scholarly journals Water stress-associated isolation barriers between two sympatric oak species

2021 ◽  
Author(s):  
Gregoire LE PROVOST ◽  
Benjamin Brachi ◽  
Isabelle Lesur ◽  
Celine Lalanne ◽  
Karine Labadie ◽  
...  

Drought and waterlogging impede tree growth and may even lead to tree death. With climate change, these environmental factors are a growing source of concern, particularly for temperate forests. Oaks, an emblematic group of tree species, have evolved a range of adaptations to cope with these constraints. The two most widely distributed European species pedunculate oak (PO) and sessile oaks (SO) have overlapping ranges, but are highly constrained locally by soil water content variation. These differences in local ecological requirements provide a powerful biological model for studying the role of ecological barriers in speciation. We used an experimental set-up mimicking the ecological preferences of these species, in which seedlings were subjected to waterlogging and drought. We studied gene expression in roots by RNA-seq and identified genes differentially expressed between treatments with different outcomes depending on species. These ″species x environment″ responsive genes revealed adaptive molecular strategies involving adventitious and lateral root formation, aerenchyma formation in PO, and osmoregulation and ABA regulation in SO. With this experimental design, we also identified genes with expression profiles presenting a ″species″ effect regardless of imposed constraints with important roles in intrinsic reproductive barriers. Finally, we compared our findings with those for a genome scan of species divergence and found that the candidate genes were enriched in highly differentiated SNPs. This suggests that many of the genes involved in the contrasting transcriptomic responses are subject to natural selection and that gene regulation helps to maintain these two different oak species in sympatry.

2020 ◽  
Author(s):  
Jianjun Li ◽  
Chenglin Ye ◽  
Cuifang Chang

Abstract Background: Trichomes comprise specialized multicellular structures that have the capacity to synthesize and secrete secondary metabolites and protect plants from biotic and abiotic stresses. However, little is known about the trichome formation mechanism during flower development in Lonicera Japonica Thunb.Results: Here, we present a genome-wide comparative transcriptome analysis between two L. japonica cultivars, toward the identification of biological processes and functional gene activities that occur during flowering stage trichome development. In this study, the density and average lengths of flower trichomes were at their highest during three green periods. Using the Illumina RNA-Seq method, we obtained 134,304 unigenes, 33,733 of which were differentially expressed. In an analysis of 40 differentially expressed unigenes (DEGs) involved in trichome development, 29 of these were transcription factors. The DEGs analysis of plant hormone signal transduction indicated that plant growth and development may be independent of GA and CTK signaling pathways, and plant stress may be independent of JA and ET signaling pathways. We successfully isolated key genes involved in the floral biosynthesis of odors, tastes, colors, and plant hormones, and proposed biosynthetic pathways for sesquiterpenoid, triterpenoid, monoterpenoid, flavonoid, and plant hormones. Furthermore, 82 DEGs were assigned to cell cycles and 2,616 were predicted as plant resistance genes (PRGs).Conclusions: This study provides a comprehensive characterization of the expression profiles of flower development during the seven developmental stages of L. japonica, thereby offering valuable insights into the molecular networks that underly flower development in L. japonica.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Xia Tang ◽  
Delong Feng ◽  
Min Li ◽  
Jinxue Zhou ◽  
Xiaoyuan Li ◽  
...  

