Sequence and characterisation of the <i>RET</i> proto‐oncogene 5′ flanking region: analysis of retinoic acid responsiveness at the transcriptional level

Patrone, Giovanna; Puliti, Aldamaria; Bocciardi, Renata; Ravazzolo, Roberto; Romeo, Giovanni

doi:10.1016/s0014-5793(97)01435-x

Cited by 29 publications

(26 citation statements)

References 60 publications

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“…For the induction of GDNF responsiveness in cultured SCG neurons from E17 rats, RA markedly induced the expression of ligandspecifying receptor component GFR␣-1 and increased the efficacy of GDNF-triggered Ret tyrosine phosphorylation. Effect of RA on the upregulation of Ret expression in cultured SCG neurons was rather small, although the significant ability of RA to upregulate the expression of Ret in tumorigenic neuroblastoma cells has been reported previously (Tahira et al, 1991;Bunone et al, 1995;Patrone et al, 1997). The expression of Ret starts from the early stage of neural crest development (Lo and Anderson, 1995;Tsuzuki et al, 1995;Durbec et al, 1996) and continues even after transfer to in vitro culture system, as shown in this study.…”

Section: Discussionsupporting

confidence: 71%

Regulation of Glial Cell Line-Derived Neurotrophic Factor Responsiveness in Developing Rat Sympathetic Neurons by Retinoic Acid and Bone Morphogenetic Protein-2

2000

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There are several lines of evidence suggesting that, in addition to neurotrophins, member(s) of glial cell line-derived neurotrophic factor (GDNF) family play important roles in the development of sympathetic neurons. However, the mechanism regulating the responsiveness of the neurons to GDNF family members is not known. Previously, we reported on the cooperative roles of bone morphogenetic protein-2 (BMP2) and retinoic acid (RA) in the enhancement of neurotrophin-3 (NT3) responsiveness in cultured sympathetic neurons dissociated from perinatal rat superior cervical ganglia (SCG). In the present study, we further examined the effects of BMP2 and RA on the regulation of the responsiveness of SCG neurons to GDNF family members. Consequently, we found that RA alone induced the responsiveness of SCG neurons specifically to GDNF by upregulating the ligand-specifying receptor for GDNF (GFR␣-1) at both the mRNA and protein levels. The expression levels of mRNAs for other ligand-specifying receptors for GDNF family (GFR␣-2 and GFR␣-3) were unaffected by RA. Although the upregulation of signal-transducing receptor Ret by the RA treatment was rather small, this treatment significantly increased the efficacy of tyrosine phosphorylation of Ret by GDNF. Experiments using synthetic retinoids suggested that RA acts through ␣-type of nuclear retinoic acid receptor to exert the induction of GDNF responsiveness. On the other hand, BMP2, which had no significant effect by itself on the GDNF responsiveness, promoted the action of RA to upregulate GFR␣-1 and enhance the GDNF responsiveness. These results indicate that RA and BMP2 play important roles in the induction of GDNF responsiveness, as well as NT3 responsiveness, of developing SCG neurons.

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Section: Discussionsupporting

confidence: 71%

Regulation of Glial Cell Line-Derived Neurotrophic Factor Responsiveness in Developing Rat Sympathetic Neurons by Retinoic Acid and Bone Morphogenetic Protein-2

2000

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“…An additional Pax3 binding site, GTGTGA, has been described for the melanocyte-specific tyrosinase-related protein-1 promoter (30). This consensus sequence is also present in MITF (23) and c-RET (29). The presence of the complimentary sequences TAAT or CAAGG was observed in the STX.…”

Section: Fig 2 Validation Of Representative Pax3 Downstream Target mentioning

confidence: 81%

Microarray Analysis Detects Novel Pax3 Downstream Target Genes

Mayanil¹,

George²,

Freilich³

et al. 2001

Journal of Biological Chemistry

106

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“…The question of whether RA receptors act by binding to enhancers in Ret regulatory sequences or by inducing expression of an intermediary transcription factor in ureteric bud cells is unclear. Several candidate RA response elements have been identified in the Ret promoter; however, none of these has been shown to drive RAdependent expression (Grice et al, 2005;Patrone et al, 1997), suggesting that RA might control Ret indirectly. Potential direct activators of Ret include Pax2 (Brophy et al, 2001), Hox genes , Ttf1 (Garcia-Barcelo et al, 2007), Nkx2.1 and Nurr1 (Nr4a2 -Mouse Genome Informatics) (Wallen et al, 2001), all of which are localized in the developing kidney.…”

Section: What Renal Cell Types Are Important For Mediating Ra-dependementioning

confidence: 99%

Non-cell-autonomous retinoid signaling is crucial for renal development

et al. 2010

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SUMMARYIn humans and mice, mutations in the Ret gene result in Hirschsprung's disease and renal defects. In the embryonic kidney, binding of Ret to its ligand, Gdnf, induces a program of epithelial cell remodeling that controls primary branch formation and branching morphogenesis within the kidney. Our previous studies showed that transcription factors belonging to the retinoic acid (RA) receptor family are crucial for controlling Ret expression in the ureteric bud; however, the mechanism by which retinoid-signaling acts has remained unclear. In the current study, we show that expression of a dominant-negative RA receptor in mouse ureteric bud cells abolishes Ret expression and Ret-dependent functions including ureteric bud formation and branching morphogenesis, indicating that RA-receptor signaling in ureteric bud cells is crucial for renal development. Conversely, we find that RA-receptor signaling in ureteric bud cells depends mainly on RA generated in nearby stromal cells by retinaldehyde dehydrogenase 2, an enzyme required for most fetal RA synthesis. Together, these studies suggest that renal development depends on paracrine RA signaling between stromal mesenchyme and ureteric bud cells that regulates Ret expression both during ureteric bud formation and within the developing collecting duct system.

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Sequence and characterisation of the RET proto‐oncogene 5′ flanking region: analysis of retinoic acid responsiveness at the transcriptional level

Cited by 29 publications

References 60 publications

Regulation of Glial Cell Line-Derived Neurotrophic Factor Responsiveness in Developing Rat Sympathetic Neurons by Retinoic Acid and Bone Morphogenetic Protein-2

Regulation of Glial Cell Line-Derived Neurotrophic Factor Responsiveness in Developing Rat Sympathetic Neurons by Retinoic Acid and Bone Morphogenetic Protein-2

Microarray Analysis Detects Novel Pax3 Downstream Target Genes

Non-cell-autonomous retinoid signaling is crucial for renal development

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