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RNA-Seq of wild type and Terc-/- in G3 tail, G3 liver, G3 testis, G3 TTF, G3 ASC, G4 early ESC, G4 late ESC

ABSTRACT: RNA-Seq of wild type and Terc-/- in G3 tail, G3 liver, G3 testis, G3 TTF, G3 ASC, G4 early ESC, G4 late ESC

PROVIDER: PRJNA764681 | ENA |

REPOSITORIES: ENA

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Expression data between WT and G3/4 Terc KO mouse ESCs during differentiation

Project description:Mammalian telomeres are formed by tandem repeats of the TTAGGG sequence, and shorten with each round of cell division in the absence of telomerase. Telomere shortening and dysfunction has been implicated in the pathology of several age-related diseases and premature ageing syndromes. Telomerase is important for telomere length maintenance. Telomerase RNA component, also known as TERC, is a component of telomerase. Terc knockout leads to telomerase deficiency and telomere shortening. Heterozygous telomerase-deficient (Terc+/-) mice were housed and bred for homozygous generation. ESC lines were generated with high efficiency from wild-type (WT, Terc+/+), heterozygous (Het, Terc+/-) and early- to late-generation (G1, G3 and G4) Terc-/- mouse blastocysts. Telomeres were shorter in Terc+/- ES cells than in WT ES cells, and further shortened from G1 to G4 Terc-/- ES cells. We took advantage of ES cell lines with various telomere lengths to investigate roles of telomere length on differentiation capacity of ES cells. We found that telomere length, but not telomerase activity, is required for differentiation of ES cells into epidermis. We performed microarray analysis to investigate differential gene expression profile at genome-wide levels between WT and G3/G4 Terc-/- (KO) mouse ES cells and during differentiation in vitro of WT and G4 Terc-/- mouse ES cells.

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RNA-Seq of wild type and Terc-/- in G3 tail, G3 liver, G3 testis, G3 TTF, G3 ASC, G4 early ESC, G4 late ESC

Project description:We aimed to see if the short telomere could affect the genome stability and the retrotransposon expression profiles.

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Project description:WES of wild type and Terc-/- in G3 tail, G3 testis, G3 TTF, G3 ASC, G3 ESC, G4 early ESC, G4 late ESC.

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Transcription profiling of testis from wild type mice and mice lacking telomerase for three generations (G3-Terc), Ku86 or both telomerase and Ku86 to identify effectors of mammalian telomere dysfunction.

Project description:Transcriptome of murine testis from wild type mice and mice lacking telomerase for three generations (G3-Terc), Ku86 or both telomerase and Ku86.

2007-09-04 | E-GEOD-2498 | biostudies-arrayexpress

Project description:WGS of wild type and Terc-/- in G4 early ESC, G4 late ESC.

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RNA-Seq of early passage wild type and short telomere G1 G4 Terc-/- ESCs.

Project description:RNA-Seq of early passage wild type and short telomere G1 G4 Terc-/- ESCs.

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Differential gene expression profiles of long bones of telomerase deficient mice (G3-mTERC-/-)

Project description:Telomere shortening due to telomerase deficiency leads to accelerated senescence of human skeletal (mesenchymal) stem cells (MSC) in vitro. In order to study the role of telomere shortening in vivo, we studied the phenotype of telomerase deficient mice caused by absence of telomerase RNA component (TERC-/-). TERC-/- exhibited accelerated age-related bone loss starting at 3 months of age and during 12 months follow up. Bone histomorphometry revealed decreased mineralized surface and bone formation rate as well as increased osteoclast number and size in TERC-/-. Also, serum total deoxy-pyridinoline (tDPD) was increased in TERC-/-. MSC isolated from TERC-/- exhibited intrinsic defects with reduced total number, lower proliferation rate, decreased expression of osteoblastic (OB) differentiation markers and formed less in vivo ectopic bone compared to WT cells. The TERC-/--MSC cultures accumulated a larger proportion of senescent Ã-galactosidase+ cells and cells exhibiting DNA damage positive for Î³-H2AX. Micro-array analysis of bones of TERC-/- and WT revealed significant over-expression of a large number of pro-inflammatory genes and signaling pathways in TERC-/- known to control osteoclast (OC) differentiation. In accordance with that, serum from TERC-/- enhanced OC formation in control bone marrow cultures. Our data demonstrate two mechanisms for age-related bone loss caused by telomerase deficiency: intrinsic osteoblastic defects and creation of pro-inflammatory osteoclast-activating microenvironment. Approaches for re-telomerization of MSC may provide a novel approach for abolishing age-related bone loss. control (WT) and the test (G3 - mTERC-/-) samples

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Post-transcriptional manipulation of TERC reverses molecular hallmarks of telomere disease

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Trichomonas vaginalis G3 strain:G3

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