In Vivo Regulation of Follicle-Stimulating Hormone Receptor by the Transcription Factors Upstream Stimulatory Factor 1 and Upstream Stimulatory Factor 2 Is Cell Specific

Hermann, Brian P.; Hornbaker, Kaori; Rice, Daren A.; Sawadogo, Michèle; Heckert, Leslie L.

doi:10.1210/en.2007-1199

Cited by 28 publications

(23 citation statements)

References 38 publications

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“…Chromatin from three independent biological preparations of THY1 + spermatogonia (each line was generated independently from multiple pups from one or more P6-P8 mouse litters) was used for ChIP essentially as described previously (Hermann et al, 2008;Hermann and Heckert, 2005). Briefly, THY1…”

Section: Chip-seqmentioning

confidence: 99%

The regulatory repertoire of PLZF and SALL4 in undifferentiated spermatogonia

Lovelace

Mutoji

et al. 2016

Development

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Spermatogonial stem cells (SSCs) maintain spermatogenesis throughout adulthood through balanced self-renewal and differentiation, yet the regulatory logic of these fate decisions is poorly understood. The transcription factors Sal-like 4 (SALL4) and promyelocytic leukemia zinc finger (PLZF; also known as ZBTB16) are known to be required for normal SSC function, but their targets are largely unknown. ChIP-seq in mouse THY1+ spermatogonia identified 4176 PLZF-bound and 2696 SALL4-bound genes, including 1149 and 515 that were unique to each factor, respectively, and 1295 that were bound by both factors. PLZF and SALL4 preferentially bound gene promoters and introns, respectively. Motif analyses identified putative PLZF and SALL4 binding sequences, but rarely both at shared sites, indicating significant non-autonomous binding in any given cell. Indeed, the majority of PLZF/SALL4 shared sites contained only PLZF motifs. SALL4 also bound gene introns at sites containing motifs for the differentiation factor DMRT1. Moreover, mRNA levels for both unique and shared target genes involved in both SSC self-renewal and differentiation were suppressed following SALL4 or PLZF knockdown. Together, these data reveal the full profile of PLZF and SALL4 regulatory targets in undifferentiated spermatogonia, including SSCs, which will help elucidate mechanisms controlling the earliest cell fate decisions in spermatogenesis.

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Section: Chip-seqmentioning

confidence: 99%

The regulatory repertoire of PLZF and SALL4 in undifferentiated spermatogonia

Lovelace

Mutoji

et al. 2016

Development

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“…Furthermore, binding of upstream transcription factor 1 Supported by Estonian Science Foundation grant 7839. 2 Correspondence: E-mail: tarmo.tiido@ut.ee (USF) homodimers or heterodimers to its DNA element, the Ebox is required for transcriptional regulation of mouse Fshr, as shown both by in vitro and in vivo studies [16].…”

Section: Introductionmentioning

confidence: 99%

“…homodimers (USF1 and USF2) and heterodimers (USF1/2), and evidence from studies in rodents document the fact that in ovary, homo-and heterodimers direct Fshr promoter activity equally well [16]. Evidence about the part played by AHR in Fshr regulation first appeared in 2007 with the demonstration that AHR deletion leads to slow ovarian follicle growth in prepubertal mice, in part because of reduced FSH responsiveness [11].…”

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confidence: 99%

The Aryl Hydrocarbon Receptor Regulates Mouse Fshr Promoter Activity Through an E-Box Binding Site1

