Long range interaction of cis‐DNA elements mediated by architectural transcription factor Bach1

Yoshida, Chikashi; Tokumasu, Fuyuki; Hohmura, Ken I.; Bungert, Jörg; Hayashi, Norio; Nagasawa, Toshiro; Engel, James Douglas; Yamamoto, Masayuki; Igarashi, Kazuhiko

doi:10.1046/j.1365-2443.1999.00291.x

Cited by 88 publications

(89 citation statements)

References 44 publications

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“…This domain mediates transcriptional repression through its ability to recruit the corepressors SMRT and N-CoR, as demonstrated for BCL-6 and PLZF (33)(34)(35). The Bach1 BTB domain mediates oligomer formation, generating a multivalent DNA-binding complex (25,32). Surprisingly, removing the BTB domain of Bach1 (Bach1⌬BTB) resulted in nuclear accumulation (Fig.…”

Section: Bach1 Export From Nuclei Is Dependent On Crm1/exportin-1-mentioning

confidence: 83%

Cadmium Induces Nuclear Export of Bach1, a Transcriptional Repressor of Heme Oxygenase-1 Gene

Sano

Tashiro

Sun

et al. 2003

Journal of Biological Chemistry

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156

128

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The export of certain nuclear proteins is involved in the regulation of various nuclear functions, including transcription. In some cases, the export of target proteins is induced upon environmental or cellular cues, resulting in conditional gene expression. The small Maf proteins appear to be critical regulators of heme oxygenase (HO)-1, an anti-oxidant defense enzyme that degrades heme into iron, carbon monoxide, and biliverdin. Although ho-1 is repressed by Bach1/small Maf heterodimers, it is activated by Nrf2/small Maf heterodimers, indicating that Bach1 and Nrf2 compete with each other. We anticipated that the nuclear concentration of Bach1 might be regulated to ensure that the entire system effectively responds to various stimuli. We carried out detailed domain analysis of Bach1 in an effort to understand how various inducers of HO-1 inactivate Bach1. We show here that cadmium, a strong inducer of HO-1, activates the nuclear export of Bach1. This cadmium-induced export of Bach1 was mediated in trans by its C-terminal region that is conserved between Bach1 and Bach2. The nuclear export of Bach2 was also induced by cadmium, indicating that the cadmium responsibility is shared between Bach1 and Bach2. The nuclear export of Bach1 was dependent on Crm1/Exportin-1 as well as the extracellular signal-regulated kinase-1/2 (ERK1/2) activity. These results indicate that the nuclear export of Bach1 constitutes an important regulatory mechanism to relieve the Bach1-mediated repression of genes such as ho-1.

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Section: Bach1 Export From Nuclei Is Dependent On Crm1/exportin-1-mentioning

confidence: 83%

Cadmium Induces Nuclear Export of Bach1, a Transcriptional Repressor of Heme Oxygenase-1 Gene

Sano

Tashiro

Sun

et al. 2003

Journal of Biological Chemistry

Self Cite

156

128

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“…Within this control region there are several elements named MAREs, which contain binding sites for the transcription factors Maf and Bach1. Using atomic force microscopy, investigators showed that distant MAREs physically interact in vitro when Maf and Bach1 are present (Yoshida et al, 1999). These interactions between MAREs might be critical for chromatin structure and gene expression (Yoshida et al, 1999).…”

Section: Interactions Between Regulatory Elementsmentioning

confidence: 99%

“…Using atomic force microscopy, investigators showed that distant MAREs physically interact in vitro when Maf and Bach1 are present (Yoshida et al, 1999). These interactions between MAREs might be critical for chromatin structure and gene expression (Yoshida et al, 1999). Although not directly related to the control of gene expression, the case of the Igh locus provides another interesting example of interactions between noncoding elements (Guo et al, 2011).…”

