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

Abstract

Abstract. By scanning electron microscopy, we have observed that a 20-min heat shock at 37~ 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~ 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 heatinduced 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.T HE effect of heat shock on the physiology and metabolism of cells has been extensively studied. Most investigations have concentrated on analyzing the molecular responses of cells to thermal stress. During heat shock, cells selectively synthesize heat shock proteins (hsps), ~ which are believed to enhance their ability to survive at the higher temperature (for reviews see 2, 14, 19).Heat shock can cause extensive cellular damage, particularly to membranous structures. These effects have been examined at the ultrastructural level and include the dispersal of the Golgi apparatus (23) and endoplasmic reticulum (3) and the swelling of mitochondria (23), which apparently lose the ability to function properly (12; for review see 11). The plasma membrane is also affected by heat shock, exhibiting increases in fluidity (13), loss of active transport activity (4) and formation of lesions large enough to allow the passage of small molecules (for review see 19). Nonmembranous structures also suffer heat-induced damage. The chromatin in nuclei condenses (20), whereas nucleoli disperse (13, 24). Bundles of actin filaments also form within the nuclei (20,23), and in the cytoplasm, the intermediate filament network collapses onto the nucleus (23).The effects of heat shock on intact organisms or tissues have been less well characterized. Embryos are highly susceptible to heat shock, however, as they often develop severe abnormalities if exposed to elevated temperatures during critical periods of their development. These effects are exemplified by mammalian embryos, which are particularly susceptible to heat-induced defects of the central nervous system 1. Abbreviation used in this paper: hsp, heat shock protein.(22), and by Drosophila larvae, which can be induced by heat shock to develop phenocopies (15). How heat shock effects developing embryos is uncertain, although some lines of evidence ...

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“…Nonetheless, it is known that they fall into at least two categories, the large secretory cells and the smaller, scattered cells (Fig. 1B-C; (Billett and Gould, 1971;Nickells et al, 1988). The large secretory cells in the Xenopus epidermis are the predominant cell type, and they are known to secrete lectin-rich mucus (Billett and Gould, 1971;Nagata, 2005).…”

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