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Related Concept Videos

Cis-regulatory Sequences02:02

Cis-regulatory Sequences

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Cis-regulatory sequences are short fragments of non-coding DNA that are present on the same chromosomes as the genes that they regulate. These fragments serve as binding sites for transcriptional regulators, proteins that are responsible for controlling gene transcription and differential gene expression across cell types in eukaryotes. Cis-regulatory sequences can be close to the gene of interest or thousands of bases away in the DNA sequence; however, those sequences that are further away are...
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Combinatorial Gene Control02:33

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Combinatorial gene control is the synergistic action of several transcriptional factors to regulate the expression of a single gene. The absence of one or more of these factors may lead to a significant difference in the level of gene expression or repression.
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Master transcription regulators are regulatory proteins that are predominantly responsible for regulating the expression of multiple genes. Often these genes work in concert to drive a  complex process. Activation of a master transcription regulator can lead to a cascade of transcriptional activation necessary for that outcome. These regulators can directly bind to the regulatory sequences of the various genes involved, or they can indirectly regulate transcription by binding to regulatory...
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Transcriptional regulators bind to specific cis-regulatory sequences in the DNA to regulate gene transcription. These cis-regulatory sequences are very short, usually less than ten nucleotide pairs in length. The short length means that there is a high probability of the exact same sequence randomly occurring throughout the genome.  Since regulators can also bind to groups of similar sequences, this further increases the chances of random binding. Transcriptional regulators form...
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Mechanism governing a stem cell-generating cis-regulatory element.

Rajendran Sanalkumar1, Kirby D Johnson, Xin Gao

  • 1Department of Cell and Regenerative Biology, Wisconsin Institutes for Medical Research, Carbone Cancer Center, University of Wisconsin School of Medicine and Public Health, Madison, WI 53705.

Proceedings of the National Academy of Sciences of the United States of America
|March 12, 2014
PubMed
Summary

Investigating GATA switch sites in gene regulation, this study found the -3.9 site is dispensable for Gata2 expression and hematopoiesis. Unique +9.5 site activity was identified for GATA factor-dependent chromatin transitions.

Keywords:
HSCscis element

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Area of Science:

  • Developmental Biology
  • Gene Regulation
  • Hematopoiesis

Background:

  • Stem and progenitor cell regulation is vital for tissue renewal.
  • Master regulatory transcription factors like GATA-2 control these processes.
  • Understanding GATA-2 control in dynamic systems is crucial but poorly understood.

Purpose of the Study:

  • To investigate the role of the -3.9 GATA switch site in Gata2 expression and hematopoiesis.
  • To compare the regulatory mechanisms of different GATA switch sites.
  • To elucidate the function of the +9.5 GATA switch site in GATA factor-dependent chromatin regulation.

Main Methods:

  • Targeted deletion of the -3.9 Gata2 locus sequence in mice.
  • Analysis of Gata2 expression and hematopoiesis in -3.9(-/-) mice.
  • Development of a Gata2 repression/reactivation assay.
  • Loss-of-function studies involving LDB1 and BRG1.

Main Results:

  • Mice lacking the -3.9 site (-3.9(-/-)) were viable with normal Gata2 expression and hematopoiesis.
  • The -3.9 site deletion did not impact embryonic or adult steady-state hematopoiesis.
  • The +9.5 site demonstrated unique activity in mediating GATA factor-dependent chromatin structural transitions.
  • LDB1 and BRG1 were found to synergize via the +9.5 site to confer GATA-2 expression.

Conclusions:

  • The -3.9 GATA switch site is not essential for Gata2 regulation or normal hematopoiesis.
  • The +9.5 site plays a critical role in GATA-2 expression through chromatin remodeling.
  • LDB1 and BRG1 are key mediators in the long-range transcriptional control of GATA-2 via the +9.5 site.
  • This mechanism is important for hematopoietic stem cell genesis and survival.