Biology subjects

Lei, Y.

Publications and source records attributed to Lei, Y..

112 records · Page 7Linked to original sources

bioRxiv2019

QTL Mapping and integration as well as candidate gene prediction for branch number in soybean

Branch number is an important factor that affects crop plant architecture and yield in soybean. With the aim of elucidating the genetic basis of branch number, we identified 10 consensus quantitative trait loci (QTLs) through preliminary mapping, which were on chromosome A1, B2, C1, C2, D1a, D1b, F, L and N, explained 0.3-33.3% of the phenotypic variance. Of these, three QTLs were identical to previously identified ones, whereas the other seven were novel. In addition, one major QTL-qBN.C2 (R2=33.3%) was detected in all three environments and another new major QTL-qBN.N (R2=19.6%) was detected in two environments (Taiyuan 2017 and Taiyuan 2018), but only in Taiyuan. Thus, the QTL x environment interaction analysis confirmed that QTL-qBN.N was strongly affected by the environment. We compared the physical positions of the QTL intervals of the candidate genes potentially involved in branching development, and five orthologous genes were ultimately selected and related to the establishment of axillae meristem organization and lateral organs, qBN.A1 (SoyZH13_05G177000.m1), qBN.C2 (SoyZH13_06G176500.m1, SoyZH13_06G185600.m1), and qBN.D1b-1 (SoyZH13_02G035400.m1, SoyZH13_02G070000.m3). The results of our study reveal a complex and relatively complete genetic architecture and can serve as a basis for the positional gene cloning of branch number in soybean.

genetics↗

bioRxiv2019

CD155/CD96 promotes immunosuppression in lung adenocarcinoma (LUAD)

Lung adenocarcinoma (LUAD) remains one of the leading causes of death in patients with cancer. The association of CD155 with CD96 transmits an inhibitory signal and suppresses antitumor immune response. This study investigates the effect of CD155/CD96 on immune suppression in LUAD. We demonstrate that LUAD patients with high CD155 expression suffer from immune suppression and experience a poor prognosis, which coincides with an inhibited AKT-mTOR signaling pathway in CD8 T cells and subsequently up-regulated CD96 expression. Moreover, the inhibition effect can be reversed by CD96 blocking antibody. High CD155 expression inhibited the release of IFN{gamma} from CD8 cells. Moreover, Blocking CD96 restored IFN{gamma} production in CD8 T cells and neutralized the inhibition of IFN{gamma} production in CD8 T cells mediated by CD155. Animal experiments showed that CD155-mediated LUAD growth might depend on its suppression antitumor immune response in the tumor microenvironment in PDX mice. In conclusion, our results suggest that LUAD cells suppress antitumor immune response in the tumor microenvironment through CD155/CD96. CD155/CD96 could be a potential therapeutic target for LUAD patients.\n\nAbbreviationsLUAD: lung adenocarcinoma; IFN{gamma}: interferon gamma; PDX: patient-derived xenograft; NSCLC: non-small cell lung cancer; PRR: poliovirus receptor-related; MDSCs: myeloid-derived suppressor cells; PRR: poliovirus receptor-related; STR: short tandem repeat; IRS: immunoreactive score; SI: staining intensity; PP: percentage of positive cells; RT-PCR: reverse transcription-polymerase chain reaction; PBS: phosphate-buffered saline; PBMCs: peripheral blood mononuclear cells; SDS-PAGE: sodium dodecyl sulfate-polyacrylamide gel electrophoresis; rCD155: recombinant human CD155; LUAD cells: lung adenocarcinoma cells; TILs: tumor-infiltrating lymphocytes; GzmB: granzyme B; IL-2 (Interleukin-2); TNF- : tumor necrosis factor-alpha; PI: propidium Iodide; PDX: patient-derived xenograft; TIGIT: T cell immunoreceptor with Igand ITIM domains; WBC: white blood cells; MFI: mean fluorescence intensity; HPF: high power field

cancer biology↗

bioRxiv2018

The ghr-miR164 and GhNAC100 module participates in cotton plant defence against Verticillium dahliae

Previous reports have shown that many miRNAs were identified at the early induction stage during which Verticillium dahliae localizes at the root surface. In this study, we constructed two sRNA libraries of cotton root responses to this fungus at the later induction stage when the pathogen enters the root vascular tissue. We identified 71 known miRNAs and 378 novel miRNAs from two pathogen-induced sRNAs and the control libraries. Combined with degradome and sRNA sequencing, 178 corresponding miRNA target genes were identified, in which 40 target genes from differentially expressed miRNAs were primarily associated with oxidation-reduction and stress responses. More importantly, we characterized the ghr-miR164-GhNAC100 module in the response of the plant to V dahliae infection. A GUS fusion reporter showed that ghr-miR164 directly cleaved the mRNA of GhNAC100 in the post-transcriptional process. ghr-miR164-silencing increased the resistance of the plant to this fungus, while the knockdown of GhNAC100 elevated the susceptibility of the plant, indicating that ghr-miR164-GhNAC100 modulates plant defence through the post-transcriptional regulation. Our data documented that there are numerous miRNAs at the later induction stage that participate in the plant response to V. dahliae, suggesting that miRNAs play important roles in plant resistance to vascular disease.\n\nHighlightAccording to degradome and sRNA sequencings of cotton root in responses to Verticillium dahliae at the later induction stage, many miRNAs and corresponding targets including ghr-miR164-GhNAC100 module participate plant defence.

molecular biology↗

bioRxiv2018

Stable changing fluid shear stress promotes osteogenesis

ObjectiveBone marrow cells encounter various chemical and mechanical stimuli from the internal environment. In vivo, fluid shear stress (FSS) is one of the primary mechanical stimuli that affect bone marrow-derived mesenchymal stem cells (BMCs) activity. Since various cases of FSS influence BMCs activity differently, the purpose of this study is to determine how BMC activity in osteogenesis and osteoclastgenesis is affected by stable and unstable changing FSS.\n\nMethodBMCs samples from the femur of the mouse, divided in to three groups: stimulate by stable changing FSS, unstable changing FSS, and no FSS. RT-PCR would be applied to detect OPG, RANKL, ALP, OCN, RUNX2, and RANK of all the samples at the 3rd day. Alizarin red staining and TRAP staining would be applied to test all the samples at the 6th day.\n\nResultsThe S group samples showed the lowest level in RANKL mRNA and showed the highest level in OPG mRNA. RANKL/OPG mRNA in the S group was the smallest during three groups. Comparing with the C group samples, RUNX2 mRNA in the S group was increased significantly. RANK mRNA in the C group was three times more than S group. S group had the largest area of mineralized nodules, and largest number of area [≥]100{micro}m, [≥]500{micro}m2 or [≥]1000{micro}m2. The area of positive TRAP stain in S group was the smallest among three groups.\n\nConclusionStable changing FSS significantly increases osteogenesis relating to OPG-RANKL-RANK pathway. Compared with unstable changing FSS, stable changing FSS afford a more appropriate stimulation to osteogenesis.\n\nAbbreviations

cell biology↗