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POLIE suppresses telomerase-mediated telomere G-strand extension and helps ensure proper telomere C-strand synthesis in trypanosomes

ABSTRACT: POLIE suppresses telomerase-mediated telomere G-strand extension and helps ensure proper telomere C-strand synthesis in trypanosomes

PROVIDER: PRJNA758389 | ENA |

REPOSITORIES: ENA

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POLIE suppresses telomerase-mediated telomere G-strand extension and helps ensure proper telomere C-strand synthesis in trypanosomes

Project description:T. brucei regularly switches its major surface antigen, VSG, to evade the mammalian host immune response. VSGs are expressed from subtelomeric loci in a strictly monoallelic manner. We identify POLIE as an intrinsic component of the T. brucei telomere complex and examined the effect of POLIE depletion on VSG expression regulation by RNAseq.

2022-01-07 | GSE182941 | GEO

End resection and telomere healing of DNA double-strand breaks during nematode programmed DNA elimination

Project description:Most DNA double-strand breaks (DSBs) are harmful to genome integrity. However, some forms of DSBs are essential to biological processes, such as meiotic recombination and V(D)J recombination. DSBs are also required for programmed DNA elimination (PDE) in ciliates and nematodes. In nematodes, the DSBs are healed with telomere addition. While telomere addition sites have been well-characterized, little is known regarding the DSBs that fragment nematode chromosomes. Here, we used embryos from the nematode Ascaris to study the timing of PDE breaks and examine the DSBs and their end processing. Using END-seq, we characterize the DSB ends and demonstrate that DNA breaks are introduced before mitosis, followed by extensive end resection. The resection profile is unique for each break site, and the resection generates 3’ overhangs before the addition of telomeres. Interestingly, telomere healing occurs much more frequently on retained DSB ends than on eliminated ends. This biased repair of the DSB in Ascaris is likely due to the sequestration of the eliminated DNA into micronuclei, preventing their ends from telomere healing. Additional DNA breaks occur within the eliminated DNA in both Ascaris and Parascaris, ensuring chromosomal breakage and providing a fail-safe mechanism for nematode PDE.

2024-03-15 | GSE260958 | GEO

Rif1 acts through Protein Phosphatase 1 and independent of replication timing to suppresses telomere extension in budding yeast

Project description:The Rif1 protein negatively regulates telomeric TG repeat length in the budding yeast S. cerevisiae, but how it prevents telomere over-extension is unknown. Rif1 was recently shown to control DNA replication by acting as a Protein Phosphatase 1 (PP1)-targeting subunit. Therefore we investigated whether Rif1 controls telomere length by targeting PP1 activity. We find that a Rif1 mutant that cannot interact with PP1 causes a long-telomere phenotype, similar to that of rif1∆ cells. Compromised PP1 function also causes telomere extension. Tethering PP1 at a specific telomere partially substitutes for Rif1 in limiting TG repeat length, confirming the importance of PP1 in telomere length control. Ablating Rif1-PP1 interaction leads to precocious activation of telomere-proximal replication origins and aberrantly early telomere replication. However, we find that Rif1 still limits telomere length even if nearby replication origins are deleted, indicating that effects of Rif1 on telomere length are not mediated through replication timing. Instead we find that, even at a telomere created after DNA synthesis during a mitotic block, Rif1-PP1 interaction is required to suppress telomere lengthening and prevent inappropriate recruitment of Tel1 kinase. Overall, our results show that Rif1 controls telomere length by recruiting PP1 to directly suppress telomerase-mediated TG repeat lengthening.

2018-02-14 | GSE109241 | GEO

MAK98 trypanosomes cultured for 7 weeks

Project description:MAK98 strain trypanosomes were cultured for 7 weeks. Control sequences are uploaded separately. These are paired reads in separate files.

2021-05-22 | E-MTAB-10466 | biostudies-arrayexpress

PUF3 RNAi in bloodstream-form trypanosomes

Project description:PUF3 was depleted by RNAi for 24h in bloodstream-form trypanosomes (Trypanosoma brucei). No effect was seen on the transcriptome.

2019-06-30 | E-MTAB-8062 | biostudies-arrayexpress

Protein arginine methylation in Trypanosomes

Project description:Protein arginine methylation in Trypanosomes

| PRJNA610785 | ENA

Telomere length effect on genes near the telomere in myoblasts

Project description:We examined differential expression of genes within 10MBs of telomeres in myoblasts with long or short telomeres We offer telomere looping with telomere length as a partial mechanistic explanation for the changes gene expression that is observed. Compare expression of genes within 10MB of the telomere in normal myoblasts with long (15 kb) and short (6 kb) telomeres.

2014-07-17 | E-GEOD-48973 | biostudies-arrayexpress

ILF3 safeguards telomere from aberrant homologous recombination as a telomeric R-loop reader

Project description:Here we found that ILF3 prefers to bind telomere R-loops and protects telomere from aberrant homologous recombination. ILF3 knockout induces TERRA aggregation onto telomere and activates telomere DNA damage response (DDR). Furthermore, ILF3 deficiency disrupts telomere homeostasis and induces abnormal ALT-mediated telomere lengthening

2022-03-04 | PXD032093 | iProX

Telomere dysfunction

Project description:We used microarrays to analyze the prevalence of signalling induced by acute telomere dysfunction (as induced by TRF2DBDM expression = Dataset 1) and in TERC- compared to TERC+ HCC (Dataset 2). Keywords: acute telomere dysfunction, hepatocellular cancer

2006-07-01 | GSE4627 | GEO

Telomere dysfunction induces Sirtuin repression that drives telomere-dependent disease

Project description:Telomere dysfunction induces Sirtuin repression that drives telomere-dependent disease

| PRJNA517700 | ENA