Abstract Fully elucidating the molecular mechanisms of non-coding RNAs (ncRNAs), including micro RNAs (miRNAs) and long non-coding RNAs (lncRNAs), underlying hepatocarcinogenesis is challenging. We characterized the expression profiles of ncRNAs and constructed a regulatory mRNA-lncRNA-miRNA (MLMI) network based on transcriptome sequencing (RNA-seq) of hepatocellular carcinoma (HCC, n = 9) patients. Of the identified miRNAs (n = 203) and lncRNAs (n = 1,090), we found 16 significantly differentially expressed (DE) miRNAs and three DE lncRNAs. The DE RNAs were highly enriched in 21 functional pathways implicated in HCC (p < 0.05), including p53, MAPK, and NAFLD signaling. Potential pairwise interactions between DE ncRNAs and mRNAs were fully characterized using in silico prediction and experimentally-validated evidence. We for the first time constructed a MLMI network of reciprocal interactions for 16 miRNAs, three lncRNAs, and 253 mRNAs in HCC. The predominant role of MEG3 in the MLMI network was validated by its overexpression in vitro that the expression levels of a proportion of MEG3-targeted miRNAs and mRNAs was changed significantly. Our results suggested that the comprehensive MLMI network synergistically modulated carcinogenesis, and the crosstalk of the network provides a new avenue to accurately describe the molecular mechanisms of hepatocarcinogenesis.


Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 1199-1199 ◽  
Author(s):  
Brian Liddicoat ◽  
Robert Piskol ◽  
Alistair Chalk ◽  
Miyoko Higuchi ◽  
Peter Seeburg ◽  
...  

Abstract The role of RNA and its regulation is becoming increasingly appreciated as a vital component of hematopoietic development. RNA editing by members of the Adenosine Deaminase Acting on RNA (ADAR) gene family is a form of post-transcriptional modification which converts genomically encoded adenosine to inosine (A-to-I) in double-stranded RNA. A-to-I editing by ADAR directly converts the sequence of the RNA substrate and can alter the structure, function, processing, and localization of the targeted RNA. ADAR1 is ubiquitously expressed and we have previously described essential roles in the development of hematopoietic and hepatic organs. Germline ablation of murine ADAR1 results in a significant upregulation of interferon (IFN) stimulated genes and embryonic death between E11.5 and E12.5 associated with fetal liver disintegration and failed hemopoiesis. To determine the biological importance of A-to-I editing by ADAR1, we generated an editing dead knock-in allele of ADAR1 (ADAR1E861A). Mice homozygous for the ADAR1E861A allele died in utero at ∼E13.5. The fetal liver (FL) was small and had significantly lower cellularity than in controls. Analysis of hemopoiesis demonstrated increased apoptosis and a loss of hematopoietic stem cells (HSC) and all mature lineages. Most notably erythropoiesis was severely impaired with ∼7-fold reduction across all erythrocyte progenitor populations compared to controls. These data are consistent with our previous findings that ADAR1 is essential for erythropoiesis (unpublished data) and suggest that the ADAR1E861A allele phenocopies the null allele in utero. To assess the requirement of A-to-I editing in adult hematopoiesis, we generated mice where we could somatically delete the wild-type ADAR1 allele and leave only ADAR1E861A expressed in HSCs (hScl-CreERAdar1fl/E861A). In comparison to hScl-CreERAdar1fl/+ controls, hScl-CreERAdar1fl/E861A mice were anemic and had severe leukopenia 20 days post tamoxifen treatment. Investigation of marrow hemopoiesis revealed a significant loss of all cells committed to the erythroid lineage in hScl-CreERAdar1fl/E861A mice, despite having elevated phenotypic HSCs. Upon withdrawal of tamoxifen diet, all blood parameters were restored to control levels within 12 weeks owing to strong selection against cells expressing only the ADAR1E861A allele. To understand the mechanism through which ADAR1 mediated A-to-I editing regulates hematopoiesis, RNA-seq was performed. Gene expression profiles showed that a loss of ADAR1 mediated A-to-I editing resulted in a significant upregulation of IFN signatures, consistent with the gene expression changes in ADAR1 null mice. To define substrates of ADAR1 we assessed A-to-I mismatches in the RNA-seq data sets. 3,560 previously known and 353 novel A-to-I editing sites were identified in our data set. However, no single editing substrate discovered could account for the IFN signature observed or the lethality of ADAR1E861A/E861A mice. These results demonstrate that ADAR1 mediated A-to-I editing is essential for the maintenance of both fetal and adult hemopoiesis in a cell-autonomous manner and a key suppressor of the IFN response in hematopoiesis. Furthermore the ADAR1E861A allele demonstrates the essential role of ADAR1 in vivo is A-to-I editing. Disclosures: Hartner: TaconicArtemis: Employment.


