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Selected Papers From the Advanced Genetics Conference 2019

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A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: closed (1 June 2020) | Viewed by 41999

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Dr. David Q-H Wang

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Albert Einstein College of Medicine, Bronx, NY 10461, USA
Interests: cholesterol and bile acid metabolism in the liver; bile; intestine; plasma; cholelithiasis; intestinal lipid absorption; nonalcoholic fatty liver disease; alcoholic liver disease; cholestasis
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Special Issue Information

Dear Colleagues,

The human genome comprises the entire genetic code of three billion letters required to create a human being, and the study of these genes is called genetics. The modification of genes to produce the desired traits in plants, animals, and microbes used for food is a process that began about 10,000 years ago. The recent years have witnessed a rapid advance in the application of genetic technology from single-cell microbial systems to eukaryotic culture systems and up to multicellular whole-animal systems. The development of genetic techniques has accelerated the growth of the biotechnology industry, resulting in a significant increase in the number of recombinant protein products on the market. As a result, new biological entities with added value for innovative medicines—such as increased stability, improved targeting, and reduced toxicity, among others—have been obtained.

Advanced Genetics 2019 is the third edition of a Genomic Medicine conference that was first started in 2017 and has since been held annually. The third edition of the meeting is scheduled to be held on 13–15 November 2019 in Baltimore, MD, USA. This meeting will provide great insights into the recent advances in the field of genetics as well as opportunities to learn more about recently used tools and techniques. Advanced Genetics 2019 will provide a platform for sharing new ideas and thoughts with other fellow researchers.

https://unitedscientificgroup.com/conferences/advanced-genetics/

Accepted abstracts from this conference will have an opportunity to be published in a Special Issue of the MDPI journal Genes (subject to peer review).

Dr. David Q-H Wang
Guest Editor

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Genes is an international peer-reviewed open access monthly journal published by MDPI.

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Keywords

next generation sequencing & genome analysis; genetics and advanced genetics; cancer genetics; evolutionary genetics; gene mutation & cloning; epigenetics; single cell genetics; microbial genomics; genetics disorders, functional genomics; animal genetics; plant genomics; immunogenetics

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Published Papers (10 papers)

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Editorial

Jump to: Research, Review

4 pages, 174 KiB

Open AccessEditorial

Emerging Trends in Deciphering the Pathogenesis of Human Diseases through Genetic Analysis

by David Q.-H. Wang

Genes 2021, 12(1), 96; https://doi.org/10.3390/genes12010096 - 13 Jan 2021

Cited by 2 | Viewed by 1941

Abstract

Any changes in gene expression or protein functions can cause abnormal anatomical, physiological, biochemical, and behavioral modifications in human beings, which can lead to disease [...] Full article

(This article belongs to the Special Issue Selected Papers From the Advanced Genetics Conference 2019)

Research

Jump to: Editorial, Review

21 pages, 2242 KiB

Open AccessArticle

MYC DNA Methylation in Prostate Tumor Tissue is Associated with Gleason Score

by Kathryn Hughes Barry, Kareshma Mohanty, Patricia A. Erickson, Difei Wang, Jianxin Shi, Gary Rose, Ashley Cellini, Kimberly Clark, Nicholas Ambulos, Jr., Jing Yin, Liying Yan, Matthew Poulin, Ann Meyer, Yuji Zhang, Søren M. Bentzen, Allen Burke, Arif Hussain and Sonja I. Berndt

