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非洲爪蟾周期性白化突变体黑素细胞的进一步研究

Further studies on the melanophores of periodic albino mutant of Xenopus laevis.

作者信息

Fukuzawa T, Ide H

出版信息

J Embryol Exp Morphol. 1986 Feb;91:65-78.

PMID:3711792
Abstract

It is still unknown why dermal melanophores disappear during larval development, and why no or very few epidermal melanophores appear during and after metamorphosis, in Xenopus laevis showing periodic albinism (ap). To elucidate these points, we investigated the occurrence of depigmentation in mutant (ap/ap) melanophores during in vitro proliferation and the incidence of melanophore differentiation from mutant melanoblasts in the skin in vitro. During in vitro proliferation of mutant melanophores, ap-type melanosomes decreased in number gradually and instead the number of premelanosomes increased in the cells, which caused depigmentation at the light microscopic level in the culture. Depigmentation was observed only in mutant melanophores, and not in wild-type (+/+) melanophores. These results suggest that autonomous depigmentation of mutant dermal melanophores is the cause of the disappearance of these cells in vivo. Dopa-positive melanoblasts were demonstrated in both wild-type and mutant skins. However, the melanoblasts of metamorphosed mutant froglets did not differentiate in vitro, while those of wild-type froglets did. These results suggest that mutant melanoblasts in the skin of froglets lose the potency to differentiate into melanophores, and that this causes the lack of mutant melanophores in the froglets. The site of action of the ap gene is also discussed.

摘要

在表现出周期性白化病(ap)的非洲爪蟾中,目前仍不清楚为什么真皮黑素细胞在幼体发育过程中会消失,以及为什么在变态期间及之后表皮黑素细胞很少出现或根本不出现。为了阐明这些问题,我们研究了突变体(ap/ap)黑素细胞在体外增殖过程中的色素脱失情况,以及突变体成黑素细胞在体外皮肤中分化为黑素细胞的发生率。在突变体黑素细胞的体外增殖过程中,ap型黑素小体数量逐渐减少,取而代之的是细胞中前黑素小体数量增加,这在培养物的光学显微镜水平上导致了色素脱失。色素脱失仅在突变体黑素细胞中观察到,而在野生型(+/+)黑素细胞中未观察到。这些结果表明,突变体真皮黑素细胞的自主色素脱失是这些细胞在体内消失的原因。在野生型和突变体皮肤中均证实了多巴阳性成黑素细胞。然而,变态后的突变体幼蛙的成黑素细胞在体外未分化,而野生型幼蛙的成黑素细胞则分化了。这些结果表明,幼蛙皮肤中的突变体成黑素细胞失去了分化为黑素细胞的能力,这导致了幼蛙中缺乏突变体黑素细胞。本文还讨论了ap基因的作用位点。

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1
Further studies on the melanophores of periodic albino mutant of Xenopus laevis.非洲爪蟾周期性白化突变体黑素细胞的进一步研究
J Embryol Exp Morphol. 1986 Feb;91:65-78.
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Melanophore differentiation in Xenopus laevis, with special reference to dorsoventral pigment pattern formation.非洲爪蟾的黑素细胞分化,特别涉及背腹色素模式的形成。
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Experimental evidence for autonomous action of the periodic albinism (ap) gene within developing retinal pigment cells and melanophores of Xenopus laevis.非洲爪蟾发育中的视网膜色素细胞和黑素细胞内周期性白化病(ap)基因自主作用的实验证据。
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Melanophore differentiation in the periodic albino mutant of Xenopus laevis.非洲爪蟾周期性白化突变体中的黑素细胞分化
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Ferritin H subunit gene is specifically expressed in melanophore precursor-derived white pigment cells in which reflecting platelets are formed from stage II melanosomes in the periodic albino mutant of Xenopus laevis.铁蛋白H亚基基因在非洲爪蟾周期性白化突变体中,于由黑素体前体衍生的白色色素细胞中特异性表达,在这些细胞中,反光血小板由II期黑素体形成。
Cell Tissue Res. 2015 Sep;361(3):733-44. doi: 10.1007/s00441-015-2133-8. Epub 2015 Feb 26.

引用本文的文献

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The origin and development of retinal pigment cells and melanophores analyzed by Xenopus black-white chimeras.通过非洲爪蟾黑白嵌合体分析视网膜色素细胞和黑素细胞的起源与发育。
Dev Growth Differ. 1995 Apr;37(2):157-166. doi: 10.1046/j.1440-169X.1995.t01-1-00004.x.
2
Periodic albinism of a widely used albino mutant of Xenopus laevis caused by deletion of two exons in the Hermansky-Pudlak syndrome type 4 gene.周期性白化症是一种广泛应用的非洲爪蟾白化突变体,由 Hermansky-Pudlak 综合征 4 型基因的两个外显子缺失引起。
Genes Cells. 2021 Jan;26(1):31-39. doi: 10.1111/gtc.12818. Epub 2020 Nov 28.
3
Ferritin H subunit gene is specifically expressed in melanophore precursor-derived white pigment cells in which reflecting platelets are formed from stage II melanosomes in the periodic albino mutant of Xenopus laevis.
铁蛋白H亚基基因在非洲爪蟾周期性白化突变体中,于由黑素体前体衍生的白色色素细胞中特异性表达,在这些细胞中,反光血小板由II期黑素体形成。
Cell Tissue Res. 2015 Sep;361(3):733-44. doi: 10.1007/s00441-015-2133-8. Epub 2015 Feb 26.
4
Unusual development of light-reflecting pigment cells in intact and regenerating tail in the periodic albino mutant of Xenopus laevis.周期性白化突变体非洲爪蟾完整和再生尾中光反射色素细胞的异常发育。
Cell Tissue Res. 2010 Oct;342(1):53-66. doi: 10.1007/s00441-010-1042-0. Epub 2010 Sep 22.