scholarly journals Author response: Embryonic origin of adult stem cells required for tissue homeostasis and regeneration

2016 ◽  
Author(s):  
Erin L Davies ◽  
Kai Lei ◽  
Christopher W Seidel ◽  
Amanda E Kroesen ◽  
Sean A McKinney ◽  
...  
eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Erin L Davies ◽  
Kai Lei ◽  
Christopher W Seidel ◽  
Amanda E Kroesen ◽  
Sean A McKinney ◽  
...  

Planarian neoblasts are pluripotent, adult somatic stem cells and lineage-primed progenitors that are required for the production and maintenance of all differentiated cell types, including the germline. Neoblasts, originally defined as undifferentiated cells residing in the adult parenchyma, are frequently compared to embryonic stem cells yet their developmental origin remains obscure. We investigated the provenance of neoblasts during Schmidtea mediterranea embryogenesis, and report that neoblasts arise from an anarchic, cycling piwi-1+ population wholly responsible for production of all temporary and definitive organs during embryogenesis. Early embryonic piwi-1+ cells are molecularly and functionally distinct from neoblasts: they express unique cohorts of early embryo enriched transcripts and behave differently than neoblasts in cell transplantation assays. Neoblast lineages arise as organogenesis begins and are required for construction of all major organ systems during embryogenesis. These subpopulations are continuously generated during adulthood, where they act as agents of tissue homeostasis and regeneration.


Author(s):  
Elena Lazzeri ◽  
Anna Peired ◽  
Lara Ballerini ◽  
Laura Lasagni

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Junjun Jing ◽  
Jifan Feng ◽  
Jingyuan Li ◽  
Hu Zhao ◽  
Thach-Vu Ho ◽  
...  

Interaction between adult stem cells and their progeny is critical for tissue homeostasis and regeneration. In multiple organs, mesenchymal stem cells (MSCs) give rise to transit amplifying cells (TACs), which then differentiate into different cell types. However, whether and how MSCs interact with TACs remains unknown. Using the adult mouse incisor as a model, we present in vivo evidence that TACs and MSCs have distinct genetic programs and engage in reciprocal signaling cross talk to maintain tissue homeostasis. Specifically, an IGF-WNT signaling cascade is involved in the feedforward from MSCs to TACs. TACs are regulated by tissue-autonomous canonical WNT signaling and can feedback to MSCs and regulate MSC maintenance via Wnt5a/Ror2-mediated non-canonical WNT signaling. Collectively, these findings highlight the importance of coordinated bidirectional signaling interaction between MSCs and TACs in instructing mesenchymal tissue homeostasis, and the mechanisms identified here have important implications for MSC–TAC interaction in other organs.


2022 ◽  
Author(s):  
Jiaxin Gong ◽  
Niraj K. Nirala ◽  
Jiazhang Chen ◽  
Fei Wang ◽  
Pengyu Gu ◽  
...  

Adult stem cells are essential for maintaining normal tissue homeostasis and supporting tissue repair. Although genetic and biochemical programs controlling adult stem cell behavior have been extensively investigated, how mechanosensing regulates stem cells and tissue homeostasis is not well understood. Here, we show that shear stress can activate enteroendocrine cells, but not other gut epithelial cell types, to regulate intestine stem cell-mediated gut homeostasis. This shear stress sensing is mediated by transient receptor potential A1 (TrpA1), a Ca2+-permeable ion channel expressed only in enteroendocrine cells among all gut epithelial cells. Genetic depletion of TrpA1 or modification of its shear stress sensing function causes reduced intestine stem cell proliferation and intestine growth. We further show that among the TrpA1 splice variants, only select isoforms are activated by shear stress. Altogether, our results suggest the naturally occurring mechanical force such as fluid passing generated shear stress regulates intestinal stem cell-mediated tissue growth by activating enteroendocrine cells, and Drosophila TrpA1 as a new shear stress sensor.


2014 ◽  
Vol 31 ◽  
pp. 8-15 ◽  
Author(s):  
Peggy Janich ◽  
Qing-Jun Meng ◽  
Salvador Aznar Benitah

2011 ◽  
Vol 17 (4) ◽  
pp. 513-519 ◽  
Author(s):  
Hilda Amalia Pasolli

AbstractAdult stem cells (SCs) are essential for tissue homeostasis and wound repair. They have the ability to both self-renew and differentiate into multiple cell types. They often reside in specialized microenvironments or niches that preserve their proliferative and tissue regenerative capacity. The murine hair follicle (HF) has a specialized and permanent compartment—the bulge, which safely lodges SCs and provides the necessary molecular cues to regulate their function. The HF undergoes cyclic periods of destruction, regeneration, and rest, making it an excellent system to study SC biology.


2019 ◽  
Author(s):  
James R. Allen ◽  
James B. Skeath ◽  
Stephen L. Johnson

AbstractAdult stem cells (ASCs) contribute to long-term homeostasis and regeneration of many adult tissues. Some ASCs proliferate continuously, others remain quiescent awaiting activation. To identify pathways that regulate ASC quiescence and tissue homeostasis, we study melanocyte stem cells (MSCs) that drive vertebrate pigmentation. In larval zebrafish, MSCs are quiescent, but can be recruited to regenerate the larval pigment pattern following melanocyte ablation. Through pharmacological experiments, we found that inhibition of GABA-A receptor function, specifically the GABA-A rho subtype, induces excessive melanocyte production in larval zebrafish. Conversely, pharmacological activation of GABA-A inhibited melanocyte regeneration. We used CRISPR to generate two mutant alleles of gabrr1, a subtype of GABA-A. Both alleles exhibited robust melanocyte overproduction, while conditional overexpression of gabrr1 inhibited larval melanocyte regeneration. Our data suggest that gabrr1 signaling is necessary and sufficient to maintain MSC quiescence and prevent excessive pigmentation of the larval zebrafish.


2005 ◽  
Vol 53 (S 3) ◽  
Author(s):  
W Röll ◽  
T Hashemi ◽  
M Breitbach ◽  
O Dewald ◽  
A Welz ◽  
...  

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