GFRα1 Is an Essential Receptor Component for GDNF in the Developing Nervous System and Kidney

Cacalano, Grace; Fariñas, Isabel; Wang, Li-Chong; Hagler, Kelly E.; Forgie, Alison; Moore, Mark; Armanini, Mark; Phillips, Heidi S.; Ryan, Anne; Reichardt, Louis F.; Hynes, Mary; Davies, Alun M.; Rosenthal, Arnon

doi:10.1016/s0896-6273(00)80514-0

Cited by 497 publications

(331 citation statements)

References 39 publications

Supporting

Mentioning

317

Contrasting

Unclassified

Order By: Relevance

“…Recent studies suggest this difference might be at least partially explained by the expression of axon guidance molecules Slit and Robo on vagal NC (De Bellard et al, 2003). In contrast to our results, mice lacking members of the glial cell line-derived neurotrophic factor signaling pathway have enteric neurons in the anterior ENS (Cacalano et al, 1998;Pichel et al, 1996;Sanchez et al, 1996), whereas mutations in endothelin 3 or endothelin receptor type B cause the loss of ENS only in the distal colon Hosoda et al, 1994). In Phox2b -/-embryos, there is an initial migration of vagal NC into the proximal gut mesentery, but these progenitors are not maintained, leaving the entire gut without innervation (Pattyn et al, 1999).…”

Section: Nc Patterningcontrasting

confidence: 99%

Requirement for Foxd3 in the maintenance of neural crest progenitors

et al. 2008

View full text Add to dashboard Cite

Understanding the molecular mechanisms of stem cell maintenance is crucial for the ultimate goal of manipulating stem cells for the treatment of disease. Foxd3 is required early in mouse embryogenesis; Foxd3 -/-embryos fail around the time of implantation, cells of the inner cell mass cannot be maintained in vitro, and blastocyst-derived stem cell lines cannot be established. Here, we report that Foxd3 is required for maintenance of the multipotent mammalian neural crest. Using tissue-specific deletion of Foxd3 in the neural crest, we show that Foxd3 flox/-; Wnt1-Cre mice die perinatally with a catastrophic loss of neural crest-derived structures. Cranial neural crest tissues are either missing or severely reduced in size, the peripheral nervous system consists of reduced dorsal root ganglia and cranial nerves, and the entire gastrointestinal tract is devoid of neural crest derivatives. These results demonstrate a global role for this transcriptional repressor in all aspects of neural crest maintenance along the anterior-posterior axis, and establish an unprecedented molecular link between multiple divergent progenitor lineages of the mammalian embryo.

show abstract

Section: Nc Patterningcontrasting

confidence: 99%

Requirement for Foxd3 in the maintenance of neural crest progenitors

et al. 2008

View full text Add to dashboard Cite

show abstract

“…The ureteric bud, kidney and enteric neurons are absent Pichel et al, 1996;Sanchez et al, 1996). The Ret and Gfrα-1 receptors have also been knocked out and show the same phenotypes, indicating that Gdnf signals through the Gfrα-1/Ret-receptor complex and is essential for postnatal survival in the mouse (Schuchardt et al, 1994;Enomoto et al, 1998;Cacalano et al, 1998;Tomac et al, 2000). Interestingly, the testicular morphology of mice lacking Gdnf, Gfrα-1 and Ret is normal before birth.…”

Section: Role Of Gdnf In the Mammalian Testismentioning

confidence: 99%

Gdnf signaling pathways within the mammalian spermatogonial stem cell niche

Hofmann

2008

Molecular and Cellular Endocrinology

201

178

View full text Add to dashboard Cite

SummaryMammalian spermatogenesis is a complex process in which male germ-line stem cells develop to ultimately form spermatozoa. Spermatogonial stem cells, or SSCs, are found in the basal compartment of the seminiferous epithelium. They self-renew to maintain the pool of stem cells throughout life, or they differentiate to generate a large number of germ cells. A balance between SSC self-renewal and differentiation in the adult testis is therefore essential to maintain normal spermatogenesis and fertility. Maintenance and self-renewal are tightly regulated by extrinsic signals from the surrounding microenvironment, called the spermatogonial stem cell niche. By physically supporting the SSCs and providing them with growth factors, the Sertoli cell is the main component of the niche. In addition, adhesion molecules that connect the SSCs to the basement membrane and cellular components of the interstitium between the seminiferous tubules are important regulators of the niche function. This review mainly focuses on glial cell line-derived neurotrophic factor (Gdnf), which is produced by Sertoli cells to maintain SSCs self-renewal, and the downstream signaling pathways induced by this crucial growth factor. Interactions between Gdnf and other signaling pathways that maintain self-renewal, as well as the role of novel SSC-and Sertoli cell-specific transcription factors, are also discussed.

show abstract

“…55 RET and GFRa-1 transduce a GDNF signal that plays a role in the development of the enteric nervous system and the kidney; thus, null mutations in GDNF, RET, and GFRa-1 display similar phenotypes. [56][57][58] Ligand binding to the RET complex triggers RET autophosphorylation, followed by interaction with effectors that include phospholipase Cg, Shc, Enigma, Grb2, Grb7/Grb10, Src kinase, and Ras-GAP, and resultant downstream signaling. [59][60][61] Mutations in the RET proto-oncogene may be associated with neoplastic disease or with a neural developmental disease.…”

Section: Rearranged During Transfection (Ret): One Receptor Two Disementioning

confidence: 99%

Receptors that mediate cellular dependence

2005

View full text Add to dashboard Cite

Cells depend for their survival on stimulation by trophic factors and other prosurvival signals, the withdrawal of which induces apoptosis, both via the loss of antiapoptotic signaling and the activation of proapoptotic signaling via specific receptors. These receptors, dubbed dependence receptors, activate apoptotic pathways following the withdrawal of trophic factors and other supportive stimuli. Such receptors may feature in developmental cell death, carcinogenesis (including metastasis), neurodegeneration, and possibly subapoptotic events such as neurite retraction and somal atrophy. Mechanistic studies of dependence receptors suggest that these receptors form ligand-dependent complexes that include specific caspases. Complex formation in the absence of ligand leads to caspase activation by a mechanism that is typically dependent on caspase cleavage of the receptor itself, releasing proapoptotic peptides. Cellular dependence receptors, considered in the aggregate, may thus form a system of molecular integration, analogous to the electrical integration system provided by dendritic arbors in the nervous system.

show abstract

GFRα1 Is an Essential Receptor Component for GDNF in the Developing Nervous System and Kidney

Cited by 497 publications

References 39 publications

Requirement for Foxd3 in the maintenance of neural crest progenitors

Requirement for Foxd3 in the maintenance of neural crest progenitors

Gdnf signaling pathways within the mammalian spermatogonial stem cell niche

Receptors that mediate cellular dependence

Contact Info

Product

Resources

About