Overlapping roles and asymmetrical cross-regulation of the USF proteins in mice

Sirito, Mario; Lin, Qun; Deng, Jian Min; Behringer, Richard R.; Sawadogo, Michèle

doi:10.1073/pnas.95.7.3758

Cited by 144 publications

(146 citation statements)

References 35 publications

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“…In this experiment, a 150-bp DNA fragment was used as the radiolabeled probe under conditions that allow separation of the complexes containing di erent USF dimers (Sirito et al, 1994(Sirito et al, , 1998. Total USF DNA-binding activity in the di erent extracts varied in proportion to the concentration of USF polypeptides detected by Western blotting, indicating that there was no di erence between cell lines in the ability of the USF proteins to bind DNA ( Figure 1).…”

Section: Expression and Dna-binding Activity Of Usf In Human Breast Cmentioning

confidence: 99%

“…In mammals, the two ubiquitously expressed genes, Usf1 and Usf2, play overlapping, essential roles in embryonic development (Sirito et al, 1998). All USF proteins interact with DNA as dimers and recognize Ebox elements characterized by a central CACGTG or CACATG sequence.…”

Section: Introductionmentioning

confidence: 99%

“…The major USF species present in most tissues and cell types is the USF1×USF2 heterodimer. USF1 homodimers are less abundant and USF2 homodimers usually quite scarce (Sirito et al, 1994(Sirito et al, , 1998Viollet et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

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Loss of USF transcriptional activity in breast cancer cell lines

1999

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USF is a family of transcription factors that are structurally related to the Myc oncoproteins and also share with Myc a common DNA-binding speci®city. USF overexpression can prevent c-Myc-dependent cellular transformation and also inhibit the proliferation of certain transformed cells. These antiproliferative activities suggest that USF inactivation could be implicated in carcinogenesis. To explore this possibility, we compared the activities of the ubiquitous USF1 and USF2 proteins in several cell lines derived from either normal breast epithelium or breast tumors. The DNAbinding activities of USF1 and USF2 were present at similar levels in all cell lines. In the non-tumorigenic MCF-10A cells, USF in general, and USF2 in particular, exhibited strong transcriptional activities. In contrast, USF1 and USF2 were completely inactive in three out of six transformed breast cell lines investigated, while the other three transformed cell lines exhibited loss of USF2 activity. Analyses in cells cultured from healthy tissue con®rmed the transcriptional activity of USF in normal human mammary epithelial cells. These results demonstrate that a partial or complete loss of USF function is a common event in breast cancer cell lines, perhaps because, like Myc overexpression, it favors rapid proliferation.

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Section: Expression and Dna-binding Activity Of Usf In Human Breast Cmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Loss of USF transcriptional activity in breast cancer cell lines

1999

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“…USF1 and USF2 are ubiquitously expressed in the adult, but neither USF1 nor USF2 null mice display a muscle phenotype. Double homozygotes die in utero, however, suggesting redundant functions (Sirito et al, 1998).…”

Section: Discussionmentioning

confidence: 99%

The A17 enhancer directs expression of Myf5 to muscle satellite cells but Mrf4 to myonuclei

Chang

Vincent

Buckingham

et al. 2007

Developmental Dynamics

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The myogenic regulatory factors, Myf5 and Mrf4, play key roles in the specification and differentiation of skeletal muscle, respectively. Many cis-acting regulatory elements at the Mrf4/Myf5 locus have been identified, including the A17 enhancer. During development, A17 in conjunction with the Mrf4 or Myf5 promoter, directs transgene expression either to embryonic or fetal muscles. We now show that this enhancer also regulates Mrf4/Myf5 transcription in the adult. A17 linked to the Myf5 promoter drives expression in muscle satellite cells, whereas with the Mrf4 promoter, A17 directs transgene expression to myonuclei. Interestingly, expression of A17-Mrf4-nlacZ transgenes in myonuclei varies between muscles, revealing muscle autonomous transcriptional regulation. During muscle repair, satellite cells are induced to proliferate and differentiate to provide new myonuclei. A17 directs Myf5 expression in satellite cell progeny while it only drives the Mrf4 promoter after differentiation. Importantly, therefore, this promoterspecific activity directed by A17 reflects aspects of the expression profiles of the endogenous Myf5 and Mrf4 genes. Developmental Dynamics 236:3419 -3426, 2007.

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“…Sirito et al, 1998), TFE-3 (Beckmann et al, 1990) and TFEB (Fisher et al, 1991). Fusion of the aminoterminal repression domain of Mad-1 to TFEB generates a protein that is capable of suppressing cellular transformation by Myc, demonstrating that these proteins have overlapping binding sites on DNA in vivo (Harper et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

DNA binding of USF is required for specific E-box dependent gene activation in vivo

et al. 1999

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Although USF-1 and -2 are the major proteins that bind to Myc-regulated E-box (CACGTG) elements in many cells, there is no clear role for USF during Mycdependent gene regulation. Using dominant negative alleles of USF-1 we now show that DNA binding by USF at a Myc-regulated E-box limits the ability of another E-box binding factor, TFE-3, to activate a target gene of Myc in vivo and to stimulate S phase entry in resting ®broblasts. Similarly, dominant negative alleles of USF-1 relieve the restriction that prevents activation of the IgH enhancer by TFE-3 in non B-cells. DNA binding activity of USF complexes is abundant in primary human B-cells and is signi®cantly downregulated during B-cell immortalization. Re-expression of USF-1 in immortalized B-cells retards proliferation. Our data establish an essential role for USF in restricting E-box dependent gene activation in vivo and suggest that this control is relaxed during cellular immortalization.

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Overlapping roles and asymmetrical cross-regulation of the USF proteins in mice

Cited by 144 publications

References 35 publications

Loss of USF transcriptional activity in breast cancer cell lines

Loss of USF transcriptional activity in breast cancer cell lines

The A17 enhancer directs expression of Myf5 to muscle satellite cells but Mrf4 to myonuclei

DNA binding of USF is required for specific E-box dependent gene activation in vivo

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