scholarly journals Genomic Insights Into the Molecular Basis of Sexual Selection in Birds

2021 ◽  
Vol 9 ◽  
Author(s):  
Shubham K. Jaiswal ◽  
Ankit Gupta ◽  
Aaron B. A. Shafer ◽  
Vishnu Prasoodanan P. K. ◽  
Nagarjun Vijay ◽  
...  
Keyword(s):  
Gene Expression ◽  
Sexual Selection ◽  
Gene Expression Regulation ◽  
Draft Genome ◽  
Honest Signal ◽  
Phenotypic Data ◽  
Genome Wide ◽  
Pavo Cristatus ◽  
Depth Analysis ◽  
Genomic Basis

Sexual selection is a well-known biological process, yet the genomic basis and patterns of sexual selection are not fully understood. The extravagant ornamental plumage of peacock (Pavo cristatus) was instrumental in shaping Charles Darwin's theory of sexual selection and is considered to be an honest signal of its immunocompetence. Here, we used the recently generated draft genome sequence of peafowl (Pavo cristatus) and carried out a comparative analysis across 11 bird genomes that encompass a range of sexual selection and also had high-quality genomic and phenotypic data publically available to study the genomic basis of sexual selection. We found that varying degree of purifying selection was the predominant mechanism of action for sexual selection at the genome-wide scale and observed that sexual selection mostly influences genes regulating gene expression and protein processing. Specifically, the genome-wide phylogenetically corrected regression analysis supported the continuous or ongoing model of sexual selection. Genes involved in nucleic acid binding and gene expression regulation, including a specific regulator of sex-determination known as TRA2A to be under positive selection in the species with high post-copulatory sexual selection manifested as high sperm competition. We also detected specific feather-related and immune-related gene-pairs evolving under similar selection pressures across the 11 species, including peacock (Pavo cristatus), which is consistent with the Hamilton-Zuk hypothesis. The comparative genomics analysis of 11 avian taxa has provided new insights on the molecular underpinnings of sexual selection and identifies specific genomic regions for future in-depth analysis.

scholarly journals Differential evolution in 3′UTRs leads to specific gene expression in Staphylococcus

2020 ◽  
Vol 48 (5) ◽  
pp. 2544-2563 ◽  
Author(s):  
Pilar Menendez-Gil ◽  
Carlos J Caballero ◽  
Arancha Catalan-Moreno ◽  
Naiara Irurzun ◽  
Inigo Barrio-Hernandez ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gene Expression Regulation ◽  
Bacterial Species ◽  
Regulatory Elements ◽  
Specific Gene ◽  
Species Differentiation ◽  
Orthologous Genes ◽  
Genome Wide ◽  
Sequence Variations ◽  
Species Specific

Abstract The evolution of gene expression regulation has contributed to species differentiation. The 3′ untranslated regions (3′UTRs) of mRNAs include regulatory elements that modulate gene expression; however, our knowledge of their implications in the divergence of bacterial species is currently limited. In this study, we performed genome-wide comparative analyses of mRNAs encoding orthologous proteins from the genus Staphylococcus and found that mRNA conservation was lost mostly downstream of the coding sequence (CDS), indicating the presence of high sequence diversity in the 3′UTRs of orthologous genes. Transcriptomic mapping of different staphylococcal species confirmed that 3′UTRs were also variable in length. We constructed chimeric mRNAs carrying the 3′UTR of orthologous genes and demonstrated that 3′UTR sequence variations affect protein production. This suggested that species-specific functional 3′UTRs might be specifically selected during evolution. 3′UTR variations may occur through different processes, including gene rearrangements, local nucleotide changes, and the transposition of insertion sequences. By extending the conservation analyses to specific 3′UTRs, as well as the entire set of Escherichia coli and Bacillus subtilis mRNAs, we showed that 3′UTR variability is widespread in bacteria. In summary, our work unveils an evolutionary bias within 3′UTRs that results in species-specific non-coding sequences that may contribute to bacterial diversity.

