Starvation resistance in planarians: multiple strategies to get a thrifty phenotype
Starvation resistance is a life‐saving mechanism for many organisms facing food availability fluctuation in the natural environment. Different strategies have been episodically identified for some model organisms, the first of which was the ability to suppress metabolic rate. Among the identified st...
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Veröffentlicht in: | The FEBS journal 2024-03, Vol.291 (5), p.965-985 |
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Sprache: | eng |
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Zusammenfassung: | Starvation resistance is a life‐saving mechanism for many organisms facing food availability fluctuation in the natural environment. Different strategies have been episodically identified for some model organisms, the first of which was the ability to suppress metabolic rate. Among the identified strategies, the ability of planarians to shrink their body under fasting conditions and revert the process after feeding (the growth–degrowth process) represents a fascinating mechanism to face long periods of fasting. The growth–degrowth process is strictly related to the capability of planarians to continuously maintain tissue homeostasis and body proportions even in challenging conditions, thanks to the presence of a population of pluripotent stem cells. Here, we take advantage of several previous studies describing the growth–degrowth process and of recent progress in the understanding of planarian homeostasis mechanisms, to identify tissue‐selective transcriptional downregulation as a driving strategy for the development of a thrifty phenotype, and the p53 transcription factor as a player in adjusting tissue homeostasis in accordance with food availability.
Starvation resistance is a lifesaving mechanism for many organisms. The ability of planarians to shrink their body under fasting conditions represents a fascinating strategy in which the p53 transcription factor operates to adjust tissue homeostasis in accordance with food availability. In starving animals, proliferative activity is supported at the expense of tissue‐selective transcriptional downregulation and thanks to the increase in cell death. |
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ISSN: | 1742-464X 1742-4658 |
DOI: | 10.1111/febs.17020 |