scholarly journals Differential cell fates of muscle stem cells are accompanied by symmetric segregation of canonical H3 histones in vivo

2018 ◽  
Author(s):  
Brendan Evano ◽  
Gilles Le Carrou ◽  
Geneviève Almouzni ◽  
Shahragim Tajbakhsh
Keyword(s):  
Stem Cells ◽  
Ex Vivo ◽  
Germline Stem Cells ◽  
Cell Fates ◽  
Evolutionary Mechanisms ◽  
Mouse Muscle ◽  
Muscle Stem Cells ◽  
Histone H3 Variant ◽  
Cell Assays

AbstractStem cells are maintained through symmetric or asymmetric cell divisions. While various mechanisms initiate asymmetric cell fates during mitosis, possible epigenetic control of this process has emerged recently. The asymmetrical distribution of a canonical histone H3 variant during mitosis in fly germline has suggested a role for partitioning old and new nucleosomes in asymmetric cell fates. Here, we provide resources for single cell assays and show the asymmetric segregation of transcription factors along with old and new DNA in mouse muscle stem cells ex vivo and in vivo. However, these differential fate outcomes contrast with a symmetric distribution of the canonical H3.1 vertebrate variant. These findings point to different evolutionary mechanisms operating in fly germline stem cells and vertebrate somatic stem cells to mitigate epigenetic regulation of asymmetric cell fates.

scholarly journals In vivo gene editing in dystrophic mouse muscle and muscle stem cells

Science ◽  
2015 ◽  
Vol 351 (6271) ◽  
pp. 407-411 ◽  
Author(s):  
M. Tabebordbar ◽  
K. Zhu ◽  
J. K. W. Cheng ◽  
W. L. Chew ◽  
J. J. Widrick ◽  
...  
Keyword(s):  
Stem Cells ◽  
Gene Editing ◽  
Mouse Muscle ◽  
Muscle Stem Cells ◽  
Dystrophic Mouse

scholarly journals Tubastatin A maintains adult skeletal muscle stem cells in a quiescent state ex vivo and improves their engraftment ability in vivo

2022 ◽  
Vol 17 (1) ◽  
pp. 82-95
Author(s):  
Marina Arjona ◽  
Armon Goshayeshi ◽  
Cristina Rodriguez-Mateo ◽  
Jamie O. Brett ◽  
Pieter Both ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Stem Cells ◽  
Ex Vivo ◽  
Quiescent State ◽  
Adult Skeletal Muscle ◽  
Muscle Stem Cells ◽  
Skeletal Muscle Stem Cells

scholarly journals Ex Vivo Expansion and In Vivo Self-Renewal of Human Muscle Stem Cells

2015 ◽  
Vol 5 (4) ◽  
pp. 621-632 ◽  
Author(s):  
Gregory W. Charville ◽  
Tom H. Cheung ◽  
Bryan Yoo ◽  
Pauline J. Santos ◽  
Gordon K. Lee ◽  
...  
Keyword(s):  
Stem Cells ◽  
Ex Vivo ◽  
Ex Vivo Expansion ◽  
Human Muscle ◽  
Self Renewal ◽  
Muscle Stem Cells

scholarly journals Asymmetric histone inheritance regulates stem cell fate in Drosophila midgut

2020 ◽  
Author(s):  
Emily Zion ◽  
Xin Chen
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Cell Fate ◽  
Biological Significance ◽  
Cell Lineage ◽  
Germline Stem Cells ◽  
Cell Fates ◽  
Stem Cell Fate ◽  
Distinct Cell

AbstractA fundamental question in developmental biology is how distinct cell fates are established and maintained through epigenetic mechanisms in multicellular organisms. Here, we report that preexisting (old) and newly synthesized (new) histones H3 and H4 are asymmetrically inherited by the distinct daughter cells during asymmetric division of Drosophila intestinal stem cells (ISCs). By contrast, in symmetrically dividing ISCs that produce two self-renewed stem cells, old and new H3 and H4 show symmetric inheritance patterns. These results indicate that asymmetric histone inheritance is tightly associated with the distinct daughter cell fates. To further understand the biological significance of this asymmetry, we express a mutant histone that compromises asymmetric histone inheritance pattern. We find increased symmetric ISC division and ISC tumors during aging under this condition. Together, our results demonstrate that asymmetric histone inheritance is important for establishing distinct cell identities in a somatic stem cell lineage, consistent with previous findings in asymmetrically dividing male germline stem cells in Drosophila. Therefore, this work sheds light on the principles of histone inheritance in regulating stem cell fate in vivo.

