scholarly journals miR-27 and miR-125 Distinctly Regulate Muscle-Enriched Transcription Factors in Cardiac and Skeletal Myocytes

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Estefania Lozano-Velasco ◽  
Jennifer Galiano-Torres ◽  
Alvaro Jodar-Garcia ◽  
Amelia E. Aranega ◽  
Diego Franco
Keyword(s):  
Transcription Factors ◽  
Cardiac Development ◽  
Protein Translation ◽  
Cell Type ◽  
Atrial Cardiomyocytes ◽  
Skeletal Myocytes ◽  
Specific Manner ◽  
A Cell ◽  
Cell Type Specific

MicroRNAs are noncoding RNAs of approximately 22–24 nucleotides which are capable of interacting with the 3′ untranslated region of coding RNAs (mRNAs), leading to mRNA degradation and/or protein translation blockage. In recent years, differential microRNA expression in distinct cardiac development and disease contexts has been widely reported, yet the role of individual microRNAs in these settings remains largely unknown. We provide herein evidence of the role of miR-27 and miR-125 regulating distinct muscle-enriched transcription factors. Overexpression of miR-27 leads to impair expression ofMstnandMyocdin HL1 atrial cardiomyocytes but not in Sol8 skeletal muscle myoblasts, while overexpression of miR-125 resulted in selective upregulation ofMef2din HL1 atrial cardiomyocytes and downregulation in Sol8 cells. Taken together our data demonstrate that a single microRNA, that is, miR-27 or miR-125, can selectively upregulate and downregulate discrete number of target mRNAs in a cell-type specific manner.

scholarly journals Mechanisms Underlying Hox-Mediated Transcriptional Outcomes

2021 ◽  
Vol 9 ◽  
Author(s):  
Brittany Cain ◽  
Brian Gebelein
Keyword(s):  
Transcription Factors ◽  
Differentially Express ◽  
Target Genes ◽  
Cell Type ◽  
Cell Fates ◽  
Specific Manner ◽  
A Cell ◽  
Cell Type Specific ◽  
Anterior Posterior ◽  
Anterior Posterior Axis

Metazoans differentially express multiple Hox transcription factors to specify diverse cell fates along the developing anterior-posterior axis. Two challenges arise when trying to understand how the Hox transcription factors regulate the required target genes for morphogenesis: First, how does each Hox factor differ from one another to accurately activate and repress target genes required for the formation of distinct segment and regional identities? Second, how can a Hox factor that is broadly expressed in many tissues within a segment impact the development of specific organs by regulating target genes in a cell type-specific manner? In this review, we highlight how recent genomic, interactome, and cis-regulatory studies are providing new insights into answering these two questions. Collectively, these studies suggest that Hox factors may differentially modify the chromatin of gene targets as well as utilize numerous interactions with additional co-activators, co-repressors, and sequence-specific transcription factors to achieve accurate segment and cell type-specific transcriptional outcomes.

scholarly journals N-cadherin (Cdh2) Maintains Migration and Postmitotic Survival of Cortical Interneuron Precursors in a Cell-Type-Specific Manner

2019 ◽  
Vol 30 (3) ◽  
pp. 1318-1329
Author(s):  
Zsófia I László ◽  
Kinga Bercsényi ◽  
Mátyás Mayer ◽  
Kornél Lefkovics ◽  
Gábor Szabó ◽  
...  
Keyword(s):  
Target Selection ◽  
Cortical Plate ◽  
Specific Factor ◽  
Cell Type ◽  
Cortical Interneuron ◽  
Specific Manner ◽  
A Cell ◽  
Cell Type Specific ◽  
Interneuron Development

Abstract The multiplex role of cadherin-based adhesion complexes during development of pallial excitatory neurons has been thoroughly characterized. In contrast, much less is known about their function during interneuron development. Here, we report that conditional removal of N-cadherin (Cdh2) from postmitotic neuroblasts of the subpallium results in a decreased number of Gad65-GFP-positive interneurons in the adult cortex. We also found that interneuron precursor migration into the pallium was already delayed at E14. Using immunohistochemistry and TUNEL assay in the embryonic subpallium, we excluded decreased mitosis and elevated cell death as possible sources of this defect. Moreover, by analyzing the interneuron composition of the adult somatosensory cortex, we uncovered an unexpected interneuron-type-specific defect caused by Cdh2-loss. This was not due to a fate-switch between interneuron populations or altered target selection during migration. Instead, potentially due to the migration delay, part of the precursors failed to enter the cortical plate and consequently got eliminated at early postnatal stages. In summary, our results indicate that Cdh2-mediated interactions are necessary for migration and survival during the postmitotic phase of interneuron development. Furthermore, we also propose that unlike in pallial glutamatergic cells, Cdh2 is not universal, rather a cell type-specific factor during this process.

scholarly journals Chromatin accessibility determines intron retention in a cell type-specific manner

