scholarly journals Functional analysis of sense organ specification in the Tribolium castaneum larva reveals divergent mechanisms in insects

BMC Biology ◽  
2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Marleen Klann ◽  
Magdalena Ines Schacht ◽  
Matthew Alan Benton ◽  
Angelika Stollewerk
Keyword(s):  
Gene Expression ◽  
Transcription Factors ◽  
Tribolium Castaneum ◽  
Dominant Role ◽  
Sense Organ ◽  
Past Research ◽  
Cell Types ◽  
Sensory Organ ◽  
Sense Organs ◽  
Evolutionary Scenario

Abstract Insects and other arthropods utilise external sensory structures for mechanosensory, olfactory, and gustatory reception. These sense organs have characteristic shapes related to their function, and in many cases are distributed in a fixed pattern so that they are identifiable individually. In Drosophila melanogaster, the identity of sense organs is regulated by specific combinations of transcription factors. In other arthropods, however, sense organ subtypes cannot be linked to the same code of gene expression. This raises the questions of how sense organ diversity has evolved and whether the principles underlying subtype identity in D. melanogaster are representative of other insects. Here, we provide evidence that such principles cannot be generalised, and suggest that sensory organ diversification followed the recruitment of sensory genes to distinct sensory organ specification mechanism. Results We analysed sense organ development in a nondipteran insect, the flour beetle Tribolium castaneum, by gene expression and RNA interference studies. We show that in contrast to D. melanogaster, T. castaneum sense organs cannot be categorised based on the expression or their requirement for individual or combinations of conserved sense organ transcription factors such as cut and pox neuro, or members of the Achaete-Scute (Tc ASH, Tc asense), Atonal (Tc atonal, Tc cato, Tc amos), and neurogenin families (Tc tap). Rather, our observations support an evolutionary scenario whereby these sensory genes are required for the specification of sense organ precursors and the development and differentiation of sensory cell types in diverse external sensilla which do not fall into specific morphological and functional classes. Conclusions Based on our findings and past research, we present an evolutionary scenario suggesting that sense organ subtype identity has evolved by recruitment of a flexible sensory gene network to the different sense organ specification processes. A dominant role of these genes in subtype identity has evolved as a secondary effect of the function of these genes in individual or subsets of sense organs, probably modulated by positional cues.

scholarly journals Sense organ formation and identity are controlled by divergent mechanisms in insects

2020 ◽  
Author(s):  
Marleen Klann ◽  
Magdalena Ines Schacht ◽  
Matthew Alan Benton ◽  
Angelika Stollewerk
Keyword(s):  
Transcription Factors ◽  
Sense Organ ◽  
Past Research ◽  
Cell Types ◽  
Functional Categories ◽  
Sense Organs ◽  
Organ Transcription ◽  
Default State ◽  
Development And Differentiation ◽  
Sensory Structures

AbstractInsects and other arthropods utilise external sensory structures for mechanosensory, olfactory and gustatory reception. These sense organs have characteristic shapes related to their function, and in many cases are distributed in a fixed pattern so that they are identifiable individually. In Drosophila melanogaster, the identity of sense organs is regulated by specific combinations of transcription factors. In other arthropods, however, sense organ subtypes cannot be linked to the same code of gene expression. This raises the questions of how sense organ diversity has evolved in arthropods, and if the D. melanogaster subtype identity principle is representative for insects. To address these questions, we analyse sense organ development in another insect, the flour beetle Tribolium castaneum. We show that in contrast to D. melanogaster, T. castaneum sense organs cannot be categorised based on their requirement for individual or combinations of the conserved sense organ transcription factors such as cut and pox-neuro and members of the Achaete-Scute (Tc ASH, Tc asense) and Atonal family (Tc atonal, Tc cato, Tc amos). Rather, these genes are required for the specification of sense organ precursors and the development and differentiation of sensory cell types in diverse external sensilla. Based on our findings and past research, we present an evolutionary scenario suggesting that sensory organs have diversified from a default state through subsequent recruitment of sensory genes to the different sense organ specification processes. A specific role for genes in subtype identity has evolved as a secondary effect of the function of these genes in individual or subsets of sense organs, which can largely not be aligned with morphological or functional categories.

scholarly journals Single-nuclei chromatin profiling of ventral midbrain reveals cell identity transcription factors and cell-type-specific gene regulatory variation

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Yujuan Gui ◽  
Kamil Grzyb ◽  
Mélanie H. Thomas ◽  
Jochen Ohnmacht ◽  
Pierre Garcia ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcription Factors ◽  
Cell Types ◽  
Mouse Strains ◽  
Cell Type ◽  
Data Set ◽  
Cell Identity ◽  
Regulatory Variation ◽  
Ventral Midbrain ◽  
Cell Type Specific

