Biology subjects

Huang, Z.

Publications and source records attributed to Huang, Z..

22 records · Page 2Linked to original sources

bioRxiv2017

NLR1-V, a CC-NBS-LRR encoding gene, is a potential candidate gene of the wheat powdery mildew resistance gene Pm21

Wheat powdery mildew caused by Blumeria graminisb f. sp. tritici is one of the most destructive diseases all over the world. Pm21, transferred from the wild Haynaldia villosa to wheat, confers broad spectrum resistance throughout the whole stage, and this gene has been widely used in wheat production for more than 20 years. Cloning the candidate gene of Pm21 is the prerequisite for elucidating the resistance mechanism, and is a valuable attempt to clone the target genes from the evolutionarily distant wild species. In this study, an innovative approach, which combined cytogenetic stocks development, mutagenesis, RenSeq and PacBio, was tried successfully to clone an NBS-LRR type gene NLR1-V from the Pm21 locus. Firstly, a powdery mildew resistant cryptic alien introgression line HP33 involved very small 6VS segment was developed, and 6 independent susceptible mutants of T6VS {middle dot} 6AL was identified. Then, the transcriptome of H. villosa was obtained by NGS and the full-length NBS-LRR gene database was constructed by RenSeq-PacBio. In the following study, two expressed NLR genes were located to the Pm21 locus using the HP33 as the mapping material, and only NLR1-V showed polymorphism between the wild T6VS {middle dot} 6AL and its six mutants. The functional analysis indicated that silencing of NLR1-V could compromise the resistance of T6VS {middle dot} 6AL completely, and could also decrease the resistance of T6VS {middle dot} 6DL dramatically. Moreover, NLR1-V could recover the resistance of the susceptible mutant and increase the resistance in the susceptible wheat. The study implied that NLR1-V, a CC-NBS-LRR encoding gene, is a potential candidate gene of the powdery mildew resistance gene Pm21.

plant biology↗

bioRxiv2017

MiR-126 impairs the intestinal barrier function via inhibiting S1PR2 mediated activation of PI3K/AKT signaling pathway

BackgroundAberrant expression of miRNAs was a critical element in the pathogenesis of inflammatory bowel disease (IBD). This study aimed to explore the involvement and mechanism of miR-126 in IBD.\n\nMethodsIn this study, the endogenous expressions of miR-126, S1PR2 and S1P in the pathological tissues of patients with IBD were detected using qRT-PCR and western blot assay, respectively. The luciferase reporter gene assay was performed to confirm the targeting regulatory relation between miR-126 and S1PR2. The transendothelial electrical resistance assay was used to measured the value of TEER.\n\nResultsThe expressions of miR-126, S1PR2 and S1P in the pathological tissues of IBD patients were significantly higher than that of the control group. Moreover, miR-126 overexpression contributed to intestinal mucosal barrier dysfunction in vitro. S1PR2 was a direct target of miR-126, and S1PR2 expression was negatively regulated by miR-126 in Caco-2 cells. However, S1PR2 activated by S1P had the protection effect for the integrity and permeability of intestinal mucosal barrier via a PI3K/Akt dependent mechanism. MiR-126 silencing possessed obvious protective effects on the intestinal barrier function, but these effects could be reversed by JTE-013 or LY294002.\n\nConclusionMiR-126 down-regulated S1PR2 and then prevented the activation of PI3K/AKT signaling pathway, which ultimately could damage intestinal mucosal barrier function.

cell biology↗

bioRxiv2017

Grid cells show field-to-field variability and this explains the aperiodic response of inhibitory interneurons

Research on network mechanisms and coding properties of grid cells assume that the firing rate of a grid cell in each of its fields is the same. Furthermore, proposed network models predict spatial regularities in the firing of inhibitory interneurons that are inconsistent with experimental data. In this paper, by analyzing the response of grid cells recorded from rats during free navigation, we first show that there are strong variations in the mean firing rate of the fields of individual grid cells and thus show that the data is inconsistent with the theoretical models that predict similar peak magnitudes. We then build a two population excitatory-inhibitory network model in which sparse spatially selective input to the excitatory cells, presumed to arise from e.g. salient external stimuli, hippocampus or a combination of both, leads to the variability in the firing field amplitudes of grid cells. We show that, when combined with appropriate connectivity between the excitatory and inhibitory neurons, the variability in the firing field amplitudes of grid cells results in inhibitory neurons that do not exhibit regular spatial firing, consistent with experimental data. Finally, we show that even if the spatial positions of the fields are maintained, variations in the firing rates of the fields of grid cells are enough to cause remapping of hippocampal cells.

neuroscience↗

bioRxiv2016

Hardy Weinberg Exact Test In Large Scale Variant Calling Quality Control

Hardy Weinberg Equilibrium (HWE) test is widely used as a quality control measure to detect sequencing artifacts like mismapping, allelic dropout and biases. However, in the high throughput sequencing era, where the sample size is beyond a thousand scale, the utility of HWE test in reducing the false positive rate remains unclear. In this paper, we demonstrate that HWE test has limited power in identifying sequencing artifacts when the variant allele frequency is lower than 1% in a variant call set produced from more than five thousand whole genome sequenced samples from two homogeneous populations. We develop a novel strategy of implementing HWE filtering in which we incorporate site frequency spectrum information and determine the p-value cutoff which optimizes the tradeoff between sensitivity and specificity. The novel strategy is shown to outperform the exact test of HWE with an empirical constant p-value cutoff regardless of the sequencing sample size. We also present best practice recommendations for identifying possible sources of false positives from large sequencing datasets based on an analysis of intrinsic biases in the variant calling process. Our novel strategy of determining the HWE test p-value cutoff and applying the test to the common variants provides a practical approach for the variant level quality controls in the upcoming sequencing projects with tens to hundreds of thousand of samples.

bioinformatics↗