Strategies to Protect Hematopoietic Stem Cells from Culture-Induced Stress Conditions

2020 ◽  
Vol 15 ◽  
Author(s):  
Fatima Aerts-Kaya
Keyword(s):  
Stem Cells ◽  
Hematopoietic Stem Cells ◽  
Ex Vivo ◽  
Stress Conditions ◽  
Stress Factors ◽  
Hematopoietic Stem ◽  
Induced Stress

: In contrast to their almost unlimited potential for expansion in vivo and despite years of dedicated research and optimization of expansion protocols, the expansion of Hematopoietic Stem Cells (HSCs) in vitro remains remarkably limited. Increased understanding of the mechanisms that are involved in maintenance, expansion and differentiation of HSCs will enable the development of better protocols for expansion of HSCs. This will allow procurement of HSCs with long-term engraftment potential and a better understanding of the effects of the external influences in and on the hematopoietic niche that may affect HSC function. During collection and culture of HSCs, the cells are exposed to suboptimal conditions that may induce different levels of stress and ultimately affect their self-renewal, differentiation and long-term engraftment potential. Some of these stress factors include normoxia, oxidative stress, extra-physiologic oxygen shock/stress (EPHOSS), endoplasmic reticulum (ER) stress, replicative stress, and stress related to DNA damage. Coping with these stress factors may help reduce the negative effects of cell culture on HSC potential, provide a better understanding of the true impact of certain treatments in the absence of confounding stress factors. This may facilitate the development of better ex vivo expansion protocols of HSCs with long-term engraftment potential without induction of stem cell exhaustion by cellular senescence or loss of cell viability. This review summarizes some of available strategies that may be used to protect HSCs from culture-induced stress conditions.

scholarly journals Dynamic integration of enteric neural stem cells in ex vivo organotypic colon cultures

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Georgina Navoly ◽  
Conor J. McCann
Keyword(s):  
Stem Cells ◽  
Neural Stem Cells ◽  
Organotypic Culture ◽  
Ex Vivo ◽  
Donor Cell ◽  
Colonic Tissue ◽  
Cell Therapies ◽  
Enteric Ganglia ◽  
Donor Cells

AbstractEnteric neural stem cells (ENSC) have been identified as a possible treatment for enteric neuropathies. After in vivo transplantation, ENSC and their derivatives have been shown to engraft within colonic tissue, migrate and populate endogenous ganglia, and functionally integrate with the enteric nervous system. However, the mechanisms underlying the integration of donor ENSC, in recipient tissues, remain unclear. Therefore, we aimed to examine ENSC integration using an adapted ex vivo organotypic culture system. Donor ENSC were obtained from Wnt1cre/+;R26RYFP/YFP mice allowing specific labelling, selection and fate-mapping of cells. YFP+ neurospheres were transplanted to C57BL6/J (6–8-week-old) colonic tissue and maintained in organotypic culture for up to 21 days. We analysed and quantified donor cell integration within recipient tissues at 7, 14 and 21 days, along with assessing the structural and molecular consequences of ENSC integration. We found that organotypically cultured tissues were well preserved up to 21-days in ex vivo culture, which allowed for assessment of donor cell integration after transplantation. Donor ENSC-derived cells integrated across the colonic wall in a dynamic fashion, across a three-week period. Following transplantation, donor cells displayed two integrative patterns; longitudinal migration and medial invasion which allowed donor cells to populate colonic tissue. Moreover, significant remodelling of the intestinal ECM and musculature occurred upon transplantation, to facilitate donor cell integration within endogenous enteric ganglia. These results provide critical evidence on the timescale and mechanisms, which regulate donor ENSC integration, within recipient gut tissue, which are important considerations in the future clinical translation of stem cell therapies for enteric disease.

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