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

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.

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

BioMed Research International ◽

10.1155/2015/391306 ◽

2015 ◽

Vol 2015 ◽

pp. 1-6 ◽

Cited By ~ 13

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.

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

10.1101/2021.02.17.431609 ◽

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.

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The role of cordycepin in cancer treatment via induction or inhibition of apoptosis: implication of polyadenylation in a cell type specific manner

Cancer Chemotherapy and Pharmacology ◽

10.1007/s00280-007-0467-y ◽

2007 ◽

Vol 61 (2) ◽

pp. 251-265 ◽

Cited By ~ 31

Author(s):

Hellinida Thomadaki ◽

Andreas Scorilas ◽

Chris Milto Tsiapalis ◽

Maria Havredaki

Keyword(s):

Cancer Treatment ◽

Cell Type ◽

Specific Manner ◽

A Cell ◽

Cell Type Specific

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

Journal of Experimental Medicine ◽

10.1084/jem.191.8.1281 ◽

2000 ◽

Vol 191 (8) ◽

pp. 1281-1292 ◽

Cited By ~ 146

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.

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