Biology subjects

Wang, J.-j.

Publications and source records attributed to Wang, J.-j..

3 recordsLinked to original sources

bioRxiv2024

dsRNAEngineer: a web-based tool of comprehensive dsRNA design for pest control

RNA interference (RNAi) is a form of gene silencing triggered by double-stranded RNA (dsRNA) that operates in all eukaryotic organisms, including insects, mites, nematodes and fungi. In the last two decades, many dsRNAs have been synthesized to silence the target genes for exploration of the underlying function in these pests. Some of them are lethal to pests or inhibit the growth of the pest population, leading to a new concept of pesticides. The generation of these environment-friendly pesticides requires precise in silico design of dsRNA molecules that are specific to target pests but do not target non-pest organisms. Current efforts for dsRNA design are mostly focused on gene sequence level, lacking comprehensive analysis of RNAi-based mode-of-action at the whole transcriptome level of given species, causing low efficiency and imprecise dsRNA target exploration. To address these limitations, we have created dsRNAEngineer, a publicly available online tool that allows a comprehensive and rational dsRNA design, incorporating hundreds of pests and non-pests transcriptomes. Developed functionalities include screen-target (screen conserved genes for co-targets of various pest species), on-target, off-target, and multi-target to generate optimal dsRNA for precise pest control. dsRNAEngineer is available at https://dsrna-engineer.cn/. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=138 SRC="FIGDIR/small/604585v1_ufig1.gif" ALT="Figure 1"> View larger version (55K): org.highwire.dtl.DTLVardef@9ee7fdorg.highwire.dtl.DTLVardef@90b015org.highwire.dtl.DTLVardef@11857eborg.highwire.dtl.DTLVardef@1340f18_HPS_FORMAT_FIGEXP M_FIG C_FIG

bioinformatics↗

bioRxiv2020

miR-100-5p downregulates mTOR to suppress the proliferation, migration and invasion of prostate cancer cells

BackgroundPrevious studies have shown that miR-100-5p expression is abnormal in prostate cancer. However, the role and regulatory mechanism of miR-100-5p requires further investigation. Thus, the aim of this study was to observe the effects of miR-100-5p on the proliferation, migration and invasion of prostate cancer (PCa) cells and to explore the potential related regulatory mechanism. MethodsDifferential miRNA expression analysis was performed using next-generation sequencing (NGS) in the PCa cell line LNCaP and the normal prostatic epithelial cell line RWPE-1. The expression levels of miR-100-5pwere detected using real-time fluorescence quantitative PCR (qRT-PCR). LNCaP cells were transfected with NC-mimics or miR-100-5p mimics by using liposome transfection. Moreover, the CCK-8 proliferation assay, cell scratch assay and Transwell assay were used to detect the effects of miR-100-5p on cell proliferation, migration and invasion. In addition, the potential target gene of miR-100-5p was predicted, and the influence of miR-100-5p on the expression of mTOR mRNA by qRT-PCR and the expression of mTOR protein was detected by western blot and immunohistochemical staining. ResultsDifferential expression analysis of high-throughput sequencing data showed low expression of miR-100-5p in the PCa cell line LNCaP. It was further confirmed by qRT-PCR that the expression of miR-100-5p in LNCaP cells was significantly lower than that in RWPE-1 cells (P<0.01). miR-100-5p expression in LNCaP cells was markedly upregulated after transfection with miR-100-5p mimics (P<0.01), while cell proliferation, migration and invasion capacities were clearly reduced (P<0.01), and mTOR mRNA and protein expression was also substantially lowered (P<0.01). Finally, we further confirmed by immunohistochemical staining that miR-100-5p regulated the expression of mTOR. ConclusionmiR-100-5p is expressed at low levels in LNCaP cells, and it can suppress LNCaP cell proliferation, migration and invasion, the mechanism of which is related to downregulating the expression of mTOR.

cancer biology↗

bioRxiv2020

The ParAs function is realized by two separate proteins in the partitioning system of Myxococcus plasmid pMF1

The par operon in the sole myxobacterial plasmid pMF1 includes a function-unknown parC gene in front of the classical parA and parB genes. Removal of parC severely reduced plasmid stability, but ex-situ compensations of parC did not restore the par system function. Individual expression of parA formed insoluble proteins, while co-expression of parC before parA produced a soluble ParC-ParA heterodimer. ParA alone had no ATPase activity and no polymerization, while ParC addition aided ParA to restore the activities. Fusing ParC and ParA in different ways all produced soluble proteins and some restored ATPase activity or increased plasmid stability. Protein interaction model analysis and experiments revealed that ParC structurally mimics the N-terminal of Ia-type SopA (ParA), endowing the Myxococcus ParA protein to play functions by shifting of ParC between two sites on ParA surface. The present results highlight that ParC functions as a part of ParA to support its soluble expression and function, and the separation of ParC and ParA into two proteins in structure enables the ParC fragment to shift in a larger range around ParA to function during partitioning. Author summaryOur work on ParC here provides a new example for the evolution of multi-domain protein. ParC and ParA are two proteins, but their expression and function act as a whole, which proposes a new regulatory model for bacterial par system, and also provides research ideas and materials for the study of functional coordination and evolution of ParA domains in the future.

microbiology↗