scholarly journals Integrative analysis reveals pathways associated with sex reversal in Cynoglossus semilaevis

PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e8801 ◽  
Author(s):  
Zhan Ye ◽  
Weifeng Wang ◽  
Yaqun Zhang ◽  
Liping Wang ◽  
Yu Cui ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Zona Pellucida ◽  
Molecular Mechanisms ◽  
Binding Protein ◽  
Sex Reversal ◽  
Cynoglossus Semilaevis ◽  
Integrative Analysis ◽  
Sperm Binding ◽  
Gene And Protein Expression ◽  
Related Transcription Factor

Sex reversal is a complex biological phenomenon exhibited by Cynoglossus semilaevis. Some genetic females may irreversibly convert to pseudomales, thus increasing aquaculture costs because males grow much more slowly than females. In this study, an integrative analysis of transcriptome and proteome was performed to compare differences in gene and protein expression in females and pseudomales after gonad differentiation in C. semilaevis. Based on RNA-Seq results, 1893 genes showed differences in expression at the transcript level between females and pseudomales. Of these differentially expressed genes (DEGs), zona pellucida sperm-binding protein 4-like (LOC103393374 , ZP4), zona pellucida sperm-binding protein 4-like (LOC103396071, ZP4) and forkhead box L2 (foxl2) were highly expressed in females and doublesex and mab-3 related transcription factor 1(dmrt1) and doublesex and mab-3 related transcription factor 3 (dmrt3) were highly expressed in pseudomales. GO enrichment analysis results indicate that wnt signaling pathways and oocyte maturation are two terms enriched in female. At the protein level, Tandem Mass Tags analysis revealed that 324 proteins differed in their relative abundance between pseudomales and females. KEGG analysis found that pseudo-highly expressed proteins were enriched in the ubiquitin mediated proteolysis pathway. For integrative analysis, the Spearman correlation coefficient between the transcriptome and proteome was 0.59. Among 52 related genes, 46 DEGs (88%) were well matched in their levels of change in protein abundance. These findings reveal major active pathways in female and pseudomale gonads after sex reversal and provide new insights into molecular mechanisms associated with sex reversal regulatory network.

scholarly journals A CCAAT/Enhancer Binding Protein β Isoform, Liver-Enriched Inhibitory Protein, Regulates Commitment of Osteoblasts and Adipocytes

2005 ◽  
Vol 25 (5) ◽  
pp. 1971-1979 ◽  
Author(s):  
Kenji Hata ◽  
Riko Nishimura ◽  
Mio Ueda ◽  
Fumiyo Ikeda ◽  
Takuma Matsubara ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Osteoblast Differentiation ◽  
Molecular Mechanisms ◽  
Binding Protein ◽  
Mesenchymal Cells ◽  
Dominant Negative ◽  
Inhibitory Protein ◽  
Enhancer Binding Protein ◽  
Ccaat Enhancer Binding Protein

ABSTRACT Although both osteoblasts and adipocytes have a common origin, i.e., mesenchymal cells, the molecular mechanisms that define the direction of two different lineages are presently unknown. In this study, we investigated the role of a transcription factor, CCAAT/enhancer binding protein β (C/EBPβ), and its isoform in the regulation of balance between osteoblast and adipocyte differentiation. We found that C/EBPβ, which is induced along with osteoblast differentiation, promotes the differentiation of mesenchymal cells into an osteoblast lineage in cooperation with Runx2, an essential transcription factor for osteogenesis. Surprisingly, an isoform of C/EBPβ, liver-enriched inhibitory protein (LIP), which lacks the transcriptional activation domain, stimulates transcriptional activity and the osteogenic action of Runx2, although LIP inhibits adipogenesis in a dominant-negative fashion. Furthermore, LIP physically associates with Runx2 and binds to the C/EBP binding element present in the osteocalcin gene promoter. These data indicate that LIP functions as a coactivator for Runx2 and preferentially promotes the osteoblast differentiation of mesenchymal cells. Thus, identification of a novel role of the C/EBPβ isoform provides insight into the molecular basis of the regulation of osteoblast and adipocyte commitment.