Genes 2021, 12(1), 12; https://doi.org/10.3390/genes12010012 - 24 Dec 2020

Cited by 6 | Viewed by 2495

Abstract

Increasing evidence suggests a role of epigenetic mechanisms at chromosome 8q24, an important cancer genetic susceptibility region, in prostate cancer. We investigated whether MYC DNA methylation at 8q24 (six CpG sites from exon 3 to the 3′ UTR) in prostate tumor was associated with tumor aggressiveness (based on Gleason score, GS), and we incorporated RNA expression data to investigate the function. We accessed radical prostatectomy tissue for 50 Caucasian and 50 African American prostate cancer patients at the University of Maryland Medical Center, selecting an equal number of GS 6 and GS 7 cases per group. MYC DNA methylation was lower in tumor than paired normal prostate tissue for all six CpG sites (median difference: −14.74 to −0.20 percentage points), and we observed similar results for two nearby sites in The Cancer Genome Atlas (p < 0.0001). We observed significantly lower methylation for more aggressive (GS 7) than less aggressive (GS 6) tumors for three exon 3 sites (for CpG 212 (chr8:128753145), GS 6 median = 89.7%; GS 7 median = 85.8%; p-value = 9.4 × 10⁻⁴). MYC DNA methylation was not associated with MYC expression, but was inversely associated with PRNCR1 expression after multiple comparison adjustment (q-value = 0.04). Findings suggest that prostate tumor MYC exon 3 hypomethylation is associated with increased aggressiveness. Full article

(This article belongs to the Special Issue Selected Papers From the Advanced Genetics Conference 2019)

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12 pages, 1599 KiB

Open AccessArticle

Estradiol Enhances Anorectic Effect of Apolipoprotein A-IV through ERα-PI3K Pathway in the Nucleus Tractus Solitarius

by Min Liu, Ling Shen, Meifeng Xu, David Q.-H. Wang and Patrick Tso

Genes 2020, 11(12), 1494; https://doi.org/10.3390/genes11121494 - 12 Dec 2020

Cited by 3 | Viewed by 2050

Abstract

Estradiol (E2) enhances the anorectic action of apolipoprotein A-IV (apoA-IV), however, the intracellular mechanisms are largely unclear. Here we reported that the phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway was significantly activated by E2 and apoA-IV, respectively, in primary neuronal cells isolated from rat embryonic brainstem. Importantly, the combination of E2 and apoA-IV at their subthreshold doses synergistically activated the PI3K/Akt signaling pathway. These effects, however, were significantly diminished by the pretreatment with LY294002, a selective PI3K inhibitor. E2-induced activation of the PI3K/Akt pathway was through membrane-associated ERα, because the phosphorylation of Akt was significantly increased by PPT, an ERα agonist, and by E2-BSA (E2 conjugated to bovine serum albumin) which activates estrogen receptor on the membrane. Centrally administered apoA-IV at a low dose (0.5 µg) significantly suppressed food intake and increased the phosphorylation of Akt in the nucleus tractus solitarius (NTS) of ovariectomized (OVX) rats treated with E2, but not in OVX rats treated with vehicle. These effects were blunted by pretreatment with LY294002. These results indicate that E2’s regulatory role in apoA-IV’s anorectic action is through the ERα-PI3K pathway in the NTS. Manipulation of the PI3K/Akt signaling activation in the NTS may provide a novel therapeutic approach for the prevention and the treatment of obesity-related disorders in females. Full article

(This article belongs to the Special Issue Selected Papers From the Advanced Genetics Conference 2019)

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17 pages, 3442 KiB

Open AccessArticle

WNT11-Conditioned Medium Promotes Angiogenesis through the Activation of Non-Canonical WNT-PKC-JNK Signaling Pathway

by Jingcai Wang, Min Gong, Shi Zuo, Jie Xu, Chris Paul, Hongxia Li, Min Liu, Yi-Gang Wang, Muhammad Ashraf and Meifeng Xu

