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Biology subjects

Li, Q.-Z.

Publications and source records attributed to Li, Q.-Z..

4 recordsLinked to original sources

MOLECULAR CHARACTERIZATION AND PROMOTER ELEMENT ANALYSIS OF GROWTH REGULATOR BRAGRF5 IN BRASSICA CAMPESTRIS L. SSP. CHINENSIS

The transcriptional regulation of eukaryotic gene expression is a critical aspect, with transcription factors playing a key role by combining with cis-acting elements in the promoter regions. Growth regulating factors (GRFs) are plant-specific transcriptional factors. The Arabidopsis thaliana growth-regulating factor gene (AtGRF5), when ectopically expressed in crops such as Beta vulgaris (sugar beet) and Brassica napus (canola), has an effect of accelerating shoot organogenesis and enhancing the efficiency of genetic transformation. However, an efficient plant regeneration and genetic transformation system in Brassica campestris L. ssp. chinensis, a major vegetable crop in China, remains to be established. In this work, we identified and characterized the AtGRF5 ortholog in B. campestris, named as BraGRF5, from BRAD database. Molecular analysis of BraGRF5 gene and exploration of its protein interaction network were further conducted. Therefore, the promoter region of BraGRF5 was thoroughly examined to determine cis-acting elements of various kinds and quantities. It is expected to provide a foundation for regulation of BraGRF5, and a informative reference for the improvement of B. campestris transformation efficiency and molecular breeding.

plant biology↗

CXCR4+ Treg cells control serum IgM levels and natural IgM autoantibody production by B1 cells in the bone marrow

Regulatory T (Treg) cells represent a specialized lineage of suppressive CD4+ T cells, whose functionality is critically dependent on their ability to migrate to, and dwell in the proximity of cells they control. Here we show that continuous expression of the chemokine receptor CXCR4 in Treg cells is required for their ability to accumulate in the bone marrow (BM). Induced CXCR4 ablation in Treg cells led to their rapid depletion and consequent increase in mature B cells, foremost B-1 subset, observed exclusively in the BM without detectable changes in plasma cells or hematopoietic stem cells or any signs of systemic or local immune activation elsewhere. Dysregulation of BM B-1 B cells was associated with a highly specific increase in IgM autoantibodies and the total serum IgM levels. Thus, Treg cells control autoreactive B-1 B cells in a CXCR4-dependent manner. These findings have significant implications for understanding of regulation of B cell autoreactivity and malignancies.

immunology↗

Advancing quality-control for NGS measurement of actionable mutations in circulating tumor DNA

The primary objective of the FDA-led Sequencing and Quality Control Phase 2 (SEQC2) project is to develop standard analysis protocols and quality control metrics for use in DNA testing to enhance scientific research and precision medicine. This study reports a targeted next generation sequencing (NGS) method that enables more accurate detection of actionable mutations in circulating tumor DNA (ctDNA) clinical specimens. This advancement was enabled by designing a synthetic internal standard spike-in for each actionable mutation target, suitable for use in NGS following hybrid-capture enrichment and unique molecular index (UMI) or non-UMI library preparation. When mixed with contrived ctDNA reference samples, internal standards enabled calculation of technical error rate, limit of blank, and limit of detection for each variant at each nucleotide position, in each sample. True positive mutations with variant allele fraction too low for detection by current practice were detected with this method, thereby increasing sensitivity.

genomics↗

Alternate models of acute dyslipidemia reveal divergent pathways upon atherosclerosis initiation

Atherosclerosis is thought to be initiated by the sub-intimal retention of apolipoprotein-B containing lipoproteins within susceptible sites of the vasculature. Understanding this initiation is not possible with current legacy mouse models of atherosclerosis. We created two mouse strains of inducible hypercholesterolemia based on conditional loss of apolipoprotein E or through inducible expression of a gain-of-function proprotein convertase subtilisin/kexin type 9 D374Y mutation. Both strains rapidly broke plasma-lipid homeostasis and converted to a state of atherogenic dyslipidemia, resulting in overt aortic-accumulation of lipoproteins within 10 days. RNA-sequencing revealed that the vascular response is completely dependent on the route taken to dyslipidemia, which nevertheless implicates known pathogenic pathways in the aetiology of atherosclerosis, and further implicates APOE as an inhibitor of inflammation. As atherosclerosis develops, a convergence of common mechanistic processes emerge in both strains with significant involvement of the immune system, and targeting of CD8 T cells can regulate a conserved aortic response. Our results define atherosclerosis initiation as highly heterogeneous process and identify multiple potential therapeutic targets that may influence disease onset.

physiology↗