Molecular analysis of cDNA coding for ZP3, a sperm binding protein of the mouse zona pellucida

1988 ◽  
Vol 127 (2) ◽  
pp. 287-295 ◽  
Author(s):  
Maurice J. Ringuette ◽  
Margaret E. Chamberlin ◽  
Anne W. Baur ◽  
Donna A. Sobieski ◽  
Jurrien Dean
Keyword(s):  
Molecular Analysis ◽  
Zona Pellucida ◽  
Binding Protein ◽  
Sperm Binding

scholarly journals Genome-wide mRNA profiling identifies X-box-binding protein 1 (XBP1) as an IRE1 and PUMA repressor

2021 ◽  
Author(s):  
Magdalena Gebert ◽  
Aleksandra Sobolewska ◽  
Sylwia Bartoszewska ◽  
Aleksandra Cabaj ◽  
David K. Crossman ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Er Stress ◽  
Cell Line ◽  
Molecular Mechanisms ◽  
Binding Protein ◽  
Bioinformatic Analysis ◽  
Competitive Inhibitor ◽  
Human Cell Line ◽  
Factor X ◽  
Stress Induction

AbstractAccumulation of misfolded proteins in ER activates the unfolded protein response (UPR), a multifunctional signaling pathway that is important for cell survival. The UPR is regulated by three ER transmembrane sensors, one of which is inositol-requiring protein 1 (IRE1). IRE1 activates a transcription factor, X-box-binding protein 1 (XBP1), by removing a 26-base intron from XBP1 mRNA that generates spliced XBP1 mRNA (XBP1s). To search for XBP1 transcriptional targets, we utilized an XBP1s-inducible human cell line to limit XBP1 expression in a controlled manner. We also verified the identified XBP1-dependent genes with specific silencing of this transcription factor during pharmacological ER stress induction with both an N-linked glycosylation inhibitor (tunicamycin) and a non-competitive inhibitor of the sarco/endoplasmic reticulum Ca2+ ATPase (SERCA) (thapsigargin). We then compared those results to the XBP1s-induced cell line without pharmacological ER stress induction. Using next‐generation sequencing followed by bioinformatic analysis of XBP1-binding motifs, we defined an XBP1 regulatory network and identified XBP1 as a repressor of PUMA (a proapoptotic gene) and IRE1 mRNA expression during the UPR. Our results indicate impairing IRE1 activity during ER stress conditions accelerates cell death in ER-stressed cells, whereas elevating XBP1 expression during ER stress using an inducible cell line correlated with a clear prosurvival effect and reduced PUMA protein expression. Although further studies will be required to test the underlying molecular mechanisms involved in the relationship between these genes with XBP1, these studies identify a novel repressive role of XBP1 during the UPR.

scholarly journals Transcription Factor 21 Promotes Chicken Adipocyte Differentiation at Least in Part via Activating MAPK/JNK Signaling

Genes ◽  
2021 ◽  
Vol 12 (12) ◽  
pp. 1971
Author(s):  
Xinyang Zhang ◽  
Bohan Cheng ◽  
Haixu Jiang ◽  
Chang Liu ◽  
Zhiping Cao ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Cell Line ◽  
Molecular Mechanisms ◽  
Binding Protein ◽  
Protein A ◽  
Peroxisome Proliferator ◽  
Jnk Pathway ◽  
Peroxisome Proliferator Activated Receptor ◽  
Fatty Acid Binding ◽  
Enhancer Binding Protein