The COP9 signalosome influences the epigenetic landscape of Arabidopsis thaliana

2018 ◽  
Vol 35 (16) ◽  
pp. 2718-2723 ◽  
Author(s):  
Tamir Tuller ◽  
Alon Diament ◽  
Avital Yahalom ◽  
Assaf Zemach ◽  
Shimshi Atar ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Arabidopsis Thaliana ◽  
Gene Expression Regulation ◽  
Developmental Pathways ◽  
Cop9 Signalosome ◽  
Supplementary Information ◽  
Loss Of Function ◽  
Genome Wide ◽  
High Level

Abstract Motivation The COP9 signalosome is a highly conserved multi-protein complex consisting of eight subunits, which influences key developmental pathways through its regulation of protein stability and transcription. In Arabidopsis thaliana, mutations in the COP9 signalosome exhibit a number of diverse pleiotropic phenotypes. Total or partial loss of COP9 signalosome function in Arabidopsis leads to misregulation of a number of genes involved in DNA methylation, suggesting that part of the pleiotropic phenotype is due to global effects on DNA methylation. Results We determined and analyzed the methylomes and transcriptomes of both partial- and total-loss-of-function Arabidopsis mutants of the COP9 signalosome. Our results support the hypothesis that the COP9 signalosome has a global genome-wide effect on methylation and that this effect is at least partially encoded in the DNA. Our analyses suggest that COP9 signalosome-dependent methylation is related to gene expression regulation in various ways. Differentially methylated regions tend to be closer in the 3D conformation of the genome to differentially expressed genes. These results suggest that the COP9 signalosome has a more comprehensive effect on gene expression than thought before, and this is partially related to regulation of methylation. The high level of COP9 signalosome conservation among eukaryotes may also suggest that COP9 signalosome regulates methylation not only in plants but also in other eukaryotes, including humans. Supplementary information Supplementary data are available at Bioinformatics online.

scholarly journals Pathogen Genetic Control of Transcriptome Variation in the Arabidopsis thaliana – Botrytis cinerea Pathosystem

Genetics ◽  
2020 ◽  
Vol 215 (1) ◽  
pp. 253-266 ◽  
Author(s):  
Nicole E. Soltis ◽  
Celine Caseys ◽  
Wei Zhang ◽  
Jason A. Corwin ◽  
Susanna Atwell ◽  
...  
Keyword(s):  
Gene Expression ◽  
Arabidopsis Thaliana ◽  
Botrytis Cinerea ◽  
Gene Expression Regulation ◽  
Expression Regulation ◽  
Necrotrophic Pathogen ◽  
Control Of Gene Expression ◽  
Genome Wide ◽  
Pathogen Control ◽  
Transcriptome Variation

In plant–pathogen relations, disease symptoms arise from the interaction of the host and pathogen genomes. Host–pathogen functional gene interactions are well described, whereas little is known about how the pathogen genetic variation modulates both organisms’ transcriptomes. To model and generate hypotheses on a generalist pathogen control of gene expression regulation, we used the Arabidopsis thaliana–Botrytis cinerea pathosystem and the genetic diversity of a collection of 96 B. cinerea isolates. We performed expression-based genome-wide association (eGWA) for each of 23,947 measurable transcripts in Arabidopsis (host), and 9267 measurable transcripts in B. cinerea (pathogen). Unlike other eGWA studies, we detected a relative absence of locally acting expression quantitative trait loci (cis-eQTL), partly caused by structural variants and allelic heterogeneity hindering their identification. This study identified several distantly acting trans-eQTL linked to eQTL hotspots dispersed across Botrytis genome that altered only Botrytis transcripts, only Arabidopsis transcripts, or transcripts from both species. Gene membership in the trans-eQTL hotspots suggests links between gene expression regulation and both known and novel virulence mechanisms in this pathosystem. Genes annotated to these hotspots provide potential targets for blocking manipulation of the host response by this ubiquitous generalist necrotrophic pathogen.

