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Diminished Jak/STAT Signaling Causes Early-Onset Aging Defects in Stem Cell Cytokinesis
Journal article   Open access   Peer reviewed

Diminished Jak/STAT Signaling Causes Early-Onset Aging Defects in Stem Cell Cytokinesis

Kari F. Lenhart, Benjamin Capozzoli, Gwen S. D. Warrick and Stephen DiNardo
Current biology, v 29(2), pp 256-267.e3
21 Jan 2019
PMID: 30612906
url
https://doi.org/10.1016/j.cub.2018.11.064View
Published, Version of Record (VoR)Open Access (Publisher-Specific) Open

Abstract

Biochemistry & Molecular Biology Biology Cell Biology Life Sciences & Biomedicine Life Sciences & Biomedicine - Other Topics Science & Technology
Tissue renewal becomes compromised with age. Although defects in niche and stem cell behavior have been implicated in promoting age-related decline, the causes of early-onset aging defects are unknown. We have identified an early consequence of aging in germline stem cells (GSCs) in the Drosophila testis. Aging disrupts the unique program of GSC cytokinesis, with GSCs failing to abscise from their daughter cells. Abscission failure significantly disrupts both self-renewal and the generation of differentiating germ cells. Extensive live imaging and genetic analyses show that abscission failure is due to inappropriate retention of F-actin at the intercellular bridges between GSC-daughter cells. Furthermore, F-actin is regulated by the Jak/STAT pathway-increasing or decreasing pathway activity can rescue or exacerbate the age-induced abscission defect, respectively. Even subtle decreases to STAT activity are sufficient to precociously age young GSCs and induce abscission failure. Thus, this work has identified the earliest age-related defect in GSCs and has revealed a unique role for an established niche signaling pathway in controlling stem cell cytokinesis and in regulating stem cell behavior with age.

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Collaboration types
Domestic collaboration
Web of Science research areas
Biochemistry & Molecular Biology
Biology
Cell Biology
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