Transcriptional Repression by XPc1, a New Polycomb Homolog in <i>Xenopus laevis</i> Embryos, Is Independent of Histone Deacetylase

Strouboulis, John; Damjanovski, Sashko; Vermaak, Danielle; Meric, Funda; Wolffe, Alan P.

doi:10.1128/mcb.19.6.3958

Cited by 30 publications

(17 citation statements)

References 96 publications

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“…Therefore, HDAC1 appears to be recruited to homeotic genes with PC complexes. In contrast to our findings, HDAC activity has not been detected in some Pc-G complexes previously isolated from Drosophila, Xenopus, and human cells (11,49,50). However, considerable amounts of Pc-G proteins remain in other chromatographic fractions and many Pc-G genes are redundant in vertebrates (11,51), suggesting that different Pc-G complexes may exist.…”

Section: Discussioncontrasting

confidence: 54%

Essential role of Drosophila Hdac1 in homeotic gene silencing

Chang

Peng

Pan

et al. 2001

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

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Deacetylation of the N-terminal tails of core histones plays a crucial role in gene silencing. Rpd3 and Hda1 represent two major types of genes encoding trichostatin A-sensitive histone deacetylases. Although they have been widely found, their cellular and developmental roles remain to be elucidated in metazoa. We show that Drosophila Hdac1, an Rpd3-type gene, interacts cooperatively with Polycomb group repressors in silencing the homeotic genes that are essential for axial patterning of body segments. The biochemical copurification and cytological colocalization of HDAC1 and Polycomb group repressors strongly suggest that HDAC1 is a component of the silencing complex for chromatin modification on specific regulatory regions of homeotic genes.Pc-G ͉ histone deacetylase ͉ Ubx ͉ PRE

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Section: Discussioncontrasting

confidence: 54%

Essential role of Drosophila Hdac1 in homeotic gene silencing

Chang

Peng

Pan

et al. 2001

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

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“…Furthermore, they are separable from the cisacting elements that initially define transcriptional status and cannot be switched back at later developmental stages. Finally, although histone deacetylase activity may be involved in some aspects of polycomb-mediated silencing (Simon and Tamkun, 2002), in the case of the Xenopus polycomb homologue XPc1 transcriptional repression has been shown to be independent of histone deacetylase activity (Strouboulis et al, 1999). These features are in common with our observations concerning Mlc3f transgene repression and we suggest that the Mlc3f promoter contains a mammalian cellular memory module.…”

Section: Discussionsupporting

confidence: 77%

Cell history determines the maintenance of transcriptional differences between left and right ventricular cardiomyocytes in the developing mouse heart

Kelly

Lemonnier

Zaffran

et al. 2003

Journal of Cell Science

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IntroductionThe establishment and maintenance of transcriptional diversity during organogenesis is a key feature of embryonic development. Within the developing heart, myocardial cells in different cardiac chambers exhibit differences in gene expression, which reflect functional compartmentalisation (Christoffels et al., 2000). These transcriptional differences are established during early heart development and prefigure the formation of the specialised left and right atrial and ventricular chambers, which direct separate systemic and pulmonary blood flows.Molecular analysis of the regulatory circuits controlling cardiomyocyte diversity has identified a small number of cisacting motifs and trans-acting factors involved in atrial versus ventricular identity and in differential gene expression between cells of the ventricular and atrioventricular canal myocardium (Wang et al., 2001;Habets et al., 2002). In addition, several cisacting elements active in cardiomyocytes of either the left or right ventricle have been defined in transgenic mice (Schwartz and Olson, 1999;Kelly et al., 1999). Although the trans-acting factors that regulate such transgenes remain unknown, mutational analysis of transcription factors expressed throughout the heart has in some cases revealed compartmentrestricted roles during early development (Lyons et al., 1995;Lin et al., 1997). A small number of cardiac transcription factors, in particular the basic helix-loop-helix (bHLH) proteins Hand1 and Hand2, and the T-box-containing regulatory factor Tbx5, show left/right differences in expression pattern in the embryonic ventricles, and the generation of null alleles in the Hand1, Hand2 and Tbx5 genes has shown that these factors are important in chamber morphogenesis (Srivastava et al., 1997;Firulli et al., 1998;Riley et al., 1998;Bruneau et al., 2001). Despite these studies, the molecular mechanisms that initiate and maintain left versus right ventricular specific gene expression are poorly understood. In particular, little is known about the factors regulating transcriptional differences between left and right ventricular chambers at later developmental stages. How left/right ventricular transcriptional differences are maintained is of major interest, as the fundamentally different roles of the two ventricles become apparent only on the separation of pulmonary and systemic circulatory systems at birth. Furthermore, in the adult, cardiac hypertrophy elicits changes in gene expression that differ in the left versus right ventricular free walls (Vikstrom et al., 1998).

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“…The serine stretch adjacent to NLS3 is perhaps the most interesting feature in MusTRD1͞BEN. Similar serine stretches are also present in transcriptional activators such as ICP4, IE180, IE62, Nopp140, PC4, Sox-4, and Sp4 (31-37); nuclear shuttling proteins such as Nopp 140 (38); and transcriptional repressors belonging to the polycomb group of proteins, such as Pc1 and cramped (39,40). Ectopic expression and subsequent Western blot analysis of TFII-I and MusTRD1͞BEN revealed that whereas TFII-I is distributed between cytoplasm (37%) and …”

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confidence: 99%

Repression of TFII-I-dependent transcription by nuclear exclusion

Tussié-Luna

Bayarsaihan²,

Ruddle³

et al. 2001

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

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TFII-I is an unusual transcription factor possessing both basal and signal-induced transcriptional functions. Here we report the characterization of a TFII-I-related factor (MusTRD1͞BEN) that regulates transcriptional functions of TFII-I by controlling its nuclear residency. MusTRD1͞BEN has five or six direct repeats, each containing helix-loop-helix motifs, and, thus, belongs to the TFII-I family of transcription factors. TFII-I and MusTRD1͞BEN, when expressed individually, show predominant nuclear localization. However, when the two proteins are coexpressed ectopically, MusTRD1͞BEN locates almost exclusively to the nucleus, whereas TFII-I is largely excluded from the nucleus, resulting in a loss of TFII-I-dependent transcriptional activation of the c-fos promoter. Mutation of a consensus nuclear localization signal in MusTRD1͞BEN results in a reversal of nuclear residency of the two proteins and a concomitant gain of c-fos promoter activity. These data suggest a means of transcriptional repression by competition at the level of nuclear occupancy.transcription factor ͉ nuclear translocation ͉ transcriptional repression

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Transcriptional Repression by XPc1, a New Polycomb Homolog in Xenopus laevis Embryos, Is Independent of Histone Deacetylase

Cited by 30 publications

References 96 publications

Essential role of Drosophila Hdac1 in homeotic gene silencing

Essential role of Drosophila Hdac1 in homeotic gene silencing

Cell history determines the maintenance of transcriptional differences between left and right ventricular cardiomyocytes in the developing mouse heart

Repression of TFII-I-dependent transcription by nuclear exclusion

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