Genes 2020, 11(11), 1277; https://doi.org/10.3390/genes11111277 - 29 Oct 2020

Cited by 13 | Viewed by 3074

Abstract

Background: We demonstrated that the transduction of Wnt11 into mesenchymal stem cells (MSCs) (MSC^Wnt11) promotes these cells differentiation into cardiac phenotypes. In the present study, we investigated the paracrine effects of MSC^Wnt11 on cardiac function and angiogenesis. Methods and Results: Conditioned medium was collected from MSC^Wnt11 (CdM^Wnt11) and their control cells (CdM^GFP). CdM^Wnt11, especially obtained from MSC^Wnt11 exposed to hypoxia, significantly promoted human umbilical vein endothelial cells (HUVECs) migration and increased capillary-like tube (CLT) formation, which was blocked by Wnt11 neutralizing antibody. Wnt11 protein was significantly higher in CdM^Wnt11 compared to that in CdM^GFP. Directly treating HUVECs with recombinant Wnt11 protein significantly increased CLT formation, which was abrogated by treating cells with the JNK inhibitor SP600125, as well as the PKC inhibitor Calphostin-C. Moreover, the transfection of Wnt11 to HUVECs (H^Wnt11) significantly increased CLT formation and HUVEC migration, as well as upregulated p-pan-PKC and p-JNK expression. Injection of CdM^Wnt11 into the peri-infarct region in a rat acute myocardial infarction (AMI) model significantly improved cardiac function, reduced infarct size, and increased myocardial blood flow and blood vessel density in the ischemic area. Conclusion: Wnt11 released from MSC^Wnt11 increased angiogenesis and improved cardiac function via non-canonical Wnt-PKC-JNK dependent pathways. Full article

(This article belongs to the Special Issue Selected Papers From the Advanced Genetics Conference 2019)

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14 pages, 2429 KiB

Open AccessArticle

OneStopRNAseq: A Web Application for Comprehensive and Efficient Analyses of RNA-Seq Data

by Rui Li, Kai Hu, Haibo Liu, Michael R. Green and Lihua Julie Zhu

Genes 2020, 11(10), 1165; https://doi.org/10.3390/genes11101165 - 2 Oct 2020

Cited by 24 | Viewed by 7462

Abstract

Over the past decade, a large amount of RNA sequencing (RNA-seq) data were deposited in public repositories, and more are being produced at an unprecedented rate. However, there are few open source tools with point-and-click interfaces that are versatile and offer streamlined comprehensive analysis of RNA-seq datasets. To maximize the capitalization of these vast public resources and facilitate the analysis of RNA-seq data by biologists, we developed a web application called OneStopRNAseq for the one-stop analysis of RNA-seq data. OneStopRNAseq has user-friendly interfaces and offers workflows for common types of RNA-seq data analyses, such as comprehensive data-quality control, differential analysis of gene expression, exon usage, alternative splicing, transposable element expression, allele-specific gene expression quantification, and gene set enrichment analysis. Users only need to select the desired analyses and genome build, and provide a Gene Expression Omnibus (GEO) accession number or Dropbox links to sequence files, alignment files, gene-expression-count tables, or rank files with the corresponding metadata. Our pipeline facilitates the comprehensive and efficient analysis of private and public RNA-seq data. Full article

(This article belongs to the Special Issue Selected Papers From the Advanced Genetics Conference 2019)

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16 pages, 2091 KiB

Open AccessArticle

MicroRNA-1253 Regulation of WASF2 (WAVE2) and its Relevance to Racial Health Disparities

by Mercy A. Arkorful, Nicole Noren Hooten, Yongqing Zhang, Amirah N. Hewitt, Lori Barrientos Sanchez, Michele K. Evans and Douglas F. Dluzen