2011 ◽  
Vol 79 (5) ◽  
pp. 1848-1854 ◽  
Author(s):  
Emilie Courtine ◽  
Frédéric Pène ◽  
Nicolas Cagnard ◽  
Julie Toubiana ◽  
Catherine Fitting ◽  
...  

ABSTRACTNF-κB is a critical regulator of gene expression during severe infections. NF-κB comprises homo- and heterodimers of proteins from the Rel family. Among them, p50 and p65 have been clearly implicated in the pathophysiology of sepsis. In contrast, the role of cRel in sepsis is still controversial and has been poorly studied in single-pathogen infections. We aimed to investigate the consequences of cRel deficiency in a cecal ligation and puncture (CLP) model of sepsis. We have approached the underlying mechanisms of host defense by analyzing bacterial clearance, systemic inflammation, and the distribution of spleen dendritic cell subsets. Moreover, by using a genome-wide technology, we have also analyzed the CLP-induced modifications in gene expression profiles both in wild-type (wt) and inrel−/−mice. The absence of cRel enhances mortality due to polymicrobial sepsis. Despite normal pathogen clearance, cRel deficiency leads to an altered systemic inflammatory response associated with a sustained loss of the spleen lymphoid dendritic cells. Furthermore, a whole-blood microarray study reveals that the differential outcome between wt andrel−/−mice during sepsis is preceded by remarkable changes in the expression of hundreds of genes involved in aspects of host-pathogen interaction, such as host survival and lipid metabolism. In conclusion, cRel is a key NF-κB member required for host antimicrobial defenses and a regulatory transcription subunit that controls the inflammatory and immune responses in severe infection.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Junjie Shao ◽  
Liqiang Wang ◽  
Xinyue Liu ◽  
Meng Yang ◽  
Haimei Chen ◽  
...  

Abstract Circular RNAs (circRNAs) play important roles in animals, plants, and fungi. However, no circRNAs have been reported in Ganoderma lucidum. Here, we carried out a genome-wide identification of the circRNAs in G.lucidum using RNA-Seq data, and analyzed their features. In total, 250 and 2193 circRNAs were identified from strand-specific RNA-seq data generated from the polyA(−) and polyA(−)/RNase R-treated libraries, respectively. Six of 131 (4.58%) predicted circRNAs were experimentally confirmed. Across three developmental stages, 731 exonic circRNAs (back spliced read counts ≥ 5) and their parent genes were further analyzed. CircRNAs were preferred originating from exons with flanking introns, and the lengths of the flanking intron were longer than those of the control introns. A total of 200 circRNAs were differentially expressed across the three developmental stages of G. lucidum. The expression profiles of 119 (16.3%) exonic circRNAs and their parent genes showed significant positive correlations (r ≥ 0.9, q < 0.01), whereas 226 (30.9%) exonic circRNAs and their parent genes exhibited significant negative correlations (r ≤ −0.9, q < 0.01), in which 53 parent genes are potentially involved in the transcriptional regulation, polysaccharide biosynthesis etc. Our results indicated that circRNAs are present in G. lucidum, with potentially important regulatory roles.


2021 ◽  
Author(s):  
Taeyoung Hwang ◽  
Sojin Kim ◽  
Tamrin Chowdhury ◽  
Hyeon Jong Yu ◽  
Kyung-Min Kim ◽  
...  