An Integrated Epigenomic Analysis Approach To Determine the Molecular Basis of Acute Leukemias.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 3276-3276
Author(s):  
Maria E. Figueroa ◽  
Kenny M. Ye ◽  
Elisabeth Paietta ◽  
John M. Greally ◽  
Ari M. Melnick
Keyword(s):  
Gene Expression ◽  
Molecular Basis ◽  
Expression Profiles ◽  
Gene Activity ◽  
Gene Copy ◽  
Comparative Genomic ◽  
Acute Leukemias ◽  
Expression Arrays ◽  
Genome Wide ◽  
Depth Analysis

Abstract Acute leukemias are classified based on their immunologic, cytogenetic and morphologic characteristics. However, in most instances, response to treatment and survival probability cannot be accurately predicted, suggesting that the disease is even more complex and heterogeneous than can be shown with current techniques. Although prognostic value has been shown for certain gene expression profiles, expression profile studies are limited by the fact that only a snapshot of mRNA content is obtained in a basal state, failing to represent how genes will respond to different stresses, also failing to detect the roles of genes expressed at lower levels for which major changes in expression levels are often lost in the “noise” of expression arrays. In order to overcome these issues and to provide a more accurate molecular phenotype of acute leukemias, we established an integrated epigenomic and genomic high-throughput platform using novel techniques and custom high-density oligonucleotide arrays. We combine studies of i) genome-wide cytosine methylation using a novel technique we developed that provides accurate quantitative determination of DNA methylation levels, using genome-wide custom oligo arrays, ii) chromatin structure by ChIP on chip for histone code settings associated with active or repressed genes using 24 K promoter tiling arrays, iii) gene copy number by array-based comparative genomic hybridization (array CGH) at 6 kb resolution genome-wide and iv) 36 K gene expression arrays. Results are validated by single locus quantitative PCR techniques. Cross platform integration is facilitated by use of NimbleGen oligo arrays for all studies and analysis using novel bioinformatics and statistical models. We used this integrative analysis platform to perform an in-depth analysis of the epigenomic basis of AML and ALL using primary patient samples and cell lines. The data allowed us to generate a “gene activity index” which identified the ability of genes to be expressed to be characterized genome-wide in AML and ALL cells. This data also allowed a much more comprehensive analysis of pathways active in these cells to be identified in comparison to expression arrays alone. Our current studies apply integrative platform and gene activity indexing to large series of patients enrolled in multicenter clinical trials in order to provide high-resolution analysis of the molecular basis of acute leukemia.

scholarly journals Regulation of Chromatin Accessibility by hypoxia and HIF

2022 ◽  
Author(s):  
Michael Batie ◽  
Julianty Frost ◽  
Dilem Shakir ◽  
Sonia Rocha
Keyword(s):  
Gene Expression ◽  
Gene Expression Regulation ◽  
Chromatin Accessibility ◽  
Adaptation To Hypoxia ◽  
Hypoxia Inducible Factors ◽  
Physiological Processes ◽  
Pathological Conditions ◽  
Genome Wide ◽  
The Family ◽  
Necessary And Sufficient

Reduced oxygen availability (hypoxia) can act as a signalling cue in physiological processes such as development, but also in pathological conditions such as cancer or ischaemic disease. As such, understanding how cells and organisms respond to hypoxia is of great importance. The family of transcription factors called Hypoxia Inducible Factors (HIFs) coordinate a transcriptional programme required for survival and adaptation to hypoxia. The effects of hypoxia and HIF on the chromatin accessibility landscape are still unclear. Here, using genome wide mapping of chromatin accessibility via ATAC-seq, we find hypoxia induces loci specific changes in chromatin accessibility enriched at hypoxia transcriptionally responsive genes. These changes are predominantly HIF dependent, reversible upon reoxygenation and partially mimicked by chemical HIF stabilisation independent of molecular dioxygenase inhibition. This work demonstrates that indeed, HIF stabilisation is necessary and sufficient to alter chromatin accessibility in hypoxia, with implications for our understanding of gene expression regulation by hypoxia and HIF.

scholarly journals Promoter Proximal Pausing Limits Tumorous Growth Induced by the Yki Transcription Factor in Drosophila

