scholarly journals Comparative transcriptome analysis of mule uncovered several heterosis-related genes for improving muscular endurance and cognition

2019 ◽  
Author(s):  
Shan Gao
Keyword(s):  
Alternative Splicing ◽  
Molecular Genetic ◽  
Hybrid Vigor ◽  
Neuronal System ◽  
Future Studies ◽  
Genome Wide ◽  
A Genome ◽  
Genetic Mechanisms ◽  
Productive Traits ◽  
Genome Wide Gene Expression

AbstractHeterosis has been widely exploited in animal and plant breeding to enhance the productive traits of hybrid progeny of two breeds or two species. Although, there were multiple models for explaining the hybrid vigor, such as dominance and over-dominance hypothesis, its underlying molecular genetic mechanisms remain equivocal. The aim of this study is through comparing the different expression genes (DEGs) and different alternative splicing (DAS) genes to explore the mechanism of heterosis. Here, we performed a genome-wide gene expression and alternative splicing analysis of two heterotic crosses between donkey and horse in three tissues. The results showed that the DAS genes influenced the heterosis-related phenotypes in a unique than DEGs and about 10% DEGs are DAS genes. In addition, over 69.7% DEGs and 87.2% DAS genes showed over-dominance or dominance, respectively. Furthermore, the “Muscle Contraction” and “Neuronal System” pathways were significantly enriched both for the DEGs and DAS genes in muscle. TNNC2 and RYR1 genes may contribute to mule’s great endurance while GRIA2 and GRIN1 genes may be related with mule’s cognition. Together, these DEGs and DAS genes provide the candidates for future studies of the genetic and molecular mechanism of heterosis in mule.

scholarly journals Comparative Transcriptome Profiling Analysis Uncovers Novel Heterosis-Related Candidate Genes Associated with Muscular Endurance in Mules

Animals ◽  
2020 ◽  
Vol 10 (6) ◽  
pp. 980
Author(s):  
Shan Gao ◽  
Hojjat Asadollahpour Nanaei ◽  
Bin Wei ◽  
Yu Wang ◽  
Xihong Wang ◽  
...  
Keyword(s):  
Alternative Splicing ◽  
Transcriptome Profiling ◽  
Muscular Endurance ◽  
Breeding Programs ◽  
Future Studies ◽  
Genome Wide ◽  
Genetic Mechanisms ◽  
Productive Traits ◽  
Genome Wide Gene Expression ◽  
Profiling Analysis

Heterosis has been widely exploited in animal and plant breeding programs to enhance the productive traits of hybrid progeny from two breeds or species. However, its underlying genetic mechanisms remain enigmatic. Transcriptome profiling analysis can be used as a method for exploring the mechanism of heterosis. Here, we performed genome-wide gene expression and alternative splicing (AS) analyses in different tissues (muscle, brain, and skin) from crosses between donkeys and horses. Our results indicated that 86.1% of the differentially expressed genes (DEGs) and 87.2% of the differential alternative splicing (DAS) genes showed over-dominance and dominance in muscle. Further analysis showed that the “muscle contraction” pathway was significantly enriched for both the DEGs and DAS genes in mule muscle tissue. Taken together, these DEGs and DAS genes could provide an index for future studies of the genetic and molecular mechanism of heterosis in the hybrids of donkey and horse.

scholarly journals Genome-wide gene expression changes in postpartum depression point towards an altered immune landscape

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Divya Mehta ◽  
Karen Grewen ◽  
Brenda Pearson ◽  
Shivangi Wani ◽  
Leanne Wallace ◽  
...  
Keyword(s):  
Gene Expression ◽  
Depressive Symptoms ◽  
Postpartum Depression ◽  
Expression Profiles ◽  
Depression Scale ◽  
Well Being ◽  
Health Concern ◽  
Genome Wide ◽  
A Genome ◽  
Genome Wide Gene Expression

