Mast cell growth factor maps near the steel locus on mouse chromosome 10 and is deleted in a number of steel alleles

Copeland, Neal G.; Gilbert, Debra J.; Cho, Brian; Donovan, Peter; Jenkins, Nancy A.; Cosman, David; Anderson, D; Lyman, Stewart D.; Williams, Douglas E.

doi:10.1016/0092-8674(90)90298-s

Cited by 577 publications

(206 citation statements)

References 38 publications

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“…Strict dependency of melanocyte lineage cells in vivo on KIT signaling was clearly indicated in the case of Kit mutant mice (Copeland et al, 1990;Nishikawa et al, 1991); and this dependency was also confirmed in our ES cell culture system (Yamane et al, 1999) Bernex et al, 1996) did not differentiate into melanocytes (Fig. 4A).…”

Section: Lack Of Kit Signaling Was Compensated By Edn3 During the Devsupporting

confidence: 80%

Cooperative and indispensable roles of endothelin 3 and KIT signalings in melanocyte development

Aoki

Motohashi

Yoshimura

et al. 2005

Developmental Dynamics

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The development of melanocytes from neural crest-derived precursor cells depends on signaling by the receptor tyrosine kinase KIT and the G protein-coupled endothelin receptor B (EDNRB) pathways. Loss-of-function mutations in either of these two signaling receptor molecules cause a loss or a marked reduction in the number of melanocyte precursors in the embryo and finally lead to loss of the coat color. Using cultures of embryonic stem (ES) cells to induce melanocyte differentiation in vitro, we investigated the requirement for EDNRB signaling during the entire developmental process of the melanocyte, in association with that for KIT signaling. During the 21-day period necessary for the induction of mature melanocytes from undifferentiated ES cells, endothelin 3 (EDN3), a ligand for EDNRB, increased the number of melanocytes in proportion to the period during which it was present. We tested the compensatory effect of EDNRB signaling on KIT signaling in vivo by using Kit W-LacZ /Kit W-LacZ ES cells and confirmed that the ectopic expression of EDN3 in the skin reduced the white spotting of Kit W57 /Kit W57 mice. KIT ligand (KITL) and EDN3 worked synergistically to induce melanocyte differentiation in vitro; however, the complete lack of EDNRB signaling attained by the use of EDN3 Ϫ/Ϫ ES cells and an EDNRB antagonist, BQ788, revealed that the resulting failure of melanocyte development was not compensated by the further activation of KIT signaling by adding KITL. Simultaneous blockade of EDNRB and KIT signalings eliminated melanocyte precursors completely, suggesting that the maintenance or survival of early melanocyte precursors at least required the existence of either EDNRB or KIT signalings. Developmental Dynamics 233:407-417, 2005.

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Section: Lack Of Kit Signaling Was Compensated By Edn3 During the Devsupporting

confidence: 80%

Cooperative and indispensable roles of endothelin 3 and KIT signalings in melanocyte development

Aoki

Motohashi

Yoshimura

et al. 2005

Developmental Dynamics

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“…Genes encoding Kit and SCF are mapped to the white spotting (W) and steel (Sl) loci in mice, respectively. [4][5][6][7][8] Both mutant mice of W and Sl loci show similar phenotypes such as severe macrocytic anemia, a decreased number of mast cells, a complete lack of coat pigmentation and infertility. 9 Further, many alleles of variable severity at both W and Sl loci have been identified.…”

Section: Introductionmentioning

confidence: 99%

Involvement of death receptor Fas in germ cell degeneration in gonads of Kit-deficient Wv/Wv mutant mice

et al. 2003

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Kit and its ligand stem cell factor (SCF) play a fundamental role in hematopoiesis, melanogenesis and gametogenesis. Homozygous W v mutant mice with a mutation in kit show abnormalities in these cell lineages. Fas is a member of the death receptor family inducing apoptosis. In this study, we generated double-mutant mice (W v /W v :Fas À/À ) and analyzed histologically their reproductive organs. In testes and ovaries of the double-mutant mice, testicular germ cells and oocytes were detected, respectively, whereas the same-aged W v /W v mice contained neither cells. In addition, inhibition of Kit signals by administration of anti-Kit mAb, which induces degeneration of testicular germ cells in vivo in wild-type mice, did not cause degeneration in Fas-deficient mice. In testicular germ cells of W v /W v mutant mice, an increase of Fas expression was observed in spermatogonia. Further, in vitro treatment with SCF was shown to downregulate Fas on fibroblasts expressing exogenous Kit through activation of PI3-kinase/Akt. All the results clearly indicate that Fasmediated apoptosis is involved in germ cell degeneration accompanied by defects in Kit-mediated signals, and Kit signaling negatively regulates Fas-mediated apoptosis in vivo.

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“…A renewed interest in these mutants came when the W and Sl gene products were characterized at the molecular level (Chabot et al, 1988;Geissler et al, 1988;Copeland et al, 1990;Huang et al, 1990;Zsebo et al, 1990;Williams et al, 1990). Thus, the complementarity of the two mutations was accounted for by the fact that the W gene encodes a transmembrane tyrosinekinase receptor, c-kit, the ligand of which turned out to be the product of the Sl gene.…”

Section: Introductionmentioning

confidence: 99%

Steel and c‐kit in the development of avian melanocytes: A study of normally pigmented birds and of the hyperpigmented mutant silky fowl

Lecoin

Lahav

Martin

et al. 1995

Developmental Dynamics

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We describe here the expression of c-kit and Steel (SZ) genes during the development of melanocytes in normally pigmented strains of chick and quail compared to unpigmented (White Leghorn) and hyperpigmented (Silky Fowl) strains of chickens. By using the quailkhick chimera system, we found that the neural crest cells, which migrate dorso-laterally in the subectodermal mesenchyme to give rise to the melanocytes, express c-kit as early as E4, that is about 2 days after they have left the neural primordium. The SZ gene is expressed from E4 onward in the epidermis but not at all in the dermis at any developmental stage. As feather buds develop, S Z mRNA becomes restricted to the apical region of the feather filaments. During formation of the barbs and barbules of the down feather, production of the Steel factor is restricted to the external epidermal cells of the barbules. The cell bodies of the c-kit-positive melanocytes are then located in the internal border of the epidermal ridges and extend their processes toward the source of the Steel factor. We propose that the spa-

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Mast cell growth factor maps near the steel locus on mouse chromosome 10 and is deleted in a number of steel alleles

Cited by 577 publications

References 38 publications

Cooperative and indispensable roles of endothelin 3 and KIT signalings in melanocyte development

Cooperative and indispensable roles of endothelin 3 and KIT signalings in melanocyte development

Involvement of death receptor Fas in germ cell degeneration in gonads of Kit-deficient Wv/Wv mutant mice

Steel and c‐kit in the development of avian melanocytes: A study of normally pigmented birds and of the hyperpigmented mutant silky fowl

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