Genetics ◽  
2020 ◽  
Vol 216 (1) ◽  
pp. 67-77 ◽  
Author(s):  
Sanket Nagarkar ◽  
Ruchi Wasnik ◽  
Pravallika Govada ◽  
Stephen Cohen ◽  
L. S. Shashidhara
Keyword(s):  
Gene Expression ◽  
Rna Polymerase Ii ◽  
Gene Expression Regulation ◽  
Regulation Of Gene Expression ◽  
Elongation Factor ◽  
Imaginal Discs ◽  
Link Type ◽  
Genome Wide ◽  
Wing Imaginal Discs ◽  
Tumorous Growth

Promoter proximal pausing (PPP) of RNA polymerase II has emerged as a crucial rate-limiting step in the regulation of gene expression. Regulation of PPP is brought about by complexes 7SK snRNP, P-TEFb (Cdk9/cycT), and the negative elongation factor (NELF), which are highly conserved from Drosophila to humans. Here, we show that RNAi-mediated depletion of bin3 or Hexim of the 7SK snRNP complex or depletion of individual components of the NELF complex enhances Yki-driven growth, leading to neoplastic transformation of Drosophila wing imaginal discs. We also show that increased CDK9 expression cooperates with Yki in driving neoplastic growth. Interestingly, overexpression of CDK9 on its own or in the background of depletion of one of the components of 7SK snRNP or the NELF complex necessarily, and specifically, needed Yki overexpression to cause tumorous growth. Genome-wide gene expression analyses suggested that deregulation of protein homeostasis is associated with tumorous growth of wing imaginal discs. As both Fat/Hippo/Yki pathway and PPP are highly conserved, our observations may provide insights into mechanisms of oncogenic function of YAP—the ortholog of Yki in humans.

scholarly journals N4-acetyldeoxycytosine DNA modification marks euchromatin regions in Arabidopsis thaliana

2022 ◽  
Vol 23 (1) ◽  
Author(s):  
Shuai Wang ◽  
Hairong Xie ◽  
Fei Mao ◽  
Haiyan Wang ◽  
Shu Wang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Genomic Dna ◽  
Gene Expression Regulation ◽  
Detection Methods ◽  
Dna Modification ◽  
Protein Coding ◽  
Transcription Start Sites ◽  
Genome Wide ◽  
Multiple Detection ◽  
Cellular Dna

Abstract Background Direct analogs of chemically modified bases that carry important epigenetic information, such as 5-methylcytosine (m5C)/5-methyldeoxycytosine (5mC), 5-hydroxymethylcytosine (hm5C)/5-hydroxymethyldeoxycytosine (5hmC), and N6-methyladenosine (m6A)/N6-methyldeoxyadenosine (6mA), are detected in both RNA and DNA, respectively. The modified base N4-acetylcytosine (ac4C) is well studied in RNAs, but its presence and epigenetic roles in cellular DNA have not been explored. Results Here, we demonstrate the existence of N4-acetyldeoxycytosine (4acC) in genomic DNA of Arabidopsis with multiple detection methods. Genome-wide profiling of 4acC modification reveals that 4acC peaks are mostly distributed in euchromatin regions and present in nearly half of the expressed protein-coding genes in Arabidopsis. 4acC is mainly located around transcription start sites and positively correlates with gene expression levels. Imbalance of 5mC does not directly affect 4acC modification. We also characterize the associations of 4acC with 5mC and histone modifications that cooperatively regulate gene expression. Moreover, 4acC is also detected in genomic DNA of rice, maize, mouse, and human by mass spectrometry. Conclusions Our findings reveal 4acC as a hitherto unknown DNA modification in higher eukaryotes. We identify potential interactions of this mark with other epigenetic marks in gene expression regulation.

Uncovering AML Subtypes and Their Biology: Applying Genome-Wide Profiling.