AbstractMaternal postpartum depression (PPD) is a significant public health concern due to the severe negative impact on maternal and child health and well-being. In this study, we aimed to identify genes associated with PPD. To do this, we investigated genome-wide gene expression profiles of pregnant women during their third trimester of pregnancy and tested the association of gene expression with perinatal depressive symptoms. A total of 137 women from a cohort from the University of North Carolina, USA were assessed. The main phenotypes analysed were Edinburgh Postnatal Depression Scale (EPDS) scores at 2 months postpartum and PPD (binary yes/no) based on an EPDS cutoff of 10. Illumina NextSeq500/550 transcriptomic sequencing from whole blood was analysed using the edgeR package. We identified 71 genes significantly associated with postpartum depression scores at 2 months, after correction for multiple testing at 5% FDR. These included several interesting candidates including TNFRSF17, previously reported to be significantly upregulated in women with PPD and MMP8, a matrix metalloproteinase gene, associated with depression in a genome-wide association study. Functional annotation of differentially expressed genes revealed an enrichment of immune response-related biological processes. Additional analysis of genes associated with changes in depressive symptoms from recruitment to 2 months postpartum identified 66 genes significant at an FDR of 5%. Of these genes, 33 genes were also associated with depressive symptoms at 2 months postpartum. Comparing the results with previous studies, we observed that 15.4% of genes associated with PPD in this study overlapped with 700 core maternal genes that showed significant gene expression changes across multiple brain regions (P = 7.9e-05) and 29–53% of the genes were also associated with estradiol changes in a pharmacological model of depression (P values range = 1.2e-4–2.1e-14). In conclusion, we identified novel genes and validated genes previously associated with oestrogen sensitivity in PPD. These results point towards the role of an altered immune transcriptomic landscape as a vulnerability factor for PPD.

Abstract 12192: MBNL1 Directly Regulates the Alternative Splicing of mRNAs That Promote Myofibroblast Differentiation

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Jennifer Davis ◽  
Michelle Sargent ◽  
Jianjian Shi ◽  
Lei Wei ◽  
Maurice S Swanson ◽  
...  
Keyword(s):  
Alternative Splicing ◽  
Molecular Mechanisms ◽  
Rna Binding ◽  
Transforming Growth Factor ◽  
Ventricular Remodeling ◽  
Cardiac Injury ◽  
Myofibroblast Differentiation ◽  
Genome Wide ◽  
A Genome

Rationale: During the cardiac injury response fibroblasts differentiate into myofibroblasts, a cell type that enhances extracellular matrix production and facilitates ventricular remodeling. To better understand the molecular mechanisms whereby myofibroblasts are generated in the heart we performed a genome-wide screen with 18,000 cDNAs, which identified the RNA-binding protein muscleblind-like splicing regulator 1 (MBNL1), suggesting a novel association between mRNA alternative splicing and the regulation of myofibroblast differentiation. Objective: To determine the mechanism whereby MBNL1 regulates myofibroblast differentiation and the cardiac fibrotic response. Methods and Results: Confirming the results from our genome wide screen, adenoviral-mediated overexpression of MBNL1 promoted transformation of rat cardiac fibroblasts and mouse embryonic fibroblasts (MEFs) into myofibroblasts, similar to the level of conversion obtained by the profibrotic agonist transforming growth factor β (TGFβ). Antithetically, Mbnl1 -/- MEFs were refractory to TGFβ-induced myofibroblast differentiation. MBNL1 expression is induced in transforming fibroblasts in response to TGFβ and angiotensin II. These results were extended in vivo by analysis of dermal wound healing, a process dependent on myofibroblast differentiation and their proper activity. By day 6 control mice had achieved 82% skin wound closure compared with only 40% in Mbnl1 -/- mice. Moreover, Mbnl1 -/- mice had reduced survival following myocardial infarction injury due to defective fibrotic scar formation and healing. High throughput RNA sequencing (RNAseq) and RNA immunoprecipitation revealed that MBNL1 directly regulates the alternative splicing of transcripts for myofibroblast signaling factors and cytoskeletal-assembly elements. Functional analysis of these factors as mediators of MBNL1 activity is also described here. Conclusions: Collectively, our data suggest that MBNL1 coordinates myofibroblast transformation by directly mediating the alternative splicing of an array of mRNAs encoding differentiation-specific signaling transcripts, which then alter the fibroblast proteome for myofibroblast structure and function.

scholarly journals Genome-Wide Analysis of Alternative Splicing during Host-Virus Interactions in Chicken

Viruses ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 2409
Author(s):  
Weiwei Liu ◽  
Yingjie Sun ◽  
Xusheng Qiu ◽  
Chunchun Meng ◽  
Cuiping Song ◽  
...  
Keyword(s):  
Alternative Splicing ◽  
Virus Infection ◽  
Immune Gene ◽  
Genome Wide Analysis ◽  
Pathogen Invasion ◽  
Avian Virus ◽  
Genome Wide ◽  
A Genome ◽  
Model Animal ◽  
Alternative Splicing Events

