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Liu, W.

Publications and source records attributed to Liu, W..

563 records · Page 32Linked to original sources

Resequencing the Escherichia coli genome by GenoCare single molecule sequencing platform

Next generation sequencing (NGS) has revolutionized life sciences research. Recently, a new class of third-generation sequencing platforms has arrived to meet increasing demands in the clinic, capable of directly measuring DNA and RNA sequences at the single-molecule level without amplification. Here, we use the new GenoCare single molecule sequencing platform from Direct Genomics to resequence the E. coli genome and show comparable performance to the Illumina MiSeq system. Our platform detects single-molecule fluorescence by total internal reflection microscopy, with sequencing-by-synthesis chemistry. With a consensus sequence of 99.71% nucleotide identity to that of the Illumina MiSeq systems, GenoCare was determined to be a reliable platform for single-molecule sequencing, with strong potential for clinical applications.

genomics↗

Combining Semantic Similarity and GO Enrichment for Computation of Functional Similarity

Functional similarity between genes is widely used in many bioinformatics applications including detecting molecular pathways, finding co-expressed genes, predicting protein-protein interactions, and prioritization of candidate genes. Methods evaluating functional similarity of genes are mostly based on semantic similarity of gene ontology (GO) terms. Though there are hundreds of functional similarity measures available in the literature, none of them considers the enrichment of the GO terms by the querying gene pair. We propose a novel method to incorporate GO enrichment into the existing functional similarity measures. Our experiments show that the inclusion of gene enrichment significantly improves the performance of 44 widely used functional similarity measures, especially in the prediction of sequence homologies, gene expression correlations, and protein-protein interactions.\n\nSoftware availabilityThe software (python code) and all the benchmark datasets evaluation (R script) are available at https://gitlab.com/liuwt/EnrichFunSim.

bioinformatics↗

Sugar metabolism changes in response to the ultraviolet B irradiation of peach (Prunus persica L.)

The protected cultivation of peach (Prunuspersica L.) trees is more economical and efficient than traditional cultivation, resulting in increased farmers incomes, but the peach sugar contents are lower than in open planting. In the greenhouse, a high-sugar variety of peach Lumi 1 was irradiated with 1.44 KJ{middle dot}m-2.d-1 intensity ultraviolet B radiation. The soluble sugar contents in fruit, peel and leaf were quantified using liquid chromatography. Overall, sucrose and sorbitol increased before the second fruit-expansion period. To further understand the mechanisms regulating sucrose and sorbitol accumulation in peach fruit, expression profiles of genes involved in sugar metabolism and transport were measured. The activity and translocation protein contents of these enzymes were measured by enzyme-linked immunosorbent assay. The increased sucrose synthase activity and sucrose transporter level in the pericarp promoted the synthesis of sucrose and intake of sucrose into fruit. Sorbitol transport into fruit was promoted by the increased sorbitol transporter protein levels in leaves. In summary, greenhouse the sucrose and sorbitol contents were increased when supplemented with 1.44 kJ{middle dot}m-2{middle dot}d-1 ultraviolet B radiation before the second fruit-expansion period of peach.

plant biology↗

Human brain-derived Aβ oligomers bind to synapses and disrupt synaptic activity in a manner that requires APP

Compelling genetic evidence links the amyloid precursor protein (APP) to Alzheimers disease (AD), and several theories have been advanced to explain the involvement of APP in AD. A leading hypothesis proposes that a small amphipathic fragment of APP, the amyloid {beta}-protein (A{beta}), self-associates to form soluble aggregates which impair synaptic and network activity. Here, we report on the plasticity-disrupting effects of A{beta} isolated from AD brain and the requirement of APP for these effects. We show that A{beta}-containing AD brain extracts block hippocampal long-term potentiation (LTP), augment glutamate release probability and disrupt the excitation/inhibition balance. Notably, these effects are associated with A{beta} localizing to synapses, and genetic ablation of APP prevents both A{beta} binding and A{beta}-mediated synaptic dysfunctions. These findings indicate a role for APP in AD pathogenesis beyond the generation of A{beta} and suggest modulation of APP expression as a therapy for AD.\n\nAcknowledgmentsWe thank Dr. Tiernan T. OMalley for useful discussions and technical advice. This work was supported by grants to DMW from the National Institutes of Health (AG046275), Bright Focus, and the United States-Israel Binational Science Foundation (2013244, DMW and IS); grants to TSJ from Alzheimers Research UK and the Scottish Government (ARUK-SPG2013-1), Wellcome Trust-University of Edinburgh Institutional Strategic Support funds, and the H2020 European Research Council (ALZSYN); and to the Massachusetts Alzheimers Disease Research Center (AG05134).

neuroscience↗

The depletion of MARVELD1 leads to placenta accreta via integrin β4-dependent trophoblast cell invasion

AstractThe mammalian placenta is a remarkable organ. It serves as the interface between the mother and the fetus. Proper invasion of trophoblast cells into the maternal decidua is required for a successful pregnancy. Previous studies have found that the adhesion molecule integrin {beta}4 plays important roles during trophoblast cell invasion. Here, we found that the overall birth rate of the MARVELD1 knockout mouse is much lower than that of the wild-type mouse (P<0.001). In E18.5 MARVELD1 knockout mice, we observed an over-invasion of trophoblast cells, and indeed, the pregnant mice had a partial placenta accreta phenotype. The HTR8/SVneo cell line was used as an in vitro model to elucidate the underlying mechanisms of MARVELD1-mediated trophoblast invasion. We detected a diminished expression of integrin {beta}4 upon the downregulation of MARVELD1 and enhanced migration and invasive abilities of trophoblast cells both in vivo and in vitro. The integrin {beta}4 rescue assay also supported the results. In conclusion, this study found that MARVELD1 mediated the invasion of trophoblast cells via regulating the expression of integrin {beta}4.

developmental biology↗