Murine Sall1 Represses Transcription by Recruiting a Histone Deacetylase Complex

Kiefer, Susan M.; McDill, Bradley W.; Yang, Jing; Rauchman, Michael

doi:10.1074/jbc.m200052200

Cited by 76 publications

(99 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Forty-eight hours after transfection cells were lysed, incubated with glutathione-Sepharose beads (Amersham Biosciences), and washed as described (28). The bound proteins were eluted in SDS gel loading buffer, separated on SDS-polyacrylamide gels, transferred to a membrane, and detected with antibodies against components of the NuRD complex.…”

Section: Methodsmentioning

confidence: 99%

MBD3L1 Is a Transcriptional Repressor That Interacts with Methyl-CpG-binding Protein 2 (MBD2) and Components of the NuRD Complex

Jiang

Jin

Pfeifer

2004

Journal of Biological Chemistry

View full text Add to dashboard Cite

Section: Methodsmentioning

confidence: 99%

MBD3L1 Is a Transcriptional Repressor That Interacts with Methyl-CpG-binding Protein 2 (MBD2) and Components of the NuRD Complex

Jiang

Jin

Pfeifer

2004

Journal of Biological Chemistry

View full text Add to dashboard Cite

“…In a BLAST search, we found that this region of BCL11 proteins has similarity to the corresponding region of the transcriptional repressors belonging to Sall family (data not shown). Recently, it has been reported that the amino-terminal region of Sall1 is required for the interaction with a corepressor complex containing HDAC1/2, RbAp46/48 and MTA1/2 (Kiefer et al, 2002), which may be the NuRD complex core. However, the component(s) of the corepressor complex that directly interacted with Sall has not been identified (Kiefer et al, 2002).…”

Section: Bcl11b Recruits Mta1 To a Targeted Promotermentioning

confidence: 99%

“…Recently, it has been reported that the amino-terminal region of Sall1 is required for the interaction with a corepressor complex containing HDAC1/2, RbAp46/48 and MTA1/2 (Kiefer et al, 2002), which may be the NuRD complex core. However, the component(s) of the corepressor complex that directly interacted with Sall has not been identified (Kiefer et al, 2002). Based on the sequence similarity between the amino-terminal regions of BCL11 and Sall proteins, and the fact that BCL11B interacts with MTA proteins through this region, it is possible that Sall proteins also associate with the MTA proteins and NuRD complex through the same amino-terminal region, and both BCL11 and Sall transcriptional repressors function through a similar mechanism.…”

Section: Bcl11b Recruits Mta1 To a Targeted Promotermentioning

confidence: 99%

“…GSTRbAp46 and GST-RbAp48 (Verreault et al, 1998) were kindly provided by Dr Bruce Stillman, GST-HDAC1 and -HDAC2 (Yang et al, 1996) were kind gifts from Dr Edward Seto and GST-MBD3 (Saito and Ishikawa, 2002) was a kind gift from Dr Fuiuki Ishikawa. The firefly luciferase reporter vectors were generous gifts from Dr Ming-Jer Tsai ((17-mer) 4 -TK-Luc) and Dr Michael Rauchman (pSV40-Luc and pG5SV40-Luc) (Klaver and Berkhout, 1994;Kiefer et al, 2002). (17-mer) 4 -TK-Luc and pG5SV40-Luc vectors contain four and five, respectively, tandem repeats of GAL4 response elements upstream of the minimal herpes simplex virus thymidine kinase (TK) and SV40 promoters respectively.…”

Section: Plasmid Constructsmentioning

confidence: 99%

See 1 more Smart Citation

BCL11B functionally associates with the NuRD complex in T lymphocytes to repress targeted promoter

et al. 2005

View full text Add to dashboard Cite

BCL11 genes play crucial roles in lymphopoiesis and have been associated with hematopoietic malignancies. Specifically, disruption of the BCL11B (B-cell chronic lymphocytic leukemia/lymphoma 11B) locus is linked to T-cell acute lymphoblastic leukemia, and the loss of heterozygosity in mice results in T-cell lymphoma. BCL11 proteins are related C 2 H 2 zinc-finger transcription factors that act as transcriptional repressors. Here, we demonstrate the association of the endogenous BCL11B with the nucleosome remodeling and histone deacetylase (NuRD) complex, one of the major transcriptional corepressor complexes in mammalian cells. BCL11B complexes from T lymphocytes possess trichostatin A-sensitive histone deacetylase activity, confirming the functionality of the complexes. Analysis of the BCL11B-NuRD association demonstrated that BCL11B directly interacted with the metastasis-associated proteins MTA1 and MTA2 through the amino-terminal region. We provide evidence for the functional requirement of MTA1 in transcriptional repression mediated by BCL11B through the following: (1) overexpression of MTA1 enhanced the transcriptional repression mediated by BCL11B, (2) knockdown of MTA1 expression by small interfering RNA inhibited BCL11B transcriptional repression activity and (3) MTA1 was specifically recruited to a BCL11B targeted promoter. Taken together, these data support the hypothesis that the NuRD complex mediates transcriptional repression function of BCL11B.