Abstract Background Cell types in ventral midbrain are involved in diseases with variable genetic susceptibility, such as Parkinson’s disease and schizophrenia. Many genetic variants affect regulatory regions and alter gene expression in a cell-type-specific manner depending on the chromatin structure and accessibility. Results We report 20,658 single-nuclei chromatin accessibility profiles of ventral midbrain from two genetically and phenotypically distinct mouse strains. We distinguish ten cell types based on chromatin profiles and analysis of accessible regions controlling cell identity genes highlights cell-type-specific key transcription factors. Regulatory variation segregating the mouse strains manifests more on transcriptome than chromatin level. However, cell-type-level data reveals changes not captured at tissue level. To discover the scope and cell-type specificity of cis-acting variation in midbrain gene expression, we identify putative regulatory variants and show them to be enriched at differentially expressed loci. Finally, we find TCF7L2 to mediate trans-acting variation selectively in midbrain neurons. Conclusions Our data set provides an extensive resource to study gene regulation in mesencephalon and provides insights into control of cell identity in the midbrain and identifies cell-type-specific regulatory variation possibly underlying phenotypic and behavioural differences between mouse strains.

scholarly journals Transcriptional Regulation of Autophagy Genes via Stage-Specific Activation of CEBPB and PPARG during Adipogenesis: A Systematic Study Using Public Gene Expression and Transcription Factor Binding Datasets

Cells ◽  
2019 ◽  
Vol 8 (11) ◽  
pp. 1321 ◽  
Author(s):  
Mahmoud Ahmed ◽  
Trang Huyen Lai ◽  
Jin Seok Hwang ◽  
Sahib Zada ◽  
Trang Minh Pham ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Transcriptional Regulation ◽  
Transcription Factors ◽  
High Throughput Sequencing ◽  
Cell Model ◽  
Cell Types ◽  
Autophagy Gene ◽  
Occupancy Patterns ◽  
Differentiation Stage

Autophagy is the cell self-eating mechanism to maintain cell homeostasis by removing damaged intracellular proteins or organelles. It has also been implicated in the development and differentiation of various cell types including the adipocyte. Several links between adipogenic transcription factors and key autophagy genes has been suggested. In this study, we tried to model the gene expression and their transcriptional regulation during the adipocyte differentiation using high-throughput sequencing datasets of the 3T3-L1 cell model. We applied the gene expression and co-expression analysis to all and the subset of autophagy genes to study the binding, and occupancy patterns of adipogenic factors, co-factors and histone modifications on key autophagy genes. We also analyzed the gene expression of key autophagy genes under different transcription factor knockdown adipocyte cells. We found that a significant percent of the variance in the autophagy gene expression is explained by the differentiation stage of the cell. Adipogenic master regulators, such as CEBPB and PPARG target key autophagy genes directly. In addition, the same factor may also control autophagy gene expression indirectly through autophagy transcription factors such as FOXO1, TFEB or XBP1. Finally, the binding of adipogenic factors is associated with certain patterns of co-factors binding that might modulate the functions. Some of the findings were further confirmed under the knockdown of the adipogenic factors in the differentiating adipocytes. In conclusion, autophagy genes are regulated as part of the transcriptional programs through adipogenic factors either directly or indirectly through autophagy transcription factors during adipogenesis.

Differential configurations involving binding of USF transcription factors and Twist1 regulate Alx3 promoter activity in mesenchymal and pancreatic cells

2013 ◽  
Vol 450 (1) ◽  
pp. 199-208 ◽  
Author(s):  
Patricia García-Sanz ◽  
Antonio Fernández-Pérez ◽  
Mario Vallejo
Keyword(s):  
Gene Expression ◽  
Transcription Factors ◽  
Promoter Activity ◽  
Cell Types ◽  
Regulatory Elements ◽  
Proximal Promoter ◽  
Homeodomain Protein ◽  
Glucose Homoeostasis ◽  
Pancreatic Cells ◽  
Primary Mouse

During embryonic development, the aristaless-type homeodomain protein Alx3 is expressed in the forehead mesenchyme and contributes to the regulation of craniofacial development. In the adult, Alx3 is expressed in pancreatic islets where it participates in the control of glucose homoeostasis. In the present study, we investigated the transcriptional regulation of Alx3 gene expression in these two cell types. We found that the Alx3 promoter contains two E-box regulatory elements, named EB1 and EB2, that provide binding sites for the basic helix–loop–helix transcription factors Twist1, E47, USF (upstream stimulatory factor) 1 and USF2. In primary mouse embryonic mesenchymal cells isolated from the forehead, EB2 is bound by Twist1, whereas EB1 is bound by USF1 and USF2. Integrity of both EB1 and EB2 is required for Twist1-mediated transactivation of the Alx3 promoter, even though Twist1 does not bind to EB1, indicating that binding of USF1 and USF2 to this element is required for Twist1-dependent Alx3 promoter activity. In contrast, in pancreatic islet insulin-producing cells, the integrity of EB2 is not required for proximal promoter activity. The results of the present study indicate that USF1 and USF2 are important regulatory factors for Alx3 gene expression in different cell types, whereas Twist1 contributes to transcriptional transactivation in mesenchymal, but not in pancreatic, cells.

