Characterization of novel endothelial-specific and smooth-muscle specific Poldip2 knockout mice
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA698620 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13604017_1.fastq.gz | Fastqsanger.gz | |||
| SRR13604017_2.fastq.gz | Fastqsanger.gz | |||
| SRR13604018_1.fastq.gz | Fastqsanger.gz | |||
| SRR13604018_2.fastq.gz | Fastqsanger.gz | |||
| SRR13604019_1.fastq.gz | Fastqsanger.gz |
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Project description:Poldip2 is a multifunctional protein whose roles are only partially understood. The previous Poldip2 knockout mouse generated by the gene trap model suffers from two limitations: perinatal lethality in homozygotes and constitutive Poldip2 inactivation. To overcome these limitations, we developed a new conditional floxed Poldip2 mouse. Here, we correctly targeted floxed Poldip2 mice to produce an endothelial-specific by crossing it with CDH5 ERT2 Cre mouse. Additionally, we also produced smooth-muscle specific Poldip2 knockout mice by crossing the flox'ed Poldip2 mice with SM22A-Cre mice. The Poldip2_EC-/- and Poldip2_SMC-/-mice were viable and showed remarkably reduced Poldip2 expression. To characterize the effect of Poldip2 ablation in the ECs and in the SMCs, we performed a RNA-seq study using the carotid arteries of these mice.
2024-01-24 | GSE165939 | GEO
Project description:Poldip2 is a multifunctional protein whose roles are only partially understood. The previous Poldip2 knockout mouse generated by the gene trap model suffers from two limitations: perinatal lethality in homozygotes and constitutive Poldip2 inactivation. To overcome these limitations, we developed a new conditional floxed Poldip2 mouse. Here, we correctly targeted floxed Poldip2 mice to produce a new constitutive knockout line by crossing with a Cre deleter. In contrast to the gene trap model, many homozygous knockout mice were viable, in spite of having no Poldip2 expression. To characterize the effect of Poldip2 ablation in the vasculature, we performed a RNA-seq study using the carotid arteries of these mice.
2021-12-20 | GSE165274 | GEO
Project description:To study the function of AMD-associated gene POLDIP2 in retinal pigment epithelial (RPE) cells, we used CRISPR/Cas to knockout POLDIP2 in the human RPE cell line ARPE19. We then performed RNA-seq to profile the transcriptome of wildtype ARPE19 and POLDIP2 knockout.
2022-10-01 | GSE207158 | GEO
Project description:We report the effect of Poldip2 knock-down on gene expression in human pulmonary endothelial cells with and without TNF-alpha challenge.
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Project description:Thiele2013 - Smooth muscle smooth muscle cells
The model of smooth muscle smooth muscle cells metabolism is derived from the community-driven global reconstruction of human metabolism (version 2.02, MODEL1109130000
).
This model is described in the article:
A community-driven global reconstruction of human metabolism.
Thiele I, et al
.
Nature Biotechnology
Abstract:
Multiple models of human metabolism have been reconstructed, but each represents only a subset of our knowledge. Here we describe Recon 2, a community-driven,
consensus 'metabolic reconstruction', which is the most comprehensive representation of human metabolism that is applicable to computational modeling. Compared
with its predecessors, the reconstruction has improved topological and functional features, including ~2x more reactions and ~1.7x more unique metabolites. Using
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data and drug information onto Recon 2 demonstrates its potential for integrating and analyzing diverse data types. Using protein expression data, we automatically
generated a compendium of 65 cell type-specific models, providing a basis for manual curation or investigation of cell-specific metabolic properties. Recon 2 will
facilitate many future biomedical studies and is freely available at http://humanmetabolism.org/.
This model is hosted on BioModels Database
and identified by: MODEL1310110025
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To cite BioModels Database, please use: BioModels Database: An enhanced,
curated and annotated resource for published quantitative kinetic models
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To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer
to CC0 Public Domain Dedication
for more information.
2005-01-01 | MODEL1310110025 | BioModels
Project description:Maternal inheritance of mitochondrial DNA (mtDNA) is highly conserved in metazoans. While many species eliminate paternal mtDNA during late sperm development to foster maternal inheritance, the regulatory mechanisms governing this process remain elusive. Through a large-scale genetic screen in Drosophila, we identified 47 mutant lines exhibiting substantial retention of mtDNA in mature sperm. We mapped one line to Poldip2, a gene predominantly expressed in the testis. Disruption of Poldip2 led to pronounced mtDNA retention in mature sperm and subsequent paternal transmission to progeny. Further investigation via imaging, biochemical analyses and ChIP assays revealed that POLDIP2 is a mitochondrial matrix protein capable of binding to mtDNA. Moreover, we uncovered that CLPX, a key component of the major mitochondrial protease, binds to POLDIP2 to co-regulate mtDNA elimination in Drosophila spermatids. This study shed light on the mechanisms underlying mtDNA removal during spermatogenesis, underscoring the pivotal role of this process in safeguarding maternal inheritance.
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Project description:The smooth muscle-specific lncRNA Carmn is required for visceral smooth muscle contractile function
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Project description:Effect of POLDIP2 knockout in ARPE-19 cells
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Project description:POLDIP2 is a multifunctional protein whose roles are only partially understood. Our laboratory previously reported physiological studies performed using a mouse gene trap model, which suffered from three limitations: perinatal lethality in homozygotes, constitutive Poldip2 inactivation and inadvertent downregulation of the adjacent Tmem199 gene. To overcome these limitations, we developed a new conditional floxed Poldip2 model. The first part of the present study shows that our initial floxed mice were affected by an unexpected mutation, which was not readily detected by Southern blotting and traditional PCR. It consisted of a 305 kb duplication around Poldip2 with retention of the wild type allele and could be traced back to the original targeted ES cell clone. We offer simple suggestions to rapidly detect similar accidents, which may affect genome editing using both traditional and CRISPR-based methods. In the second part of the present study, correctly targeted floxed Poldip2 mice were generated and used to produce a new constitutive knockout line by crossing with a Cre deleter. In contrast to the gene trap model, many homozygous knockout mice were viable, in spite of having no POLDIP2 expression. To further characterize the effects of Poldip2 ablation in the vasculature, RNA-seq and RT-qPCR experiments were performed in constitutive knockout arteries. Results show that POLDIP2 inactivation affects multiple cellular processes and provide new opportunities for future in-depth study of its functions.
| S-EPMC8687530 | biostudies-literature
Project description:Canine primary endothelial cells (ECs) and vascular smooth muscle cells (vSMCs) were isolated from the vena cava, vena porta and aorta. All tissue sources were derived from three donors for accurate comparison and to reduce inter-animal variation. We used a recently established technique for the isolation of primary ECs with a lesser chance of contamination that can also be used on small vessels. This same vessel was also used for the isolation of vSMCs
2018-08-03 | GSE118029 | GEO