Amputation induces stem cell mobilization to sites of injury during planarian regeneration.
How adult stem cell populations are recruited for tissue renewal and repair is a fundamental question of biology. Mobilization of stem cells out of their niches followed by correct migration and differentiation at a site of tissue turnover or injury are important requirements for proper tissue maintenance and regeneration. However, we understand little about the mechanisms that control this process, possibly because the best studied vertebrate adult stem cell systems are not readily amenable to in vivo observation. Furthermore, few clear examples of the recruitment of fully potent stem cells, compared with limited progenitors, are known. Here, we show that planarian stem cells directionally migrate to amputation sites during regeneration. We also show that during tissue homeostasis they are stationary. Our study not only uncovers the existence of specific recruitment mechanisms elicited by amputation, but also sets the stage for the systematic characterization of evolutionarily conserved stem cell regulatory processes likely to inform stem cell function and dysfunction in higher organisms, including humans.
Department of Neurobiology and Anatomy, University of Utah School of Medicine, Salt Lake City, UT 84132, USA.
Otto C
OC
Guedelhoefer
Alejandro
A
Sánchez Alvarado
D000671:Amputation, Surgical; D000818:Animals; D002465:Cell Movement / Q000502:physiology* / Q000528:radiation effects; D005260:Female; D008297:Male; D010932:Planarians / Q000166:cytology / Q000502:physiology* / Q000528:radiation effects; D011833:Radiation Injuries, Experimental / Q000473:pathology / Q000503:physiopathology / Q000628:therapy; D012038:Regeneration / Q000502:physiology* / Q000528:radiation effects; D012100:Reproduction, Asexual / Q000502:physiology / Q000528:radiation effects; D019529:Sexuality / Q000502:physiology; D033581:Stem Cell Transplantation; D013234:Stem Cells / Q000502:physiology* / Q000528:radiation effects; D014947:Wounds and Injuries / Q000473:pathology / Q000503:physiopathology