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Título

Downregulation of mTOR Signaling Increases Stem Cell Population Telomere Length during Starvation of Immortal Planarians

AutorIglesias, Marta CSIC ORCID ; Felix, Daniel A.; Gutiérrez-Gutiérrez, Óscar; De Miguel-Bonet, Maria del Mar; Sahu, Sounak; Fernández-Varas, Beatriz CSIC; Perona Abellón, Rosario CSIC ORCID; Aboobaker, A. Aziz; Flores, Ignacio; González-Estévez, Cristina
Palabras clavePlanarian
MTOR
Starvation
Stem cell
Telomere
Aging
Neoblast
Fasting
Immortal
SMG-1
Fecha de publicación13-ago-2019
EditorElsevier BV
CitaciónStem Cell Reports 13(2): 405-418 (2019)
ResumenReduction of caloric intake delays and prevents age-associated diseases and extends the life span in many organisms. It may be that these benefits are due to positive effects of caloric restriction on stem cell function. We use the planarian model Schmidtea mediterranea, an immortal animal that adapts to long periods of starvation by shrinking in size, to investigate the effects of starvation on telomere length. We show that the longest telomeres are a general signature of planarian adult stem cells. We also observe that starvation leads to an enrichment of stem cells with the longest telomeres and that this enrichment is dependent on mTOR signaling. We propose that one important effect of starvation for the rejuvenation of the adult stem cell pool is through increasing the median telomere length in somatic stem cells. Such a mechanism has broad implications for how dietary effects on aging are mediated at the whole-organism level. González-Estévez and colleagues show that long telomeres are a signature of planarian stem cells. They find that in the immortal planarian, starvation leads to an enrichment of stem cells with the longest telomeres dependent on mTOR signaling. They propose that starvation contributes to the rejuvenation of the adult stem cell pool by increasing their telomere length.
Versión del editorhttp://dx.doi.org/10.1016/j.stemcr.2019.06.005
URIhttp://hdl.handle.net/10261/206481
DOI10.1016/j.stemcr.2019.06.005
E-ISSN2213-6711
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