Genes 2020, 11(5), 572; https://doi.org/10.3390/genes11050572 - 20 May 2020

Cited by 4 | Viewed by 3848

Abstract

The prevalence of hypertension among African Americans (AAs) in the US is among the highest of any demographic and affects over two-thirds of AA women. Previous data from our laboratory suggest substantial differential gene expression (DGE) of mRNAs and microRNAs (miRNAs) exists within peripheral blood mononuclear cells (PBMCs) isolated from AA and white women with or without hypertension. We hypothesized that DGE by race may contribute to racial differences in hypertension. In a reanalysis of our previous dataset, we found that the Wiskott–Aldrich syndrome protein Verprolin-homologous protein 2 (WASF2 (also known as WAVE2)) is differentially expressed in AA women with hypertension, along with several other members of the actin cytoskeleton signaling pathway that plays a role in cell shape and branching of actin filaments. We performed an in silico miRNA target prediction analysis that suggested miRNA miR-1253 regulates WASF2. Transfection of miR-1253 mimics into human umbilical vein endothelial cells (HUVECs) and human aortic endothelial cells (HAECs) significantly repressed WASF2 mRNA and protein levels (p < 0.05), and a luciferase reporter assay confirmed that miR-1253 regulates the WASF2 3′ UTR (p < 0.01). miR-1253 overexpression in HUVECs significantly increased HUVEC lamellipodia formation (p < 0.01), suggesting the miR-1253–WASF2 interaction may play a role in cell shape and actin cytoskeleton function. Together, we have identified novel roles for miR-1253 and WASF2 in a hypertension-related disparities context. This may ultimately lead to the discovery of additional actin-related genes which are important in the vascular-related complications of hypertension and influence the disproportionate susceptibility to hypertension among AAs in general and AA women in particular. Full article

(This article belongs to the Special Issue Selected Papers From the Advanced Genetics Conference 2019)

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8 pages, 229 KiB

Open AccessArticle

The Association between ABCB1 C1236T/C3435T SNPs and H. pylori Infection among Jordanians

by Mohammed N. BaniHani, Omar F. Khabour, Karem H. Alzoubi, Nabil A. Bashir, Muhamad Ali K. Shakhatreh, Salsabeel H. Sabi and Nasr Alrabadi

Genes 2020, 11(1), 63; https://doi.org/10.3390/genes11010063 - 5 Jan 2020

Cited by 4 | Viewed by 2578

Abstract

Infection with Helicobacter pylori (H. pylori) is very common and affecting about 50% of the worldwide population. Several genetic variations have been implicated in determining the clinical susceptibility to this infection. In the current study, we examined the association between C1236T (rs1045642) and C3435T (rs1045642) single nucleotide polymorphisms (SNPs) in the ABCB1 gene and the prevalence of H. pylori infection among Jordanians. A total of 412 subjects (257 H. pylori-positive cases and 155 H. pylori-negative controls) were recruited and participated in the study, and the genotyping of the ABCB1 gene was performed using RFLP-PCR techniques. A significant association was detected between C1236T and H. pylori infection (p < 0.01). The frequency of CT genotype was significantly higher in the positive cases (40.1%) compared to the controls (21.3%). In addition, the C3435T SNP was weakly associated with H. pylori infection (p = 0.077). Haplotype analysis of C1236T and C3435T SNPs showed that the TT haplotype was present in 22.7% of the positive cases compared to 30.7% of the negative controls (p < 0.05, odds ratio = 0.663, 95% CI: (0.483–0.911)). Consequently, the TT haplotype seems to decrease the risk of H. pylori infection. In conclusion, the current results suggest an association between ABCB1 SNPs and H. pylori infection in the Jordanian population. Full article

(This article belongs to the Special Issue Selected Papers From the Advanced Genetics Conference 2019)

Review

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21 pages, 1733 KiB

Open AccessReview

An Update on the Lithogenic Mechanisms of Cholecystokinin a Receptor (CCKAR), an Important Gallstone Gene for Lith13

