levels combined with higher blood urea nitrogen and serum creatinine. Western blot analysis showed enhanced levels of atherosclerosis inflammatory response proteins. However, there were no other risk indicators for the pathogenesis of atherosclerosis, including increased fasting glucose, altered lipid and atherosclerosis characterized cardiovascular and histological manifestations. In contrast, collar placement Uox-KO mice showed severe neointimal changes in histology staining consistent with increases in intimal area and increases in proliferating cell nuclear antigen (PCNA) - and F4/80-positive cells. Allopurinol reduced neointimal areas induced by the perivascular collar in hyperuricemic mice accompanied by decreased expression of PCNA- and F4/80-positive cells (P< 0.05). ULT alleviated atherosclerosis inflammatory response factors and reactive oxygen species intensities in both collar placement Uox-KO mice and urate-stimulated HUVECs. In vitro results using HUVECs showed ROS was induced by urate and ROS induction was abrogated using antioxidants. These data demonstrate that urate per se does not trigger atherosclerosis intima lesions in mice. Urate worsens carotid neointimal lesions induced by the perivascular collar and urate-lowering therapy partially abrogates the effects. The current study warrants the further human based study on the possible benefits of urate-lowering therapy in atherosclerosis patients with HU.\n\nSummary statementWe generated a carotid collar placement atherosclerosis model in the novel spontaneous HU Uox-KO mouse and demonstrate that urate plays a contributing rather than a causal role in the carotid neointimal lesions, while urate-lowering treatment may bring additional benefits in this HU mouse model.

physiology↗