scholarly journals Spatial transcriptomics reveals the architecture of the tumor/microenvironment interface

2020 ◽  
Author(s):  
Miranda V. Hunter ◽  
Reuben Moncada ◽  
Joshua M. Weiss ◽  
Itai Yanai ◽  
Richard M. White
Keyword(s):  
Gene Expression ◽  
Transcription Factors ◽  
Tumor Microenvironment ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Cell Types ◽  
Human Melanoma ◽  
Zebrafish Model ◽  
Interface Cell ◽  
Ets Family

SUMMARYDuring tumor progression, cancer cells come into contact with new cell types in the microenvironment, but it is unclear how tumor cells adapt to new environments. Here, we integrate spatial transcriptomics and scRNA-seq to characterize tumor/microenvironment interactions during the initial steps of invasion. Using a zebrafish model of melanoma, we identify a unique “interface” cell state at the tumor/microenvironment boundary. This interface is composed of specialized tumor and microenvironment cells that upregulate a common set of cilia genes, and cilia proteins are enriched only where the tumor contacts the microenvironment. Cilia gene expression is regulated by ETS-family transcription factors, which normally act to suppress cilia genes outside of the interface. An ETS-driven interface is conserved across ten patient samples, suggesting it is a conserved feature of human melanoma. Our results demonstrate the power of spatial transcriptomic approaches in uncovering mechanisms that allow tumors to invade into the microenvironment.

scholarly journals Positional specificity of different transcription factor classes within enhancers

2018 ◽  
Vol 115 (30) ◽  
pp. E7222-E7230 ◽  
Author(s):  
Sharon R. Grossman ◽  
Jesse Engreitz ◽  
John P. Ray ◽  
Tung H. Nguyen ◽  
Nir Hacohen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Transcription Factors ◽  
Binding Sites ◽  
Cell Types ◽  
Regulatory Sequences ◽  
Functional Characteristics ◽  
Positional Specificity ◽  
Chromatin Remodelers ◽  
Positional Bias

Gene expression is controlled by sequence-specific transcription factors (TFs), which bind to regulatory sequences in DNA. TF binding occurs in nucleosome-depleted regions of DNA (NDRs), which generally encompass regions with lengths similar to those protected by nucleosomes. However, less is known about where within these regions specific TFs tend to be found. Here, we characterize the positional bias of inferred binding sites for 103 TFs within ∼500,000 NDRs across 47 cell types. We find that distinct classes of TFs display different binding preferences: Some tend to have binding sites toward the edges, some toward the center, and some at other positions within the NDR. These patterns are highly consistent across cell types, suggesting that they may reflect TF-specific intrinsic structural or functional characteristics. In particular, TF classes with binding sites at NDR edges are enriched for those known to interact with histones and chromatin remodelers, whereas TFs with central enrichment interact with other TFs and cofactors such as p300. Our results suggest distinct regiospecific binding patterns and functions of TF classes within enhancers.

scholarly journals Nfat

2002 ◽  
Vol 156 (5) ◽  
pp. 771-774 ◽  
Author(s):  
Valerie Horsley ◽  
Grace K. Pavlath
Keyword(s):  
Gene Expression ◽  
T Cells ◽  
Transcription Factors ◽  
Immune System ◽  
Cell Types ◽  
Cytokine Gene Expression ◽  
Nuclear Factor ◽  
Cytokine Gene ◽  
Activated T Cells ◽  
Control Of Gene Expression

The nuclear factor of activated T cells (NFAT) proteins are a family of transcription factors whose activation is controlled by calcineurin, a Ca2+-dependent phosphatase. Originally identified in T cells as inducers of cytokine gene expression, NFAT proteins play varied roles in cells outside of the immune system. This review addresses the recent data implicating NFAT in the control of gene expression influencing the development and adaptation of numerous mammalian cell types.

