Abstract
The cnidarian Hydra is known for its unlimited lifespan and non-senescence, due to the indefinite self-renewal capacity of its stem cells. While proteins of the Lamin family are recognized as critical factors affecting senescence and longevity in human and mice, their putative role in the extreme longevity and non-senescence in long-living animals remains unknown. Here we analyze the role of a single lamin protein in non-senescence of Hydra. We demonstrate that proliferation of stem cells in Hydra is robust against the disturbance of Lamin expression and localization. While Lamin is indispensable for Hydra, the stem cells tolerate overexpression, downregulation and mislocalization of Lamin, and disturbances in the nuclear envelope structure. This extraordinary robustness may underlie the indefinite self-renewal capacity of stem cells and the non-senescence of Hydra. A relatively low complexity of the nuclear envelope architecture in basal Metazoa might allow for their extreme lifespans, while an increasing complexity of the nuclear architecture in bilaterians resulted in restricted lifespans.
Highlights
The freshwater polyp Hydra belongs to the Cnidaria phylum, and represents a rare case of an animal with extreme longevity
The transcriptional factor FoxO was found as critical regulator of Hydra stem cell homeostasis and longevity, supporting the view that components of the insulin/insulin-like growth factor signaling pathways govern lifespan throughout the animal kingdom [7,8,9,10]
A vast diversity of ageing patterns and lifespans has been reported across the animal kingdom, from fastageing short-living species as mayflies and turquoise killifish to species with a remarkable longevity and a negligible senescence - as clams and Hydra [4,41,42,43]
Summary
The freshwater polyp Hydra belongs to the Cnidaria phylum, and represents a rare case of an animal with extreme longevity. Diverse experimental models corroborate the importance of the proper Lamin primary sequence, expression levels, and processing for the tissue homeostasis and lifespan [20,27,28,29,30] Taken together, these findings point to the central role of Lamins in maintaining stem-cell activity and tissue homeostasis, as well as in controlling cellular and organismal senescence in model animals [14,17,31]. Www.aging-us.com proliferation displays an extraordinary robustness against the Lamin disturbance This may play a critical role in the unlimited self-renewal capacity of Hydra stem cells and its non-senescence
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