The molecular mechanisms of transcription factor 21 (TCF21) in regulating chicken adipogenesis remain unclear. Thus, the current study was designed to investigate the signaling pathway mediating the effect of TCF21 on chicken adipogenesis. Immortalized chicken preadipocytes cell line (ICP), a preadipocyte cell line stably overexpressing TCF21 (LV-TCF21) and a control preadipocyte cell line (LV-control) were used in the current study. We found that the phosphorylation of c-Jun N-terminal kinases (JNK) was significantly elevated in LV-TCF21 compared to LV-control. After treating ICP cells with a JNK inhibitor SP600125, the differentiation of ICP was inhibited, as evidenced by decreased accumulation of lipid droplets and reduced expression of peroxisome proliferator-activated receptor γ (PPARγ), CCAAT/enhancer binding protein α (C/EBPα), adipocyte fatty acid binding protein (A-FABP), and lipoprotein lipase (LPL). Moreover, we found that the inhibition of JNK by SP600125 remarkably impaired the ability of TCF21 to drive adipogenesis. Taken together, our results suggest that TCF21 promotes the differentiation of adipocytes at least in part via activating MAPK/JNK pathway.

scholarly journals Promoter-Proximal Chromatin Domain Insulator Protein BEAF Mediates Local and Long-Range Communication with a Transcription Factor and Directly Activates a Housekeeping Promoter in Drosophila

Genetics ◽  
2020 ◽  
Vol 215 (1) ◽  
pp. 89-101 ◽  
Author(s):  
Yuankai Dong ◽  
S. V. Satya Prakash Avva ◽  
Mukesh Maharjan ◽  
Janice Jacobi ◽  
Craig M. Hart
Keyword(s):  
Gene Regulation ◽  
Transcription Factor ◽  
Molecular Mechanisms ◽  
Binding Protein ◽  
Housekeeping Genes ◽  
Bimolecular Fluorescence Complementation ◽  
Chromatin Domain ◽  
Direct Role ◽  
Transcription Start Sites ◽  
Genome Wide

BEAF (Boundary Element-Associated Factor) was originally identified as a Drosophila melanogaster chromatin domain insulator-binding protein, suggesting a role in gene regulation through chromatin organization and dynamics. Genome-wide mapping found that BEAF usually binds near transcription start sites, often of housekeeping genes, suggesting a role in promoter function. This would be a nontraditional role for an insulator-binding protein. To gain insight into molecular mechanisms of BEAF function, we identified interacting proteins using yeast two-hybrid assays. Here, we focus on the transcription factor Serendipity δ (Sry-δ). Interactions were confirmed in pull-down experiments using bacterially expressed proteins, by bimolecular fluorescence complementation, and in a genetic assay in transgenic flies. Sry-δ interacted with promoter-proximal BEAF both when bound to DNA adjacent to BEAF or > 2-kb upstream to activate a reporter gene in transient transfection experiments. The interaction between BEAF and Sry-δ was detected using both a minimal developmental promoter (y) and a housekeeping promoter (RpS12), while BEAF alone strongly activated the housekeeping promoter. These two functions for BEAF implicate it in playing a direct role in gene regulation at hundreds of BEAF-associated promoters.

scholarly journals Genome-Wide mRNA Profiling Identifies X-Box-Binding Protein 1 (XBP1) As An IRE1 And PUMA Repressor

2021 ◽  
Author(s):  
Magdalena Gebert ◽  
Aleksandra Sobolewska ◽  
Sylwia Bartoszewska ◽  
Aleksandra Cabaj ◽  
David K. Crossman ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Er Stress ◽  
Cell Line ◽  
Molecular Mechanisms ◽  
Binding Protein ◽  
Bioinformatic Analysis ◽  
Competitive Inhibitor ◽  
Human Cell Line ◽  
Factor X ◽  
Stress Induction