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. sci-12-sci-12
Author(s):  
Ruud Delwel
Keyword(s):  
Gene Expression ◽  
Gene Expression Profiling ◽  
Chromosomal Aberrations ◽  
Expression Profiling ◽  
Chromosomal Abnormalities ◽  
Gene Expression Signature ◽  
Hematopoietic Stem ◽  
Genome Wide ◽  
Number Of Patients ◽  
Depth Analysis

Classification of AML subtypes based on chromosomal abnormalities is clinically relevant, as several of them are associated with distinct clinical behavior. For instance, recurring reciprocal translocations t(15;17), t(8;21), or inv(16)(p13q22)/t(16;16) predict favorable prognosis, whereas other chromosomal aberrations, such as t(6;9), −7/7q- or inv(3;3)/t(3;3), are associated with inferior outcome. In approximately 40–50% of AML patients no chromosomal aberrations have been identified. In ~75% of this latter patient group molecular lesions have been found, particularly in CEBPA, NPM1, or FLT3 (FLT3-ITD). Importantly, CEBPA or NPM1 single mutants associate with a favorable outcome, whereas cases that carry NPM1 as well as FLT3-ITD mutations correspond with unfavorable prognosis. In approximately 25% of AML no (cyto)genetic abnormalities have been found so far. We have carried out gene expression profiling (GEP) to uncover novel AML subtypes and obtain insight on the biology of these leukemias. By applying GEP to a large cohort of human AML (n>550), we identified subgroups of patients with a gene expression signature similar to that of cases with known chromosomal or molecular aberrations. We will discuss two examples. 1) AML cases that carry chromosome 3q26 lesions show high expression of EVI1, the gene that resides in this locus. Gene expression analysis revealed a significant number of patients without 3q26 cytogenetic lesions but with high EVI1 expression. Importantly, although those cases appeared frequently cytogenetically normal, fluorescent in situ hybridization (FISH) using EVI1 genomic probes revealed complex 3q26 abnormalities in ~50% of those cases. In the other half, no aberrations have been found so far. These data appear clinically relevant, as high EVI1 expression levels associate with poor treatment outcome. Consequently, we have developed an EVI1 specific Q-PCR assay to be used as a diagnostic test in AML. 2) Using gene expression profiling, we identified a novel AML subgroup that showed a gene expression profile highly similar to that of CEBPAmut AML cases. A closer look at those leukemias revealed that the CEBPA gene was switched off by promoter hypermethylation, explaining the high similarity with CEBPAmut AML. In depth analysis of the GEP data further demonstrated that this particular AML subgroup carried myeloid as well as T-lymphoid features, in particular high levels of the T cell marker CD7. Interestingly, hematopoietic stem cells isolated from conditional CEBPA knock out mice showed high CD7 expression as well, which could be reverted by reintroduction of CEBPA. These results indicate that absence of CEBPA in the leukemia subgroup explains, at least in part, the unique biological features identified by GEP. Finally, using a novel genome-wide promoter methylation assay we found that CEBPA methylation was associated with aberrant hypermethylation of many genes. Taken together, these data suggest the existence of a previously unrecognized subtype of AML, which results from aberrant epigenetic programming.

scholarly journals IFI16 promotes human embryonic stem cell trilineage specification through interaction with p53

2020 ◽  
Vol 5 (1) ◽  
Author(s):  
Qian He ◽  
Zubiao Wu ◽  
Wei Yang ◽  
Doukou Jiang ◽  
Chaofeng Hu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gene Expression Regulation ◽  
Embryonic Stem ◽  
The Self ◽  
Self Renewal ◽  
Genome Wide ◽  
Inducible Protein ◽  
Jnk Activation ◽  
External Signals ◽  
Differentiation Gene

Abstract Transcriptional regulation plays an essential role in the self-renewal and differentiation of human embryonic stem cells (hESCs). However, how external signals disrupt the self-renewal regulatory network and further drive hESC differentiation remains largely unknown. Here, we found the immune regulative protein, gamma-interferon-inducible protein 16 (IFI16) was involved in the regulation of both self-renewal and differentiation gene expression during hESC trilineage specification through interaction with p53. IFI16 expression levels were upregulated through JNK activation. IFI16 knockdown delayed the downregulation of self-renewal gene expression and suppressed the upregulation of differentiation gene expression, while IFI16 overexpression accelerated trilineage specification. Furthermore, IFI16 stabilized p53-binding in the genome through IFI16-p53 interaction and differentially regulated self-renewal and differentiation gene expression. Together, our results suggest a particular role of IFI16 in differential gene expression regulation during trilineage specification of hESCs in a manner that is dependent on the genome-wide profile of p53-binding directed by IFI16-p53 interaction.

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