Please use this identifier to cite or link to this item:
Title: JNK controls the onset of mitosis of planarian stem cells and triggers apoptotic cell death required for regeneration and remodeling
Author: Almuedo Castillo, María
Crespo, Xenia
Saló i Boix, Emili
Adell i Creixell, Teresa
Seebeck, F.
Bartscherer, Kerstin
Keywords: Apoptosi
Cèl·lules mare
Stem cells
Issue Date: 2014
Publisher: Public Library of Science (PLoS)
Abstract: Regeneration of lost tissues depends on the precise interpretation of molecular signals that control and coordinate the onset of proliferation, cellular differentiation and cell death. However, the nature of those molecular signals and the mechanisms that integrate the cellular responses remain largely unknown. The planarian flatworm is a unique model in which regeneration and tissue renewal can be comprehensively studied in vivo. The presence of a population of adult pluripotent stem cells combined with the ability to decode signaling after wounding enable planarians to regenerate a complete, correctly proportioned animal within a few days after any kind of amputation, and to adapt their size to nutritional changes without compromising functionality. Here, we demonstrate that the stress-activated c-jun-NH2-kinase (JNK) links wound-induced apoptosis to the stem cell response during planarian regeneration. We show that JNK modulates the expression of wound-related genes, triggers apoptosis and attenuates the onset of mitosis in stem cells specifically after tissue loss. Furthermore, in pre-existing body regions, JNK activity is required to establish a positive balance between cell death and stem cell proliferation to enable tissue renewal, remodeling and the maintenance of proportionality. During homeostatic degrowth, JNK RNAi blocks apoptosis, resulting in impaired organ remodeling and rescaling. Our findings indicate that JNK-dependent apoptotic cell death is crucial to coordinate tissue renewal and remodeling required to regenerate and to maintain a correctly proportioned animal. Hence, JNK might act as a hub, translating wound signals into apoptotic cell death, controlled stem cell proliferation and differentiation, all of which are required to coordinate regeneration and tissue renewal.
Note: Reproducció del document publicat a: 10.1371/journal.pgen.1004400
It is part of: PLoS Genetics, 2014, vol. 10, num. 6
Related resource:
ISSN: 1553-7390
Appears in Collections:Articles publicats en revistes (Genètica, Microbiologia i Estadística)

Files in This Item:
File Description SizeFormat 
634708.pdf2.97 MBAdobe PDFView/Open

This item is licensed under a Creative Commons License Creative Commons