HOX paralogs selectively convert binding of ubiquitous transcription factors into tissue-specific patterns of enhancer activationCitation formats

  • External authors:
  • Laure Bridoux
  • Peyman Zarrineh
  • Joshua Mallen
  • Victor Latorre
  • Frank Ladam
  • Marta Losa
  • Charles Sagerstrom

Standard

HOX paralogs selectively convert binding of ubiquitous transcription factors into tissue-specific patterns of enhancer activation. / Bridoux, Laure; Zarrineh, Peyman; Mallen, Joshua; Phuycharoen, Mike; Latorre, Victor; Ladam, Frank; Losa, Marta; Baker, Syed Murtuza; Sagerstrom, Charles; Mace, Kimberly A; Rattray, Magnus; Bobola, Nicoletta.

In: PLoS Genetics, Vol. 16, No. 12, e1009162, 14.12.2020, p. e1009162.

Research output: Contribution to journalArticlepeer-review

Harvard

APA

Vancouver

Author

Bridoux, Laure ; Zarrineh, Peyman ; Mallen, Joshua ; Phuycharoen, Mike ; Latorre, Victor ; Ladam, Frank ; Losa, Marta ; Baker, Syed Murtuza ; Sagerstrom, Charles ; Mace, Kimberly A ; Rattray, Magnus ; Bobola, Nicoletta. / HOX paralogs selectively convert binding of ubiquitous transcription factors into tissue-specific patterns of enhancer activation. In: PLoS Genetics. 2020 ; Vol. 16, No. 12. pp. e1009162.

Bibtex

@article{5b6cbe33f9e7459f945c3b1bf57b763b,
title = "HOX paralogs selectively convert binding of ubiquitous transcription factors into tissue-specific patterns of enhancer activation",
abstract = "Gene expression programs determine cell fate in embryonic development and their dysregulation results in disease. Transcription factors (TFs) control gene expression by binding to enhancers, but how TFs select and activate their target enhancers is still unclear. HOX TFs share conserved homeodomains with highly similar sequence recognition properties, yet they impart the identity of different animal body parts. To understand how HOX TFs control their specific transcriptional programs in vivo, we compared HOXA2 and HOXA3 binding profiles in the mouse embryo. HOXA2 and HOXA3 directly cooperate with TALE TFs and selectively target different subsets of a broad TALE chromatin platform. Binding of HOX and tissue-specific TFs convert low affinity TALE binding into high confidence, tissue-specific binding events, which bear the mark of active enhancers. We propose that HOX paralogs, alone and in combination with tissue-specific TFs, generate tissue-specific transcriptional outputs by modulating the activity of TALE TFs at selected enhancers.",
keywords = "Amino Acid Motifs, Animals, Enhancer Elements, Genetic, Gene Expression Regulation, Developmental, Homeodomain Proteins/chemistry, Mice, Organ Specificity, Protein Binding, Transcription Factors/metabolism, Transcriptional Activation, Zebrafish",
author = "Laure Bridoux and Peyman Zarrineh and Joshua Mallen and Mike Phuycharoen and Victor Latorre and Frank Ladam and Marta Losa and Baker, {Syed Murtuza} and Charles Sagerstrom and Mace, {Kimberly A} and Magnus Rattray and Nicoletta Bobola",
year = "2020",
month = dec,
day = "14",
doi = "10.1371/journal.pgen.1009162",
language = "English",
volume = "16",
pages = "e1009162",
journal = "PL o S Genetics",
issn = "1553-7390",
publisher = "Public Library of Science",
number = "12",

}

RIS

TY - JOUR

T1 - HOX paralogs selectively convert binding of ubiquitous transcription factors into tissue-specific patterns of enhancer activation

AU - Bridoux, Laure

AU - Zarrineh, Peyman

AU - Mallen, Joshua

AU - Phuycharoen, Mike

AU - Latorre, Victor

AU - Ladam, Frank

AU - Losa, Marta

AU - Baker, Syed Murtuza

AU - Sagerstrom, Charles

AU - Mace, Kimberly A

AU - Rattray, Magnus

AU - Bobola, Nicoletta

PY - 2020/12/14

Y1 - 2020/12/14

N2 - Gene expression programs determine cell fate in embryonic development and their dysregulation results in disease. Transcription factors (TFs) control gene expression by binding to enhancers, but how TFs select and activate their target enhancers is still unclear. HOX TFs share conserved homeodomains with highly similar sequence recognition properties, yet they impart the identity of different animal body parts. To understand how HOX TFs control their specific transcriptional programs in vivo, we compared HOXA2 and HOXA3 binding profiles in the mouse embryo. HOXA2 and HOXA3 directly cooperate with TALE TFs and selectively target different subsets of a broad TALE chromatin platform. Binding of HOX and tissue-specific TFs convert low affinity TALE binding into high confidence, tissue-specific binding events, which bear the mark of active enhancers. We propose that HOX paralogs, alone and in combination with tissue-specific TFs, generate tissue-specific transcriptional outputs by modulating the activity of TALE TFs at selected enhancers.

AB - Gene expression programs determine cell fate in embryonic development and their dysregulation results in disease. Transcription factors (TFs) control gene expression by binding to enhancers, but how TFs select and activate their target enhancers is still unclear. HOX TFs share conserved homeodomains with highly similar sequence recognition properties, yet they impart the identity of different animal body parts. To understand how HOX TFs control their specific transcriptional programs in vivo, we compared HOXA2 and HOXA3 binding profiles in the mouse embryo. HOXA2 and HOXA3 directly cooperate with TALE TFs and selectively target different subsets of a broad TALE chromatin platform. Binding of HOX and tissue-specific TFs convert low affinity TALE binding into high confidence, tissue-specific binding events, which bear the mark of active enhancers. We propose that HOX paralogs, alone and in combination with tissue-specific TFs, generate tissue-specific transcriptional outputs by modulating the activity of TALE TFs at selected enhancers.

KW - Amino Acid Motifs

KW - Animals

KW - Enhancer Elements, Genetic

KW - Gene Expression Regulation, Developmental

KW - Homeodomain Proteins/chemistry

KW - Mice

KW - Organ Specificity

KW - Protein Binding

KW - Transcription Factors/metabolism

KW - Transcriptional Activation

KW - Zebrafish

U2 - 10.1371/journal.pgen.1009162

DO - 10.1371/journal.pgen.1009162

M3 - Article

C2 - 33315856

VL - 16

SP - e1009162

JO - PL o S Genetics

JF - PL o S Genetics

SN - 1553-7390

IS - 12

M1 - e1009162

ER -