The chicken is a model animal for the study of evolution, immunity and development. In addition to their use as a model organism, chickens also represent an important agricultural product. Pathogen invasion has already been shown to modulate the expression of hundreds of genes, but the role of alternative splicing in avian virus infection remains unclear. We used RNA-seq data to analyze virus-induced changes in the alternative splicing of Gallus gallus, and found that a large number of alternative splicing events were induced by virus infection both in vivo and in vitro. Virus-responsive alternative splicing events preferentially occurred in genes involved in metabolism and transport. Many of the alternatively spliced transcripts were also expressed from genes with a function relating to splicing or immune response, suggesting a potential impact of virus infection on pre-mRNA splicing and immune gene regulation. Moreover, exon skipping was the most frequent AS event in chickens during virus infection. This is the first report describing a genome-wide analysis of alternative splicing in chicken and contributes to the genomic resources available for studying host–virus interaction in this species. Our analysis fills an important knowledge gap in understanding the extent of genome-wide alternative splicing dynamics occurring during avian virus infection and provides the impetus for the further exploration of AS in chicken defense signaling and homeostasis.

scholarly journals Generation and Transcriptome Profiling of Slr1-d7 and Slr1-d8 Mutant Lines with a New Semi-Dominant Dwarf Allele of SLR1 Using the CRISPR/Cas9 System in Rice

2020 ◽  
Vol 21 (15) ◽  
pp. 5492 ◽  
Author(s):  
Yu Jin Jung ◽  
Jong Hee Kim ◽  
Hyo Ju Lee ◽  
Dong Hyun Kim ◽  
Jihyeon Yu ◽  
...  
Keyword(s):  
Gene Expression Analysis ◽  
Transcriptome Profiling ◽  
Rna Seq ◽  
Loss Of Function ◽  
Amino Acid Motif ◽  
Dwarf Phenotype ◽  
Genome Wide ◽  
A Genome ◽  
Mutant Lines ◽  
Genome Wide Gene Expression

The rice SLR1 gene encodes the DELLA protein (protein with DELLA amino acid motif), and a loss-of-function mutation is dwarfed by inhibiting plant growth. We generate slr1-d mutants with a semi-dominant dwarf phenotype to target mutations of the DELLA/TVHYNP domain using CRISPR/Cas9 genome editing in rice. Sixteen genetic edited lines out of 31 transgenic plants were generated. Deep sequencing results showed that the mutants had six different mutation types at the target site of the TVHYNP domain of the SLR1 gene. The homo-edited plants selected individuals without DNA (T-DNA) transcribed by segregation in the T1 generation. The slr1-d7 and slr1-d8 plants caused a gibberellin (GA)-insensitive dwarf phenotype with shrunken leaves and shortened internodes. A genome-wide gene expression analysis by RNA-seq indicated that the expression levels of two GA-related genes, GA20OX2 (Gibberellin oxidase) and GA3OX2, were increased in the edited mutant plants, suggesting that GA20OX2 acts as a convert of GA12 signaling. These mutant plants are required by altering GA responses, at least partially by a defect in the phytohormone signaling system process and prevented cell elongation. The new mutants, namely, the slr1-d7 and slr1-d8 lines, are valuable semi-dominant dwarf alleles with potential application value for molecule breeding using the CRISPR/Cas9 system in rice.

scholarly journals Population Genomic Evidence Reveals Subtle Patterns of Differentiation in the Trophically Polymorphic Cuatro Ciénegas Cichlid, Herichthys minckleyi

2019 ◽  
Vol 110 (3) ◽  
pp. 361-369 ◽  
Author(s):  
Katherine L Bell ◽  
Chris C Nice ◽  
Darrin Hulsey
Keyword(s):  
Gene Flow ◽  
Biological Diversity ◽  
Molecular Genetic ◽  
Molecular Ecology ◽  
Cichlid Fish ◽  
Genome Wide ◽  
A Genome ◽  
The Face ◽  
Or Gene ◽  
Herichthys Minckleyi

Abstract In recent decades, an increased understanding of molecular ecology has led to a reinterpretation of the role of gene flow during the evolution of reproductive isolation and biological novelty. For example, even in the face of ongoing gene flow strong selection may maintain divergent polymorphisms, or gene flow may introduce novel biological diversity via hybridization and introgression from a divergent species. Herein, we elucidate the evolutionary history and genomic basis of a trophically polymorphic trait in a species of cichlid fish, Herichthys minckleyi. We explored genetic variation at 3 hierarchical levels; between H. minckleyi (n = 69) and a closely related species Herichthys cyanoguttatus (n = 10), between H. minckleyi individuals from 2 geographic locations, and finally between individuals with alternate morphotypes at both a genome-wide and locus-specific scale. We found limited support for the hypothesis that the H. minckleyi polymorphism is the result of ongoing hybridization between the 2 species. Within H. minckleyi we found evidence of geographic genetic structure, and using traditional population genetic analyses found that individuals of alternate morphotypes within a pool appear to be panmictic. However, when we used a locus-specific approach to examine the relationship between multi-locus genotype, tooth size, and geographic sampling, we found the first evidence for molecular genetic differences between the H. minckleyi morphotypes.