Abstract Accumulation of misfolded proteins in ER activates the unfolded protein response (UPR), a multifunctional signaling pathway that is important for cell survival. The UPR is regulated by three ER transmembrane sensors, one of which is inositol-requiring protein 1 (IRE1). IRE1 activates a transcription factor, X-box binding protein 1 (XBP1), by removing a 26-base intron from XBP1 mRNA that generates spliced XBP1 mRNA (XBP1s). To search for XBP1 transcriptional targets, we utilized an XBP1s-inducible human cell line to limit XBP1 expression in a controlled manner. We also verified the identified XBP1-dependent genes with specific silencing of this transcription factor during pharmacological ER stress induction with both an N-linked glycosylation inhibitor (tunicamycin) and a non-competitive inhibitor of the sarco/endoplasmic reticulum Ca2+ ATPase (SERCA) (thapsigargin). We then compared those results to the XBP1s-induced cell line without pharmacological ER stress induction. Using next‐generation sequencing followed by bioinformatic analysis of XBP1 binding motifs, we defined an XBP1 regulatory network and identified XBP1 as a repressor of PUMA (a proapoptotic gene) and IRE1 mRNA expression during the UPR. Our results indicate impairing IRE1 activity during ER stress conditions accelerates cell death in ER stressed cells, whereas elevating XBP1 expression during ER stress using an inducible cell line correlated with a clear prosurvival effect and reduced PUMA protein expression. Although further studies will be required to test the underlying molecular mechanisms involved the relationship between these genes with XBP1, these studies identify a novel repressive role of XBP1 during the UPR.

scholarly journals Cleidocranial dysplasia. A molecular and clinical review.

2018 ◽  
Vol 8 (1) ◽  
pp. 35-38
Author(s):  
Andrea Avendaño ◽  
Francisco Cammarata-Scalisi ◽  
Mochamad Fahlevi Rizal ◽  
Sarworini Bagio Budiardjo ◽  
Margaretha Suharsini ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Molecular Mechanisms ◽  
Target Genes ◽  
Autosomal Dominant ◽  
Cleidocranial Dysplasia ◽  
Supernumerary Teeth ◽  
Phenotypic Characteristics ◽  
Autosomal Dominant Disorder ◽  
Dental Abnormalities ◽  
Related Transcription Factor

Cleidocranial dysplasia (CCD) is a rare autosomal dominant disorder characterized by skeletal and dental abnormalities primarily, short stature, aplasia or hypoplasia of clavicles, open fontanelles and supernumerary teeth. Heterozygous mutations of the runt related transcription factor 2 (RUNX2) gene have been found in approximately 60-70% of cases leaving a large number of cases with no defined genetic cause which led us to delve into molecular mechanisms underlying CCD and thus to detect potential target genes to be explored in these patients. In this review we also highlight very broadly the phenotypic characteristics of previously reported patients with CCD.

scholarly journals Intestinal epithelial cell endoplasmic reticulum stress promotes MULT1 up-regulation and NKG2D-mediated inflammation

2017 ◽  
Vol 214 (10) ◽  
pp. 2985-2997 ◽  
Author(s):  
Shuhei Hosomi ◽  
Joep Grootjans ◽  
Markus Tschurtschenthaler ◽  
Niklas Krupka ◽  
Juan D. Matute ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Transcription Factor ◽  
Epithelial Cells ◽  
Er Stress ◽  
Intestinal Inflammation ◽  
Binding Protein ◽  
Lymphoid Cells ◽  
Intestinal Epithelial ◽  
Related Transcription Factor ◽  
Factor C

Endoplasmic reticulum (ER) stress is commonly observed in intestinal epithelial cells (IECs) and can, if excessive, cause spontaneous intestinal inflammation as shown by mice with IEC-specific deletion of X-box–binding protein 1 (Xbp1), an unfolded protein response–related transcription factor. In this study, Xbp1 deletion in the epithelium (Xbp1ΔIEC) is shown to cause increased expression of natural killer group 2 member D (NKG2D) ligand (NKG2DL) mouse UL16-binding protein (ULBP)–like transcript 1 and its human orthologue cytomegalovirus ULBP via ER stress–related transcription factor C/EBP homology protein. Increased NKG2DL expression on mouse IECs is associated with increased numbers of intraepithelial NKG2D-expressing group 1 innate lymphoid cells (ILCs; NK cells or ILC1). Blockade of NKG2D suppresses cytolysis against ER-stressed epithelial cells in vitro and spontaneous enteritis in vivo. Pharmacological depletion of NK1.1+ cells also significantly improved enteritis, whereas enteritis was not ameliorated in Recombinase activating gene 1−/−;Xbp1ΔIEC mice. These experiments reveal innate immune sensing of ER stress in IECs as an important mechanism of intestinal inflammation.

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