Visceral Regeneration in a Sea Cucumber Involves Extensive Expression of Survivin and Mortalin Homologs in the Mesothelium
Mashanov, Vladimir S.
Zueva, Olga R.
Garcia-Arraras, Jose E.
MetadataShow full item record
Background: The proper balance of cell division and cell death is of crucial importance for all kinds of developmental processes and for maintaining tissue homeostasis in mature tissues. Dysregulation of this balance often results in severe pathologies, such as cancer. There is a growing interest in understanding the factors that govern the interplay between cell death and proliferation under various conditions. Survivin and mortalin are genes that are known to be implicated in both mitosis and apoptosis and are often expressed in tumors.Results: The present study takes advantage of the ability of the sea cucumber Holothuria glaberrima Selenka, 1867 (Holothuroidea, Aspidochirota) to discard its viscera and completely regrow them. This visceral regeneration involves an extensive expression of survivin and mortalin transcripts in the gut mesothelium (the outer tissue layer of the digestive tube), which coincides in time with drastic de-differentiation and a burst in cell division and apoptosis. Double labeling experiments (in situ hybridization combined with TUNEL assay or with BrdU immunohistochemistry) suggest that both genes support cell proliferation, while survivin might also be involved in suppression of the programmed cell death.Conclusions: Visceral regeneration in the sea cucumber H. glaberrima is accompanied by elevated levels of cell division and cell death, and, moreover, involves expression of pro-cancer genes, such as survivin and mortalin, which are known to support proliferation and inhibit apoptosis. Nevertheless, once regeneration is completed and the expression pattern of both genes returns to normal, the regrown digestive tube shows no anomalies. This strongly suggests that sea cucumbers must possess some robust cancer-suppression mechanisms that allow rapid re-growth of the adult tissues without leading to runaway tumor development.