Section: Interactions Between Regulatory Elementsmentioning

confidence: 99%

Multiple layers of complexity in cis‐regulatory regions of developmental genes

Frankel

2012

Developmental Dynamics

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Genomes contain the necessary information to ensure that genes are expressed in the right place, at the right time, and with the proper rate. Metazoan developmental genes often possess long stretches of DNA flanking their coding sequences and/or large introns which contain elements that influence gene expression. Most of these regulatory elements are relatively small and can be studied in isolation. For example, transcriptional enhancers, the elements that generate the expression pattern of a gene, have been traditionally studied with reporter constructs in transgenic animals. These studies have provided and will provide invaluable insights into enhancer evolution and function. However, this experimental approach has its limits; often, enhancer elements do not faithfully recapitulate native expression patterns. This fact suggests that additional information in cis-regulatory regions modulates the activity of enhancers and other regulatory elements. Indeed, recent studies have revealed novel functional aspects at the level of whole cis-regulatory regions. First, the discovery of ''shadow enhancers.'' Second, the ubiquitous interactions between cis-regulatory elements. Third, the notion that some cis-regulatory regions may not function in a modular manner. Last, the effect of chromatin conformation on cis-regulatory activity. In this article, I describe these recent findings and discuss open questions in the field.

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“…Bach2⌬BTB lacked the BTB domain that is specific to Bach1 and Bach2 among the NF-E2-related factors. The BTB (Broad-Complex, Tramtrack, and Bric-a-brac) domain is found in more than 100 human proteins (32) and mediates oligomer formation (33)(34)(35)(36), DNA loop generation (37), and nuclear foci formation (34,35,38). Bach2⌬Zip lacked the leucine zipper region that mediates dimerization with small Maf family factors and is thus essential for DNA binding.…”

Section: Effects Of Bach2 On the Related Enhancers Tre Mare Andmentioning

confidence: 99%

Activation of Maf/AP-1 Repressor Bach2 by Oxidative Stress Promotes Apoptosis and Its Interaction with Promyelocytic Leukemia Nuclear Bodies

Muto¹,

Tashiro²,

Tsuchiya³

et al. 2002

Journal of Biological Chemistry

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The oxidative stress response operates by inducing the expression of genes that counteract the stress. We show here that the oxidative stress-responsive transcription factor Bach2 is a generic inhibitor of gene expression directed by the 12-O-tetradecanoylphorbol-13-acetate response element, the Maf recognition element, and the antioxidant-responsive element. The Bach2-enhanced green fluorescent protein bicistronic retrovirus was used to monitor the fate of Bach2-expressing cells at the single cell level. Bach2 exerted an inhibitory effect on NIH3T3 cell proliferation and caused massive apoptosis upon mild oxidative stress in both NIH3T3 and Raji B-lymphoid cells. Interestingly, Bach1, a highly homologous protein, could not induce cell death, demonstrating the specificity for the apoptosis induction. Although both oxidative stress and leptomycin B, an inhibitor of nuclear export, induce nuclear accumulation of Bach2, the leptomycin B-induced nuclear accumulation of Bach2 was not sufficient to elicit apoptosis. Upon oxidative stress, Bach2 formed nuclear foci that associated with promyelocytic leukemia nuclear bodies. Our results suggest that Bach2 constitutes a cell lineage-specific system that couples oxidative stress and cell death and that inhibition of 12-O-tetradecanoylphorbol-13-acetate response element, the Maf recognition element, and the antioxidant-responsive element upon oxidative stress may be critical determinants for apoptosis.

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Long range interaction of cis‐DNA elements mediated by architectural transcription factor Bach1

Cited by 88 publications

References 44 publications

Cadmium Induces Nuclear Export of Bach1, a Transcriptional Repressor of Heme Oxygenase-1 Gene

Cadmium Induces Nuclear Export of Bach1, a Transcriptional Repressor of Heme Oxygenase-1 Gene

Multiple layers of complexity in cis‐regulatory regions of developmental genes

Activation of Maf/AP-1 Repressor Bach2 by Oxidative Stress Promotes Apoptosis and Its Interaction with Promyelocytic Leukemia Nuclear Bodies

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