Estrogen receptor action through target genes with classical and alternative response elements

2003 ◽  
Vol 75 (11-12) ◽  
pp. 1757-1769 ◽  
Author(s):  
P. J. Kushner ◽  
P. Webb ◽  
R. M. Uht ◽  
M.-M. Liu ◽  
R. H. Price
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Transcription Factors ◽  
Target Genes ◽  
Cell Types ◽  
Binding Domain ◽  
Environmental Estrogens ◽  
Alternative Response ◽  
Promoter Elements ◽  
Response Elements

The estrogen receptors alpha and beta (ERα and ERβ) mediate the changes in gene expression from physiological and environmental estrogens. Early studies identified classical estrogen response elements (EREs) in the promoter region of target genes whose expression is regulated by estrogen and to which the ERs bind via their DNA-binding domain (DBD). EREs in the pituitary prolactin promoter, for example, mediate an activation by both ERα and ERβ albeit with different affinities for different ligands. Full activation in most cell types requires the integrity of the activation function 2 (AF-2) in the receptors ligand binding domain (LBD), which is engaged by estrogens and disengaged by tamoxifen, raloxifene, and other antiestrogens. However, in some cells and ERE contexts, the AF-1 in the ERα amino terminal domain (NTD) is sufficient. We now know that ERs also regulate expression of target genes that do not have EREs, but instead have various kinds of alternative response elements that bind heterologous transcription factors whose activity is regulated by interactions with ERs. Thus, ERα activates genes, including collagenase and cyclin D1, an important mediator of cellular proliferation, by AP-1 and CRE sites, which bind Jun/Fos or Jun/ATF-2 transcription factors. ERα also activates gene expression through GC-rich elements that bind the SP1 transcription factor. Finally, we also know that ERs mediate inhibition of the expression of many genes. In one well-studied instance, ERs counterexpression of genes involved in the inflammatory response by inhibiting the action at tumor necrosis factor response elements (TNF-REs) that bind the NFkappaB transcription factor. ERβ is especially efficient at this inhibition. ERα activation of AP-1/CRE target genes is of special interest because of the putative role of these target genes in mediating proliferation. The AF-1 and AF-2 functions of ERα are both needed for this activation in most cell types. However, in uterine cells, the AF-1 function is sufficient. Thus, the antiestrogen tamoxifen, which allows AF-1, mimics estrogen and drives activation of AP-1/CRE target genes and proliferation of uterine cells. This estrogen-like action, which can increase the risk of uterine cancer, complicates the use of tamoxifen to prevent breast cancer. Surprisingly, ERβ inhibits AP-1/CRE target genes in the presence of estrogen. When both receptors are present, ERβ efficiently opposes activation by ERα. Moreover, ERβ activates the AP-1/CRE target genes in the presence of antiestrogens especially so-called "complete" antiestrogens raloxifene, and ICI 182, 780. We here review the evidence for different kinds of promoter elements that mediate ER action, for the differential ligand preferences of ERα and ERβ at these different elements, and the potential mechanisms by which they are mediated. One attractive strategy for the investigation and comparison of potential environmental estrogens is to assay their activity in cell culture systems using reporter genes with simplified promoter elements. Thus, the findings of complexity in ERα and ERβ activation at different types of response elements needs to be taken into account in the development and interpretation of assays using simplified promoter elements systems.

scholarly journals Evidence for the temporal regulation of insect segmentation by a conserved set of developmental transcription factors

2017 ◽  
Author(s):  
Erik Clark ◽  
Andrew D. Peel
Keyword(s):  
Gene Expression ◽  
Drosophila Melanogaster ◽  
Transcription Factors ◽  
Tribolium Castaneum ◽  
Fruit Fly ◽  
Temporal Regulation ◽  
Gap Gene ◽  
Spatiotemporal Information ◽  
Segmentation Gene Expression ◽  
Pair Rule

ABSTRACTLong-germ insects, such as the fruit fly Drosophila melanogaster, pattern their segments simultaneously, whereas short germ insects, such as the beetle Tribolium castaneum, pattern their segments sequentially, from anterior to posterior. While the two modes of segmentation at first appear to be very different, many details of segmentation gene expression are surprisingly similar between long-germ and short-germ species. Collectively, these observations hint that insect segmentation may involve fairly conserved patterning mechanisms, which occur within an evolutionarily malleable spatiotemporal framework. Based on genetic and comparative evidence, we now propose that, in both Drosophila and Tribolium embryos, the temporal progression of the segmentation process is regulated by a temporal sequence of Caudal, Dichaete, and Odd-paired expression. These three transcription factors are broadly expressed in segmenting tissues, providing spatiotemporal information that intersects with the information provided by periodically-expressed segmentation genes such as the pair-rule factors. However, they are deployed differently in long-germ versus short-germ insects, acting as simple timers in Drosophila, but as smooth, retracting wavefronts in Tribolium, compatible with either gap gene-based or oscillator-based generation of periodicity, respectively.

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