show abstract

“…MTA1 is a transcriptional modulator and appears to have an important role in cellular identity as its expression has been correlated with invasive cancers and metastasis (10) and as loss of MTA1 in ES cells impairs their pluripotency (4). Although SALL4 and MTA1 have also been found to associate with the nucleosome remodelling and histone deacetylase (NuRD) complex (11)(12)(13), most NuRD components did not appear to associate with the NODE complex (4).…”

mentioning

confidence: 99%

Members of the NODE (Nanog and Oct4-associated deacetylase) complex and SOX-2 promote the initiation of a natural cellular reprogramming event in vivo

Kagias

Ahier

Fischer

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Differentiated cells can be forced to change identity, either to directly adopt another differentiated identity or to revert to a pluripotent state. Direct reprogramming events can also occur naturally. We recently characterized such an event in Caenorhabditis elegans, in which a rectal cell switches to a neuronal cell. Here we have used this single-cell paradigm to investigate the molecular requirements of direct cell-type conversion, with a focus on the early steps. Our genetic analyses revealed the requirement of sem-4/Sall, egl-27/ Mta, and ceh-6/Oct, members of the NODE complex recently identified in embryonic stem (ES) cells, and of the OCT4 partner sox-2, for the initiation of this natural direct reprogramming event. These four factors have been shown to individually impact on ES cell pluripotency; however, whether they act together to control cellular potential during development remained an open question. We further found that, in addition to acting at the same time, these factors physically associate, suggesting that they could act together as a NODE-like complex during this in vivo process. Finally, we have elucidated the functional domains in EGL-27/MTA that mediate its reprogramming activity in this system and have found that modulation of the posterior HOX protein EGL-5 is a downstream event to allow the initiation of Y identity change. Our data reveal unique in vivo functions in a natural direct reprogramming event for these genes that impact on ES cells pluripotency and suggest that conserved nuclear events could be shared between different cell plasticity phenomena across phyla.transdifferentiation | regenerative medicine | metaplasia | SANT H ow differentiated cells can switch their identity is a fascinating question that has attracted much attention in the last decade. A number of studies have shown how strikingly easily a differentiated cell can be experimentally reprogrammed not only into an embryonic stem cell-like state (1) but also into another, different, differentiated identity (2). Remarkably, this process, called direct cell-type conversion or transdifferentiation, also occurs naturally (2).The molecular mechanisms underlying these events are still unclear and it remains to be determined whether key elements are shared between natural and induced reprogramming events. Factors used to reprogram differentiated cells to a stem cell-like state are important for embryonic stem (ES) cell self-renewal (1). Several studies have shed light on the molecular networks that maintain ES cell pluripotency (3). Key factors have been identified, such as Nanog (3) or SOX2 and OCT4 that are required for ES cell pluripotency and that, together with additional factors, can force fibroblasts into embryonic-like stem cells (1, 3). Besides these pluripotency factors, transcriptional repression complexes have been found necessary for ES cell self-renewal, but whether and how these complexes act together to control cellular potential during development remain to be determined. Among them, the NODE (Nanog and O...

show abstract

Murine Sall1 Represses Transcription by Recruiting a Histone Deacetylase Complex

Cited by 76 publications

References 30 publications

MBD3L1 Is a Transcriptional Repressor That Interacts with Methyl-CpG-binding Protein 2 (MBD2) and Components of the NuRD Complex

MBD3L1 Is a Transcriptional Repressor That Interacts with Methyl-CpG-binding Protein 2 (MBD2) and Components of the NuRD Complex

BCL11B functionally associates with the NuRD complex in T lymphocytes to repress targeted promoter

Members of the NODE (Nanog and Oct4-associated deacetylase) complex and SOX-2 promote the initiation of a natural cellular reprogramming event in vivo

Contact Info

Product

Resources

About