Enhancer function regulated by combinations of transcription factors and cofactors

Nakagawa, Takeya; Yoneda, Mitsuhiro; Higashi, Miki; Ohkuma, Yoshiaki; Ito, Takashi

doi:10.1111/gtc.12634

Cited by 17 publications

(9 citation statements)

References 157 publications

(179 reference statements)

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“…Additional enhancer hallmarks include H3K79 trimethylation and CREB-binding protein (CBP)/p300 recruitment [30,31]. Enhancers are bound by the bromodomain and extra-terminal (BET) protein BRD4 and by members of the mediator and P-TEFb complexes [32,33,34,35]. Recent single-cell analysis of gene transcription revealed further details on the inter-dependencies of these factors in enhancer function [36].…”

Section: Promoters Enhancers and Super-enhancersmentioning

confidence: 99%

Dysregulated Transcriptional Control in Prostate Cancer

Baumgart

Nevedomskaya

Haendler

2019

IJMS

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Recent advances in whole-genome and transcriptome sequencing of prostate cancer at different stages indicate that a large number of mutations found in tumors are present in non-protein coding regions of the genome and lead to dysregulated gene expression. Single nucleotide variations and small mutations affecting the recruitment of transcription factor complexes to DNA regulatory elements are observed in an increasing number of cases. Genomic rearrangements may position coding regions under the novel control of regulatory elements, as exemplified by the TMPRSS2-ERG fusion and the amplified enhancer identified upstream of the androgen receptor (AR) gene. Super-enhancers are increasingly found to play important roles in aberrant oncogenic transcription. Several players involved in these processes are currently being evaluated as drug targets and may represent new vulnerabilities that can be exploited for prostate cancer treatment. They include factors involved in enhancer and super-enhancer function such as bromodomain proteins and cyclin-dependent kinases. In addition, non-coding RNAs with an important gene regulatory role are being explored. The rapid progress made in understanding the influence of the non-coding part of the genome and of transcription dysregulation in prostate cancer could pave the way for the identification of novel treatment paradigms for the benefit of patients.

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Section: Promoters Enhancers and Super-enhancersmentioning

confidence: 99%

Dysregulated Transcriptional Control in Prostate Cancer

Baumgart

Nevedomskaya

Haendler

2019

IJMS

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“…In other eukaryotes, TFs associate with each other and form complexes to either activate or repress gene expression 39 . ApiAP2s are known to associate with each other 20 and differential association may impact their activity.…”

Section: Discussionmentioning

confidence: 99%

TgAP2IX-5 is a key transcriptional regulator of the asexual cell cycle division in Toxoplasma gondii

et al. 2021

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Apicomplexan parasites have evolved efficient and distinctive strategies for intracellular replication where the timing of emergence of the daughter cells (budding) is a decisive element. However, the molecular mechanisms that provide the proper timing of parasite budding remain unknown. Using Toxoplasma gondii as a model Apicomplexan, we identified a master regulator that controls the timing of the budding process. We show that an ApiAP2 transcription factor, TgAP2IX-5, controls cell cycle events downstream of centrosome duplication. TgAP2IX-5 binds to the promoter of hundreds of genes and controls the activation of the budding-specific cell cycle expression program. TgAP2IX-5 regulates the expression of specific transcription factors that are necessary for the completion of the budding cycle. Moreover, TgAP2IX-5 acts as a limiting factor that ensures that asexual proliferation continues by promoting the inhibition of the differentiation pathway. Therefore, TgAP2IX-5 is a master regulator that controls both cell cycle and developmental pathways.

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“…This might explain the short timeframe when TgAP2IX-5 is expressed during the cell cycle since its expression might be self-limiting. In other eukaryotes, TF associate in complex to either activate or repress gene expression [36]. ApiAP2s are known to associate with each other [21] and differential association may impact their activity.…”

Section: Discussionmentioning

confidence: 99%

A single master regulator controls asexual cell cycle division patterns inToxoplasma gondii

Khelifa

Guillen

Lesage

et al. 2020

Preprint

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All apicomplexan parasites have complex life cycles exhibiting division characterized by a tightly regulated cell cycle control, resulting in the emergence of daughter parasites in possession of a single nucleus and a complete set of organelles. Apicomplexa have evolved efficient and distinctive strategies for intracellular replication where the timing of emergence of the daughter cells, a process termed "budding", is a decisive element. However, the molecular mechanisms that provide the proper timing of parasite budding remain unknown.Using Toxoplasma gondii as a model Apicomplexa, we identified a master regulator that controls the timing of the budding process. We show that an ApiAP2 transcription factor, TgAP2IX-5, controls cell cycle events downstream of centrosome duplication including organelle division and segregation. TgAP2IX-5 binds to the promoter of hundreds of genes and controls the activation of the budding-specific cell cycle expression program. We show that TgAP2IX-5 regulates the expression of specific transcription factors that are necessary for the completion of the budding cycle. TgAP2IX-5 acts as a licensing factor that ensures that asexual proliferation continues by promoting the inhibition of the differentiation pathway at each round of the cell cycle. Therefore, TgAP2IX-5 is a master regulator that controls both cell cycle and developmental pathways.

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Enhancer function regulated by combinations of transcription factors and cofactors

Cited by 17 publications

References 157 publications

Dysregulated Transcriptional Control in Prostate Cancer

Dysregulated Transcriptional Control in Prostate Cancer

TgAP2IX-5 is a key transcriptional regulator of the asexual cell cycle division in Toxoplasma gondii

A single master regulator controls asexual cell cycle division patterns inToxoplasma gondii

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