Abstract BackgroundAlu is a primate-specific repeat element in the human genome and has been increasingly appreciated as a regulatory element in many biological processes. But the role of Alu has not been studied comprehensively in brain tumor because an evolutionary perspective has been the subject of little research in brain tumor. We aim to investigate the relevance of Alu to the gliomagenesis.MethodsUsing a total of 41 pairs of neurotypicial brain tissue samples and samples of diverse gliomas, we performed strand-specific RNA-seq and analyzed two Alu-associated post-transcriptional regulations, A-to-I editing and circular RNAs, and Alu expression in a genome-wide way. ResultsWe found that while both A-to-I editing and circular RNA are decreased overall in gliomas, grade 2 oligodendrogliomas do not show this same pattern of global changes. Instead, in comparison with other gliomas, oligodendrogliomas showed a higher proportion of perturbed Alu RNA. Adenosine deaminase acting on RNA 2 (ADAR2) was down-regulated in gliomas other than grade 2 oligodendrogliomas, contributing to the observed Alu-associated perturbation. ConclusionsOur results demonstrate that Alu is associated with glioma development and grade 2 oligodendroglioma exhibits a unique pattern of Alu-associated post-transcriptional regulations, which provides an insight to gliomagenesis from the perspective of an evolutionary genetic element.


F1000Research ◽  
2017 ◽  
Vol 6 ◽  
pp. 2162 ◽  
Author(s):  
Travis L. Jensen ◽  
Michael Frasketi ◽  
Kevin Conway ◽  
Leigh Villarroel ◽  
Heather Hill ◽  
...  

RNA-Seq is increasingly being used to measure human RNA expression on a genome-wide scale. Expression profiles can be interrogated to identify and functionally characterize treatment-responsive genes. Ultimately, such controlled studies promise to reveal insights into molecular mechanisms of treatment effects, identify biomarkers, and realize personalized medicine. RNA-Seq Reports (RSEQREP) is a new open-source cloud-enabled framework that allows users to execute start-to-end gene-level RNA-Seq analysis on a preconfigured RSEQREP Amazon Virtual Machine Image (AMI) hosted by AWS or on their own Ubuntu Linux machine. The framework works with unstranded, stranded, and paired-end sequence FASTQ files stored locally, on Amazon Simple Storage Service (S3), or at the Sequence Read Archive (SRA). RSEQREP automatically executes a series of customizable steps including reference alignment, CRAM compression, reference alignment QC, data normalization, multivariate data visualization, identification of differentially expressed genes, heatmaps, co-expressed gene clusters, enriched pathways, and a series of custom visualizations. The framework outputs a file collection that includes a dynamically generated PDF report using R, knitr, and LaTeX, as well as publication-ready table and figure files. A user-friendly configuration file handles sample metadata entry, processing, analysis, and reporting options. The configuration supports time series RNA-Seq experimental designs with at least one pre- and one post-treatment sample for each subject, as well as multiple treatment groups and specimen types. All RSEQREP analyses components are built using open-source R code and R/Bioconductor packages allowing for further customization. As a use case, we provide RSEQREP results for a trivalent influenza vaccine (TIV) RNA-Seq study that collected 1 pre-TIV and 10 post-TIV vaccination samples (days 1-10) for 5 subjects and two specimen types (peripheral blood mononuclear cells and B-cells).


F1000Research ◽  
2018 ◽  
Vol 6 ◽  
pp. 2162 ◽  
Author(s):  
Travis L. Jensen ◽  
Michael Frasketi ◽  
Kevin Conway ◽  
Leigh Villarroel ◽  
Heather Hill ◽  
...  