by Helen H. Wang, Piero Portincasa, Min Liu, Patrick Tso and David Q.-H. Wang

Genes 2020, 11(12), 1438; https://doi.org/10.3390/genes11121438 - 29 Nov 2020

Cited by 12 | Viewed by 5932

Abstract

The cholecystokinin A receptor (CCKAR) is expressed predominantly in the gallbladder and small intestine in the digestive system, where it is responsible for CCK’s regulation of gallbladder and small intestinal motility. The effect of CCKAR on small intestinal transit is a physiological response for regulating intestinal cholesterol absorption. The CCKAR gene has been identified to be an important gallstone gene, Lith13, in inbred mice by a powerful quantitative trait locus analysis. Knockout of the CCKAR gene in mice enhances cholesterol cholelithogenesis by impairing gallbladder contraction and emptying, promoting cholesterol crystallization and crystal growth, and increasing intestinal cholesterol absorption. Clinical and epidemiological studies have demonstrated that several variants in the CCKAR gene are associated with increased prevalence of cholesterol cholelithiasis in humans. Dysfunctional gallbladder emptying in response to exogenously administered CCK-8 is often found in patients with cholesterol gallstones, and patients with pigment gallstones display an intermediate degree of gallbladder motility defect. Gallbladder hypomotility is also revealed in some subjects without gallstones under several conditions: pregnancy, total parenteral nutrition, celiac disease, oral contraceptives and conjugated estrogens, obesity, diabetes, the metabolic syndrome, and administration of CCKAR antagonists. The physical–chemical, genetic, and molecular studies of Lith13 show that dysfunctional CCKAR enhances susceptibility to cholesterol gallstones through two primary mechanisms: impaired gallbladder emptying is a key risk factor for the development of gallbladder hypomotility, biliary sludge (the precursor of gallstones), and microlithiasis, as well as delayed small intestinal transit augments cholesterol absorption as a major source for the hepatic hypersecretion of biliary cholesterol and for the accumulation of excess cholesterol in the gallbladder wall that further worsens impaired gallbladder motor function. If these two defects in the gallbladder and small intestine could be prevented by the potent CCKAR agonists, the risk of developing cholesterol gallstones could be dramatically reduced. Full article

(This article belongs to the Special Issue Selected Papers From the Advanced Genetics Conference 2019)

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13 pages, 240 KiB

Open AccessReview

Origin of Genome Instability and Determinants of Mutational Landscape in Cancer Cells

by Sonam Mehrotra and Indraneel Mittra

Genes 2020, 11(9), 1101; https://doi.org/10.3390/genes11091101 - 21 Sep 2020

Cited by 8 | Viewed by 3625

Abstract

Genome instability is a crucial and early event associated with an increased predisposition to tumor formation. In the absence of any exogenous agent, a single human cell is subjected to about 70,000 DNA lesions each day. It has now been shown that physiological cellular processes including DNA transactions during DNA replication and transcription contribute to DNA damage and induce DNA damage responses in the cell. These processes are also influenced by the three dimensional-chromatin architecture and epigenetic regulation which are altered during the malignant transformation of cells. In this review, we have discussed recent insights about how replication stress, oncogene activation, chromatin dynamics, and the illegitimate recombination of cell-free chromatin particles deregulate cellular processes in cancer cells and contribute to their evolution. The characterization of such endogenous sources of genome instability in cancer cells can be exploited for the development of new biomarkers and more effective therapies for cancer treatment. Full article

(This article belongs to the Special Issue Selected Papers From the Advanced Genetics Conference 2019)

22 pages, 2437 KiB

Open AccessReview

Gut Microbiota between Environment and Genetic Background in Familial Mediterranean Fever (FMF)

by Agostino Di Ciaula, Alessandro Stella, Leonilde Bonfrate, David Q. H. Wang and Piero Portincasa

Genes 2020, 11(9), 1041; https://doi.org/10.3390/genes11091041 - 3 Sep 2020

Cited by 17 | Viewed by 8007

Abstract

The gastrointestinal tract hosts the natural reservoir of microbiota since birth. The microbiota includes various bacteria that establish a progressively mutual relationship with the host. Of note, the composition of gut microbiota is rather individual-specific and, normally, depends on both the host genotype and environmental factors. The study of the bacterial profile in the gut demonstrates that dominant and minor phyla are present in the gastrointestinal tract with bacterial density gradually increasing in oro-aboral direction. The cross-talk between bacteria and host within the gut strongly contributes to the host metabolism, to structural and protective functions. Dysbiosis can develop following aging, diseases, inflammatory status, and antibiotic therapy. Growing evidences show a possible link between the microbiota and Familial Mediterranean Fever (FMF), through a shift of the relative abundance in microbial species. To which extent such perturbations of the microbiota are relevant in driving the phenotypic manifestations of FMF with respect to genetic background, remains to be further investigated. Full article

(This article belongs to the Special Issue Selected Papers From the Advanced Genetics Conference 2019)

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