2021 ◽  
Author(s):  
Veronika Petrova ◽  
Renhua Song ◽  
Karl J.V. Nordström ◽  
Jörn Walter ◽  
Justin J.-L. Wong ◽  
...  
Keyword(s):  
Nucleosome Occupancy ◽  
Intron Retention ◽  
Chromatin Accessibility ◽  
Lymphoid Cells ◽  
Cell Type ◽  
Systematic Analysis ◽  
Specific Manner ◽  
A Cell ◽  
Cell Type Specific

SummaryDynamic intron retention (IR) in vertebrate cells is of widespread biological importance. Aberrant IR is associated with numerous human diseases including cancer. Despite consistent reports demonstrating intrinsic sequence features that predispose introns to become retained, conflicting findings about cell type-specific IR regulation demand a systematic analysis in a controlled experimental setting. We integrated matched transcriptomics and epigenetics data (including DNA methylation, nucleosome occupancy, histone modifications) from primary human myeloid and lymphoid cells. Using machine learning we trained two complementary models to determine the role of epigenetic factors in the regulation of IR. We show that increased chromatin accessibility contributes substantially to the retention of introns in a cell-specific manner. We also confirm that intrinsic characteristics of introns are key for them to evade splicing. With mounting reports linking pathogenic alterations to RNA processing, our findings may have profound implications for the design of therapeutic approaches targeting aberrant splicing.

scholarly journals Rel Induces Interferon Regulatory Factor 4 (IRF-4) Expression in Lymphocytes

2000 ◽  
Vol 191 (8) ◽  
pp. 1281-1292 ◽  
Author(s):  
Raelene J. Grumont ◽  
Steve Gerondakis
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Nuclear Factor Κb ◽  
Wild Type ◽  
Cell Type ◽  
Regulatory Factor ◽  
Specific Manner ◽  
A Cell ◽  
Cell Type Specific ◽  
Interferon Regulatory Factor 4

In lymphocytes, the Rel transcription factor is essential in establishing a pattern of gene expression that promotes cell proliferation, survival, and differentiation. Here we show that mitogen-induced expression of interferon (IFN) regulatory factor 4 (IRF-4), a lymphoid-specific member of the IFN family of transcription factors, is Rel dependent. Consistent with IRF-4 functioning as a repressor of IFN-induced gene expression, the absence of IRF-4 expression in c-rel−/− B cells coincided with a greater sensitivity of these cells to the antiproliferative activity of IFNs. In turn, enforced expression of an IRF-4 transgene restored IFN modulated c-rel−/− B cell proliferation to that of wild-type cells. This cross-regulation between two different signaling pathways represents a novel mechanism that Rel/nuclear factor κB can repress the transcription of IFN-regulated genes in a cell type–specific manner.

PLAG1 enhances the stemness profiles of acinar cells in normal human salivary glands in a cell type-specific manner

2020 ◽  
Vol 62 (1) ◽  
pp. 99-106 ◽  
Author(s):  
Yuriko Goto ◽  
Miho Ibi ◽  
Hirotaka Sato ◽  
Junichi Tanaka ◽  
Rika Yasuhara ◽  
...  
Keyword(s):  
Salivary Glands ◽  
Acinar Cells ◽  
Cell Type ◽  
Specific Manner ◽  
A Cell ◽  
Normal Human ◽  
Cell Type Specific

scholarly journals NF-κB/Rel Transcription Factors in Pancreatic Cancer: Focusing on RelA, c-Rel, and RelB

Cancers ◽  
2019 ◽  
Vol 11 (7) ◽  
pp. 937 ◽  
Author(s):  
Derya Kabacaoglu ◽  
Dietrich A. Ruess ◽  
Jiaoyu Ai ◽  
Hana Algül
Keyword(s):  
Transcription Factors ◽  
Ductal Adenocarcinoma ◽  
Cell Type ◽  
Dual Nature ◽  
Ability To Act ◽  
Cell Type Specific ◽  
Additional Tumor ◽  
Light Chain Enhancer ◽  
Oncogenic Function

Regulation of Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB)/Rel transcription factors (TFs) is extremely cell-type-specific owing to their ability to act disparately in the context of cellular homeostasis driven by cellular fate and the microenvironment. This is also valid for tumor cells in which every single component shows heterogenic effects. Whereas many studies highlighted a per se oncogenic function for NF-κB/Rel TFs across cancers, recent advances in the field revealed their additional tumor-suppressive nature. Specifically, pancreatic ductal adenocarcinoma (PDAC), as one of the deadliest malignant diseases, shows aberrant canonical-noncanonical NF-κB signaling activity. Although decades of work suggest a prominent oncogenic activity of NF-κB signaling in PDAC, emerging evidence points to the opposite including anti-tumor effects. Considering the dual nature of NF-κB signaling and how it is closely linked to many other cancer related signaling pathways, it is essential to dissect the roles of individual Rel TFs in pancreatic carcinogenesis and tumor persistency and progression. Here, we discuss recent knowledge highlighting the role of Rel TFs RelA, RelB, and c-Rel in PDAC development and maintenance. Next to providing rationales for therapeutically harnessing Rel TF function in PDAC, we compile strategies currently in (pre-)clinical evaluation.

Sign in / Sign up

Export Citation Format

Share Document