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Accelerated evolution in the human lineage led to gain and loss of transcriptional enhancers in the RBFOX1 locus

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE242504 | GEO | 2024/05/21

REPOSITORIES: GEO

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Accelerated evolution in the human lineage led to gain and loss of transcriptional enhancers in the <i>RBFOX1</i> locus.

Project description:A long-standing goal of evolutionary biology is to decode how changes in gene regulatory networks contribute to human-specific traits. Human accelerated regions (HARs) are prime candidates for driving gene regulatory modifications in human development. The RBFOX1 locus is densely populated with HARs, providing a set of potential regulatory elements that could have changed its expression in the human lineage. Here, we examined the role of RBFOX1-HARs using transgenic zebrafish reporter assays and identified 15 transcriptional enhancers that are active in the developing nervous system, 9 of which displayed differential activity between the human and chimpanzee sequences. The engineered loss of two selected RBFOX1-HARs in knockout mouse models modified Rbfox1 expression at specific developmental stages and tissues in the brain, influencing the expression and splicing of a high number of Rbfox1 target genes. Our results provided insight into the spatial and temporal changes in gene expression driven by RBFOX1-HARs.

| S-EPMC11204294 | biostudies-literature

Accelerated evolution in the human lineage led to gain and loss of transcriptional enhancers in the RBFOX1 locus [cortex]

Project description:A long-standing goal of evolutionary biology is to decode how changes in gene regulatory networks contribute to human-specific traits. Human Accelerated Regions (HARs) are prime candidates for driving gene regulatory modifications in human development. The RBFOX1 locus is densely populated with HARs, providing a set of potential regulatory elements that could have changed its expression in the human lineage. Here we examined the role of RBFOX1-HARs using transgenic zebrafish reporter assays and identified fifteen transcriptional enhancers that are active in the developing nervous system, ten of which displayed differential expression between the human and chimpanzee sequences. The engineered loss of two selected RBFOX1-HARs in knockout mouse models increased Rbfox1 expression at specific developmental stages and tissues in the brain, influencing the expression and splicing of a high number of Rbfox1 target genes. Our results provided insight into the spatial and temporal changes in gene expression driven by RBFOX1-HARs.

2024-05-21 | GSE242503 | GEO

Accelerated evolution in the human lineage led to gain and loss of transcriptional enhancers in the RBFOX1 locus [midbrain]

2024-05-21 | GSE242502 | GEO

Accelerated evolution in the human lineage led to gain and loss of transcriptional enhancers in the RBFOX1 locus

Project description:Accelerated evolution in the human lineage led to gain and loss of transcriptional enhancers in the RBFOX1 locus

| PRJNA1013588 | ENA

Accelerated evolution in the human lineage led to gain and loss of transcriptional enhancers in the RBFOX1 locus [cortex]

Project description:Accelerated evolution in the human lineage led to gain and loss of transcriptional enhancers in the RBFOX1 locus [cortex]

| PRJNA1013594 | ENA

Accelerated evolution in the human lineage led to gain and loss of transcriptional enhancers in the RBFOX1 locus [midbrain]

Project description:Accelerated evolution in the human lineage led to gain and loss of transcriptional enhancers in the RBFOX1 locus [midbrain]

| PRJNA1013592 | ENA

Evolution of a complex locus: exon gain, loss and divergence at the Gr39a locus in Drosophila.

Project description:BackgroundGene families typically evolve by gene duplication followed by the adoption of new or altered gene functions. A different way to evolve new but related functions is alternative splicing of existing exons of a complex gene. The chemosensory gene families of animals are characterised by numerous loci of related function. Alternative splicing has only rarely been reported in chemosensory loci, for example in 5 out of around 120 loci in Drosophila melanogaster. The gustatory receptor gene Gr39a has four large exons that are alternatively spliced with three small conserved exons. Recently the genome sequences of eleven additional species of Drosophila have become available allowing us to examine variation in the structure of the Gr39a locus across a wide phylogenetic range of fly species.Methodology/principal findingsWe describe a fifth exon and show that the locus has a complex evolutionary history with several duplications, pseudogenisations and losses of exons. PAML analyses suggested that the whole gene has a history of purifying selection, although this was less strong in exons which underwent duplication.Conclusions/significanceEstimates of functional divergence between exons were similar in magnitude to functional divergence between duplicated genes, suggesting that exon divergence is broadly equivalent to gene duplication.

| S-EPMC2204066 | biostudies-literature

Evolution of transcriptional enhancers and animal diversity.

Project description:Deciphering the genetic bases that drive animal diversity is one of the major challenges of modern biology. Although four decades ago it was proposed that animal evolution was mainly driven by changes in cis-regulatory DNA elements controlling gene expression rather than in protein-coding sequences, only now are powerful bioinformatics and experimental approaches available to accelerate studies into how the evolution of transcriptional enhancers contributes to novel forms and functions. In the introduction to this Theme Issue, we start by defining the general properties of transcriptional enhancers, such as modularity and the coexistence of tight sequence conservation with transcription factor-binding site shuffling as different mechanisms that maintain the enhancer grammar over evolutionary time. We discuss past and current methods used to identify cell-type-specific enhancers and provide examples of how enhancers originate de novo, change and are lost in particular lineages. We then focus in the central part of this Theme Issue on analysing examples of how the molecular evolution of enhancers may change form and function. Throughout this introduction, we present the main findings of the articles, reviews and perspectives contributed to this Theme Issue that together illustrate some of the great advances and current frontiers in the field.

| S-EPMC3826491 | biostudies-other

Lineage-specific accelerated sequences underlying primate evolution.

Project description:Understanding the mechanisms underlying phenotypic innovation is a key goal of comparative genomic studies. Here, we investigated the evolutionary landscape of lineage-specific accelerated regions (LinARs) across 49 primate species. Genomic comparison with dense taxa sampling of primate species significantly improved LinAR detection accuracy and revealed many novel human LinARs associated with brain development or disease. Our study also yielded detailed maps of LinARs in other primate lineages that may have influenced lineage-specific phenotypic innovation and adaptation. Functional experimentation identified gibbon LinARs, which could have participated in the developmental regulation of their unique limb structures, whereas some LinARs in the Colobinae were associated with metabolite detoxification which may have been adaptive in relation to their leaf-eating diet. Overall, our study broadens knowledge of the functional roles of LinARs in primate evolution.

| S-EPMC10413682 | biostudies-literature

CHD1 Loss Alters AR Binding at Lineage-Specific Enhancers and Modulates Distinct Transcriptional Programs to Drive Prostate Tumorigenesis.

Project description:Deletion of the gene encoding the chromatin remodeler CHD1 is among the most common alterations in prostate cancer (PCa); however, the tumor-suppressive functions of CHD1 and reasons for its tissue-specific loss remain undefined. We demonstrated that CHD1 occupied prostate-specific enhancers enriched for the androgen receptor (AR) and lineage-specific cofactors. Upon CHD1 loss, the AR cistrome was redistributed in patterns consistent with the oncogenic AR cistrome in PCa samples and drove tumor formation in the murine prostate. Notably, this cistrome shift was associated with a unique AR transcriptional signature enriched for pro-oncogenic pathways unique to this tumor subclass. Collectively, these data credential CHD1 as a tumor suppressor in the prostate that constrains AR binding/function to limit tumor progression.

| S-EPMC6467783 | biostudies-literature

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