Teino

Kuuse

Ingerpuu

et al. 2012

Biology of Reproduction

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The aryl hydrocarbon receptor (AHR) mediates the toxicity of a variety of environmental chemicals. Apart from this, an understanding is emerging that the AHR has a fundamental role in female reproduction. Evidence suggests that AHR participates in regulation of follicle-stimulating hormone receptor (Fshr) transcript level in mouse ovary by binding to the promoter of this gene in vivo. The purpose of this study was to demonstrate the molecular interplay of the Fshr promoter involved in the transactivation by AHR in mouse granulosa cells. We found that AHR activates the Fshr promoter through the region from À209 to À99 bp. In this region, the importance of the E-box motif was revealed by site-directed mutagenesis followed by promoter analysis. By focusing on the DNA/protein interactions, we defined the fact that the intact E-box but not upstream transcription factor 1 (USF1), which is known to bind this motif, is necessary for AHR binding to mouse Fshr promoter. Furthermore, by constructing AHR mutants defective in DNA interaction, we confirmed the importance of DNA binding for AHR's ability to bind to and activate Fshr promoter. Collectively, the present study demonstrates that AHR modulates Fshr transactivation by its direct association through an E-box and not by recruitment via interaction with USFs. These observations suggest that although AHR and USF may respond to different signals, they compete on binding to the same E-box. Our data, together with that from one prior study suggesting involvement of E-box motif in AHR-mediated transcription, provide novel understanding of the way in which AHR may regulate its target genes through E-box sites.

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“…Other conserved regulatory elements also include an E box, which binds upstream stimulatory factor 1 (USF1) and USF2 in vitro [12,13,21] and in vivo [22,23] as well as a CRE-like sequence probably involved in cAMP mediated transcriptional regulation [16]. The neotomodon FSHR promoter also contains novel putative cis-acting elements for transcription factors of the HMG-box SRY/Sox family, which seem to be important in the positive transcriptional regulation of the nFSHR gene, since elimination of the region containing these putative SRY binding sites significantly reduced reporter activity.…”

Section: Discussionmentioning

confidence: 99%

Molecular cloning and functional analysis of the FSH receptor gene promoter from the volcano mouse (Neotomodon alstoni alstoni)

Pérez‐Solis

Macías

Acosta-MontesdeOca

et al. 2009

Endocr

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To gain further insights on the genetic divergence and the species-specific characteristics of the follicle-stimulating hormone receptor (FSHR), we cloned 946 bp of the 5'-flanking region of the FSHR gene from the volcano mouse (Neotomodon alstoni alstoni), and compared its features with those from other mammalian species. The sequence of neotomodon FSHR (nFSHR) gene from the translation initiation site to -946 is 74, 71, 64, and 59% homologous to rat, mouse (129/J), human, and sheep, respectively. The nFSHR 5'-flanking region exhibits new interesting putative cis-regulatory elements including those for the SRY transcription factor, which had not been previously related to the FSHR gene. The transcriptional regulation properties of nFSHR gene were studied in mouse Sertoli (MSC-1) and non-Sertoli (H441) cell lines, and compared with those obtained with similar 129/J constructs. All constructs tested were more active in H441 than in MSC-1 cells. The low transcription levels detected in MSC-1 cells probably reflect the recruitment of Sertoli cells-specific nuclear factors that repress transcription of the FSHR gene. In H441 cells, 129/J constructs were more active than their neotomodon counterparts, indicating important species-specific differences in their transcription pattern. Functional analysis of a series of progressive 5'-deletion mutants identified regions involved in positive and negative transcriptional regulation as well as the strongest minimal promoter spanning 260 bp upstream the translation initiation site. The identification of inhibitory nuclear transcription factors, which are apparently expressed in MSC-1 cells, may contribute to a better understanding of the transcriptional regulation of the FSHR gene.

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In Vivo Regulation of Follicle-Stimulating Hormone Receptor by the Transcription Factors Upstream Stimulatory Factor 1 and Upstream Stimulatory Factor 2 Is Cell Specific

Cited by 28 publications

References 38 publications

The regulatory repertoire of PLZF and SALL4 in undifferentiated spermatogonia

The regulatory repertoire of PLZF and SALL4 in undifferentiated spermatogonia

The Aryl Hydrocarbon Receptor Regulates Mouse Fshr Promoter Activity Through an E-Box Binding Site1

Molecular cloning and functional analysis of the FSH receptor gene promoter from the volcano mouse (Neotomodon alstoni alstoni)

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