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Distinct stress-inducible and developmentally regulated heat shock transcription factors in Xenopus oocytes.非洲爪蟾卵母细胞中不同的应激诱导型和发育调控型热休克转录因子。
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本文引用的文献

1
Central nervous system and facial defects associated with maternal hyperthermia at four to 14 weeks' gestation.妊娠4至14周时母体发热相关的中枢神经系统和面部缺陷。
Pediatrics. 1981 Jun;67(6):785-9.
2
Changes in chromatin and the phosphorylation of nuclear proteins during heat shock of Achlya ambisexualis.两性绵霉热激过程中染色质及核蛋白磷酸化的变化
Mol Cell Biol. 1984 Jul;4(7):1198-205. doi: 10.1128/mcb.4.7.1198-1205.1984.
3
Human heat shock gene expression and the modulation of plasma membrane Na+, K+-ATPase activity.人类热休克基因表达与质膜钠钾ATP酶活性的调节
FEBS Lett. 1982 Apr 5;140(1):45-8. doi: 10.1016/0014-5793(82)80517-6.
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Embryonic stress hypothesis of teratogenesis.致畸作用的胚胎应激假说。
Am J Med. 1984 Feb;76(2):293-301. doi: 10.1016/0002-9343(84)90788-5.
5
A major developmental transition in early Xenopus embryos: I. characterization and timing of cellular changes at the midblastula stage.非洲爪蟾早期胚胎发育中的一个主要转变:I. 囊胚中期细胞变化的特征与时间进程
Cell. 1982 Oct;30(3):675-86. doi: 10.1016/0092-8674(82)90272-0.
6
The origin, distribution and disappearance of surface cilia during embryonic development of Rana pipiens as revealed by scanning electron microscopy.用扫描电子显微镜揭示的牛蛙胚胎发育过程中表面纤毛的起源、分布和消失情况。
Am J Anat. 1974 Nov;141(3):341-59. doi: 10.1002/aja.1001410306.
7
Acquisition of the heat-shock response and thermotolerance during early development of Xenopus laevis.非洲爪蟾早期发育过程中热休克反应和耐热性的获得
Dev Biol. 1985 Feb;107(2):483-9. doi: 10.1016/0012-1606(85)90329-x.
8
Morphological study of the mammalian stress response: characterization of changes in cytoplasmic organelles, cytoskeleton, and nucleoli, and appearance of intranuclear actin filaments in rat fibroblasts after heat-shock treatment.哺乳动物应激反应的形态学研究:热休克处理后大鼠成纤维细胞中细胞质细胞器、细胞骨架和核仁变化的特征以及核内肌动蛋白丝的出现
J Cell Biol. 1985 Oct;101(4):1198-211. doi: 10.1083/jcb.101.4.1198.
9
Cellular and biochemical events in mammalian cells during and after recovery from physiological stress.哺乳动物细胞在生理应激期间及恢复过程中和恢复后的细胞及生化事件。
J Cell Biol. 1986 Nov;103(5):2035-52. doi: 10.1083/jcb.103.5.2035.
10
Heat shock causes destabilization of specific mRNAs and destruction of endoplasmic reticulum in barley aleurone cells.热激会导致大麦糊粉层细胞中特定mRNA的稳定性丧失以及内质网的破坏。
Proc Natl Acad Sci U S A. 1986 Mar;83(5):1354-8. doi: 10.1073/pnas.83.5.1354.

热休克对非洲爪蟾幼体表皮形态和蛋白质合成的影响。

The effects of heat shock on the morphology and protein synthesis of the epidermis of Xenopus laevis larvae.

作者信息

Nickells R W, Cavey M J, Browder L W

机构信息

Department of Biological Sciences, University of Calgary, Alberta, Canada.

出版信息

J Cell Biol. 1988 Mar;106(3):905-14. doi: 10.1083/jcb.106.3.905.

DOI:10.1083/jcb.106.3.905
PMID:3346329
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2115074/
Abstract

By scanning electron microscopy, we have observed that a 20-min heat shock at 37 degrees C, although not lethal, causes extensive damage to the epidermis of 30-h and 2-d (post-fertilization) Xenopus laevis larvae. The primary effects of heat shock are the apical swelling of the epidermal cells, giving the epidermis a "cobblestone" appearance, and the selective shedding of the ciliated cells. The shed cells may be cell fragments, however, because some of them are anucleate. Shed cells also exhibit the enriched synthesis of a group of heat shock proteins of 62,000 D molecular weight, suggesting that these proteins are specific to the shed cells. Prolonged heat shock of these larvae (i.e., 30 min at 37 degrees C) results in the complete disintegration of the epidermis, followed by larval death. At later stages of development (3-d and 4-d post-fertilization), the epidermis becomes more resistant to heat-induced damage inflicted by a 20-min heat shock. This increase in resistance coincides with the development of large secretory cells and the loss of ciliated cells in the epidermis and thus parallels a change in the state of histological differentiation.

摘要

通过扫描电子显微镜,我们观察到,在37摄氏度下进行20分钟的热休克处理,虽然不会致命,但会对受精后30小时和2天的非洲爪蟾幼虫的表皮造成广泛损伤。热休克的主要影响是表皮细胞顶端肿胀,使表皮呈现“鹅卵石”外观,以及纤毛细胞的选择性脱落。然而,脱落的细胞可能是细胞碎片,因为其中一些是无核的。脱落的细胞还表现出一组分子量为62000道尔顿的热休克蛋白的合成增加,这表明这些蛋白质是脱落细胞特有的。对这些幼虫进行长时间的热休克处理(即37摄氏度下30分钟)会导致表皮完全解体,随后幼虫死亡。在发育的后期阶段(受精后3天和4天),表皮对20分钟热休克造成的热诱导损伤更具抵抗力。这种抵抗力的增加与表皮中大型分泌细胞的发育以及纤毛细胞的丧失同时发生,因此与组织学分化状态的变化平行。