RNA-Seq is increasingly being used to measure human RNA expression on a genome-wide scale. Expression profiles can be interrogated to identify and functionally characterize treatment-responsive genes. Ultimately, such controlled studies promise to reveal insights into molecular mechanisms of treatment effects, identify biomarkers, and realize personalized medicine. RNA-Seq Reports (RSEQREP) is a new open-source cloud-enabled framework that allows users to execute start-to-end gene-level RNA-Seq analysis on a preconfigured RSEQREP Amazon Virtual Machine Image (AMI) hosted by AWS or on their own Ubuntu Linux machine via a Docker container or installation script. The framework works with unstranded, stranded, and paired-end sequence FASTQ files stored locally, on Amazon Simple Storage Service (S3), or at the Sequence Read Archive (SRA). RSEQREP automatically executes a series of customizable steps including reference alignment, CRAM compression, reference alignment QC, data normalization, multivariate data visualization, identification of differentially expressed genes, heatmaps, co-expressed gene clusters, enriched pathways, and a series of custom visualizations. The framework outputs a file collection that includes a dynamically generated PDF report using R, knitr, and LaTeX, as well as publication-ready table and figure files. A user-friendly configuration file handles sample metadata entry, processing, analysis, and reporting options. The configuration supports time series RNA-Seq experimental designs with at least one pre- and one post-treatment sample for each subject, as well as multiple treatment groups and specimen types. All RSEQREP analyses components are built using open-source R code and R/Bioconductor packages allowing for further customization. As a use case, we provide RSEQREP results for a trivalent influenza vaccine (TIV) RNA-Seq study that collected 1 pre-TIV and 10 post-TIV vaccination samples (days 1-10) for 5 subjects and two specimen types (peripheral blood mononuclear cells and B-cells).


2018 ◽  
Vol 115 (13) ◽  
pp. E2930-E2939 ◽  
Author(s):  
David Angeles-Albores ◽  
Carmie Puckett Robinson ◽  
Brian A. Williams ◽  
Barbara J. Wold ◽  
Paul W. Sternberg

RNA-sequencing (RNA-seq) is commonly used to identify genetic modules that respond to perturbations. In single cells, transcriptomes have been used as phenotypes, but this concept has not been applied to whole-organism RNA-seq. Also, quantifying and interpreting epistatic effects using expression profiles remains a challenge. We developed a single coefficient to quantify transcriptome-wide epistasis that reflects the underlying interactions and which can be interpreted intuitively. To demonstrate our approach, we sequenced four single and two double mutants of Caenorhabditis elegans. From these mutants, we reconstructed the known hypoxia pathway. In addition, we uncovered a class of 56 genes with HIF-1–dependent expression that have opposite changes in expression in mutants of two genes that cooperate to negatively regulate HIF-1 abundance; however, the double mutant of these genes exhibits suppression epistasis. This class violates the classical model of HIF-1 regulation but can be explained by postulating a role of hydroxylated HIF-1 in transcriptional control.


PLoS ONE ◽  
2021 ◽  
Vol 16 (10) ◽  
pp. e0258291
Author(s):  
Braulio Valdebenito-Maturana ◽  
Esteban Arancibia ◽  
Gonzalo Riadi ◽  
Juan Carlos Tapia ◽  
Mónica Carrasco

Transposable Elements (TEs) are ubiquitous genetic elements with the ability to move within a genome. TEs contribute to a large fraction of the repetitive elements of a genome, and because of their nature, they are not routinely analyzed in RNA-Seq gene expression studies. Amyotrophic Lateral Sclerosis (ALS) is a lethal neurodegenerative disease, and a well-accepted model for its study is the mouse harboring the human SOD1G93A mutant. In this model, landmark stages of the disease can be recapitulated at specific time points, making possible to understand changes in gene expression across time. While there are several works reporting TE activity in ALS models, they have not explored their activity through the disease progression. Moreover, they have done it at the expense of losing their locus of expression. Depending on their genomic location, TEs can regulate genes in cis and in trans, making locus-specific analysis of TEs of importance in order to understand their role in modulating gene expression. Particularly, the locus-specific role of TEs in ALS has not been fully elucidated. In this work, we analyzed publicly available RNA-Seq datasets of the SOD1G93A mouse model, to understand the locus-specific role of TEs. We show that TEs become up-regulated at the early stages of the disease, and via statistical associations, we speculate that they can regulate several genes, which in turn might be contributing to the genetic dysfunction observed in ALS.


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