scholarly journals Evaluating the contribution of cell-type specific alternative splicing to variation in lipid levels

2019 ◽  
Author(s):  
K.A.B. Gawronski ◽  
W. Bone ◽  
Y. Park ◽  
E. Pashos ◽  
X. Wang ◽  
...  
Keyword(s):  
Alternative Splicing ◽  
Quantitative Trait ◽  
Cell Types ◽  
Genome Wide Association ◽  
Genome Wide Association Studies ◽  
Lipid Levels ◽  
Cell Type ◽  
Genome Wide ◽  
Genetic Mechanisms ◽  
Cell Type Specific

AbstractBackgroundGenome-wide association studies have identified 150+ loci associated with lipid levels. However, the genetic mechanisms underlying most of these loci are not well-understood. Recent work indicates that changes in the abundance of alternatively spliced transcripts contributes to complex trait variation. Consequently, identifying genetic loci that associate with alternative splicing in disease-relevant cell types and determining the degree to which these loci are informative for lipid biology is of broad interest.Methods and ResultsWe analyze gene splicing in 83 sample-matched induced pluripotent stem cell (iPSC) and hepatocyte-like cell (HLC) lines (n=166), as well as in an independent collection of primary liver tissues (n=96). We observe that transcript splicing is highly cell-type specific, and the genes that are differentially spliced between iPSCs and HLCs are enriched for metabolism pathway annotations. We identify 1,381 HLC splicing quantitative trait loci (sQTLs) and 1,462 iPSC sQTLs and find that sQTLs are often shared across cell types. To evaluate the contribution of sQTLs to variation in lipid levels, we conduct colocalization analysis using lipid genome-wide association data. We identify 19 lipid-associated loci that colocalize either with an HLC expression quantitative trait locus (eQTL) or sQTL. Only one locus colocalizes with both an sQTL and eQTL, indicating that sQTLs contribute information about GWAS loci that cannot be obtained by analysis of steady-state gene expression alone.ConclusionsThese results provide an important foundation for future efforts that use iPSC and iPSC-derived cells to evaluate genetic mechanisms influencing both cardiovascular disease risk and complex traits in general.

scholarly journals Identification of Genes Regulating Cell Death inStaphylococcus aureus

2019 ◽  
Author(s):  
Rebecca Yee ◽  
Jie Feng ◽  
Jiou Wang ◽  
Jiazhen Chen ◽  
Ying Zhang
Keyword(s):  
Cell Death ◽  
Acetic Acid ◽  
Drug Targets ◽  
Opportunistic Pathogen ◽  
Infection Model ◽  
Chronic Infections ◽  
Bacterial Cell Death ◽  
Genome Wide ◽  
A Genome ◽  
Genetic Mechanisms

AbstractStaphylococcus aureusis an opportunistic pathogen that causes acute and chronic infections. Due toS. aureus’ s highly resistant and persistent nature, it is paramount to identify better drug targets in order to eradicateS. aureusinfections. Despite the efforts in understanding bacterial cell death, the genes and pathways ofS. aureuscell death remain elusive. Here, we performed a genome-wide screen using a transposon mutant library to study the genetic mechanisms involved inS. aureuscell death. Using a precisely controlled heat-ramp and acetic acid exposure assays, mutations in 27 core genes (hsdR1, hslO, nsaS, sspA, folD, mfd, vraF, kdpB, USA300HOU_2684, 0868, 0369, 0420, 1154, 0142, 0930, 2590, 0997, 2559, 0044, 2004, 1209, 0152, 2455, 0154, 2386, 0232, 0350 involved in transporters, transcription, metabolism, peptidases, kinases, transferases, SOS response, nucleic acid and protein synthesis) caused the bacteria to be more death-resistant. In addition, we identified mutations in core 10 genes (capA, gltT, mnhG1,USA300HOU_1780, 2496, 0200, 2029, 0336, 0329, 2386, involved in transporters, metabolism, transcription, cell wall synthesis) from heat-ramp and acetic acid that caused the bacteria to be more death-sensitive or with defect in persistence. Interestingly, death-resistant mutants were more virulent than the parental strain USA300 and caused increased mortality in aCaenorhabditis elegansinfection model. Conversely, death-sensitive mutants were less persistent and formed less persister cells upon exposure to different classes of antibiotics. These findings provide new insights into the mechanisms ofS. aureuscell death and offer new therapeutic targets for developing more effective treatments caused byS. aureus.

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