Nuclear protein binding to the 5' enhancer region of the intracisternal A particle long terminal repeat.

Zierler, M K; Christy, Robert J.; Huang, Ru Chih C.

doi:10.1016/s0021-9258(19)36817-6

Cited by 11 publications

(2 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…D Confirming RepEnTools ’ findings, UHRF1 enrichment is found over the entire length of many IAP-LTRs at regions overlapping the H3K4me1-K9me3 double mark. IAP-LTRs contain experimentally validated enhancer sequences [ 57 , 58 ]. E UHRF1 is enriched at the 5′ end of IAPEz longer than 5 kb, colocalising with H3K4me1- K9me3, and it was implicated in silencing IAPEz-gag expression [ 54 , 59 ].…”

Section: Resultsmentioning

confidence: 99%

RepEnTools: an automated repeat enrichment analysis package for ChIP-seq data reveals hUHRF1 Tandem-Tudor domain enrichment in young repeats

Choudalakis,

Bashtrykov,

Jeltsch

2024

Mobile DNA

View full text Add to dashboard Cite

Background Repeat elements (REs) play important roles for cell function in health and disease. However, RE enrichment analysis in short-read high-throughput sequencing (HTS) data, such as ChIP-seq, is a challenging task. Results Here, we present RepEnTools, a software package for genome-wide RE enrichment analysis of ChIP-seq and similar chromatin pulldown experiments. Our analysis package bundles together various software with carefully chosen and validated settings to provide a complete solution for RE analysis, starting from raw input files to tabular and graphical outputs. RepEnTools implementations are easily accessible even with minimal IT skills (Galaxy/UNIX). To demonstrate the performance of RepEnTools, we analysed chromatin pulldown data by the human UHRF1 TTD protein domain and discovered enrichment of TTD binding on young primate and hominid specific polymorphic repeats (SVA, L1PA1/L1HS) overlapping known enhancers and decorated with H3K4me1-K9me2/3 modifications. We corroborated these new bioinformatic findings with experimental data by qPCR assays using newly developed primate and hominid specific qPCR assays which complement similar research tools. Finally, we analysed mouse UHRF1 ChIP-seq data with RepEnTools and showed that the endogenous mUHRF1 protein colocalizes with H3K4me1-H3K9me3 on promoters of REs which were silenced by UHRF1. These new data suggest a functional role for UHRF1 in silencing of REs that is mediated by TTD binding to the H3K4me1-K9me3 double mark and conserved in two mammalian species. Conclusions RepEnTools improves the previously available programmes for RE enrichment analysis in chromatin pulldown studies by leveraging new tools, enhancing accessibility and adding some key functions. RepEnTools can analyse RE enrichment rapidly, efficiently, and accurately, providing the community with an up-to-date, reliable and accessible tool for this important type of analysis.

show abstract

Section: Resultsmentioning

confidence: 99%

RepEnTools: an automated repeat enrichment analysis package for ChIP-seq data reveals hUHRF1 Tandem-Tudor domain enrichment in young repeats

Choudalakis,

Bashtrykov,

Jeltsch

2024

Mobile DNA

View full text Add to dashboard Cite

show abstract

“…The transcriptional activation of escapee IAPEz copies posed the exciting possibility that some of these integrants may harbour intact enhancers that could activate host genes. Indeed, as IAPs are derived from retroviruses, they have a putative enhancer in the U3 region (Mietz et al ., 1987; Zierler et al, 1992). We asked if the IAP U3 could act as a classical enhancer by cloning the IAP575 U3 sequence into a reporter construct upstream of a minimal SV40 promoter in sense and antisense configurations.…”

Section: Resultsmentioning

confidence: 99%

Co-option of endogenous retroviruses through genetic escape from TRIM28 repression

Enriquez-Gasca

Gould

Tunbak

et al. 2022

Preprint

View full text Add to dashboard Cite

Endogenous retroviruses (ERVs) have rewired host gene networks through co-option of their enhancers. To explore which ERVs get co-opted and why, we tracked the epigenetic fate of murine IAPEz elements using an in vitro model of embryonic stem cell (ESC) to neural progenitor cell (NPC) differentiation. TRIM28-repression depended on a 190bp sequence, previously shown to confer IAPEzs with retrotransposition activity. A subset of IAPEzs (~15%) exhibit genetic divergence from this sequence, which we term escapees. While repressed IAPEzs succumb to a previously undocumented epigenetic handover from H3K9me3 in ESCs to H3K27me3 in NPCs, escapee IAPEzs evade repression, resulting in their transcriptional derepression in NPCs. Escapee IAPEzs enhance expression of nearby neural genes and contribute to gene expression differences between mouse strains, which we discern by employing IAPEz insertion polymorphisms. In sum, co-opted ERVs stem from genetic escapees that have lost vital sequences required for both TRIM28 restriction and autonomous retrotransposition.

show abstract

Reverse Transcriptase: Mediator of Genomic Plasticity

Brosius

Tiedge

1996

Molecular Evolution of Viruses — Past and Present

View full text Add to dashboard Cite

Nuclear protein binding to the 5' enhancer region of the intracisternal A particle long terminal repeat.

Cited by 11 publications

References 42 publications

RepEnTools: an automated repeat enrichment analysis package for ChIP-seq data reveals hUHRF1 Tandem-Tudor domain enrichment in young repeats

RepEnTools: an automated repeat enrichment analysis package for ChIP-seq data reveals hUHRF1 Tandem-Tudor domain enrichment in young repeats

Co-option of endogenous retroviruses through genetic escape from TRIM28 repression

Reverse Transcriptase: Mediator of Genomic Plasticity

Contact Info

Product

Resources

About