Control of nerve cell formation from multipotent stem cells in Hydra

1979 ◽  
Vol 40 (1) ◽  
pp. 193-205 ◽  
Author(s):  
S. Berking

Feeding of starved animals provides a very short signal which determines stem cells to differentiate into nerve cells after the next mitosis. Only those stem cells become determined which are just in the middle of their S-phase at the time of feeding. Stem cells of any other stage of the cycle do not become determined. Nerve cell determination is suppressed by very low concentrations of an endogenous inhibitor. The inhibitor exerts its effect only during the first half of the S-phase, not before and not after this period. Based on these finding it is proposed that stem cells are susceptible to 2 different signals during the first half of their S-phase; one signal allows the development into nerve cells, the other prevents this development. Within this period the decision whether to become a nerve cell or not is reversible. It becomes fixed at the end of this period.

Development ◽  
2001 ◽  
Vol 128 (20) ◽  
pp. 4093-4101 ◽  
Author(s):  
Paul Badenhorst

Neurons and glia are often derived from common multipotent stem cells. In Drosophila, neural identity appears to be the default fate of these precursors. Stem cells that generate either neurons or glia transiently express neural stem cell-specific markers. Further development as glia requires the activation of glial-specific regulators. However, this must be accompanied by simultaneous repression of the alternate neural fate. I show that the Drosophila transcriptional repressor Tramtrack is a key repressor of neuronal fates. It is expressed at high levels in all mature glia of the embryonic central nervous system. Analysis of the temporal profile of Tramtrack expression in glia shows that it follows that of existing glial markers. When expressed ectopically before neural stem cell formation, Tramtrack represses the neural stem cell-specific genes asense and deadpan. Surprisingly, Tramtrack protein levels oscillate in a cell cycle-dependent manner in proliferating glia, with expression dropping before replication, but re-initiating after S phase. Overexpression of Tramtrack blocks glial development by inhibiting S-phase and repressing expression of the S-phase cyclin, cyclin E. Conversely, in tramtrack mutant embryos, glia are disrupted and undergo additional rounds of replication. I propose that Tramtrack ensures stable mature glial identity by both repressing neuroblast-specific genes and controlling glial cell proliferation.


Development ◽  
1980 ◽  
Vol 60 (1) ◽  
pp. 373-387
Author(s):  
Stefan Berking

Budding in Hydra starts as an evagination of the double-layered tissue in the parent animal's gastric region. Five hours later the density of nerve cells in the bud's tissue doubles, representing the first detectable difference from the cellular composition of the surrounding tissue. These new nerve cells derive from multipotent stem cells which are in S-phase one day before evagination starts. Some of the bud's new nerve cells derive from stem cells which have migrated into the future bud's tissue after their commitment, apparently attracted by the bud anlage. The bud anlage recruits precursors of nerve cells even during starvation, during which nerve cell production ceases in other parts of the body. Furthermore, the bud anlage controls the duration of the development from commitment to final differentiation of the resulting nerve cells. Experiments with an inhibitor purified from hydra tissue indicate a tight correlation between stages of preparatory bud development and stages of recruitment of nerve cells for the bud. Whether or not precursors of nerve cells are involved in the control of bud formation in normal hydra, as compared to epithelial hydra which still bud though consisting of epithelial cells only, will be discussed.


RSC Advances ◽  
2016 ◽  
Vol 6 (12) ◽  
pp. 10159-10161 ◽  
Author(s):  
Zhe-Zhen Yu ◽  
Qing-Hua Wu ◽  
Shang-Li Zhang ◽  
Jun-Ying Miao ◽  
Bao- Xiang Zhao ◽  
...  

We identified two amino acid-coated magnetic nanoparticles that promoted mesenchymal stem cell growth without the need for transfection agents by increasing the proportion of cells in the S phase.


2020 ◽  
Author(s):  
Rui-Fang Li ◽  
Guo-Xing Nan ◽  
Dan Wang ◽  
Chang Gao ◽  
Juan Yang ◽  
...  

Abstract Background : The effects of Simian virus 40 T antigen (SV40T) on various kinds of cells are different. Previous researchers failed to use SV40T immortalized nerve cells. However, they argued that SV40T caused nerve cell transformation. No one further study what is the specific effect of SV40T on nerve cells. We transfected Schwann cells (SCs) that did not have differentiation ability with MPH 86 plasmid containing SV40T in order to explore the effects of SV40T on Schwann cells. Methods: SCs were transfected with MPH 86 plasmid carrying the SV40T gene and cultured in different media, as well as co-cultured with neural stem cells (NSCs). In our study, SCs overexpressing SV40T were defined as SV40T-SCs. The proliferation of these cells was detected by WST-1, and the expression of different biomarkers was analyzed by qPCR and immunohistochemistry. Results: SV40T induced the characteristics of NSCs, such as the ability to grow in suspension, form spheroid colonies and proliferate rapidly, in the SCs, which were reversed by knocking out SV40T by the Flip-adenovirus . In addition, SV40T up-regulated the neurocrest markers Nestin, Pax3 and Slug, and down-regulated S100b as well as the late differentiation markers MBP, GFAP and Olig1/2. These cells also expressed NSC markers like Nestin, SOX2, CD133 and SSEA-1, as well as early development markers of embryonic stem cells (ESCs) like BMP4, C-myc, OCT4 and Gbx2. Co-culturing with NSCs induced differentiation of the SV40T-SCs into neuronal and glial cells. Conclusions: SV40T reprograms Schwann cells to stem-like cells at the stage of neural crest cells that can differentiate to terminal nerve cells. Background : The effects of Simian virus 40 T antigen (SV40T) on various kinds of cells are different. Previous researchers failed to use SV40T immortalized nerve cells. However, they argued that SV40T caused nerve cell transformation. No one further study what is the specific effect of SV40T on nerve cells.


Development ◽  
1990 ◽  
Vol 109 (4) ◽  
pp. 897-904 ◽  
Author(s):  
E. Hobmayer ◽  
T.W. Holstein ◽  
C.N. David

Differentiation of sensory nerve cells in tentacles of Hydra magnipapillata was investigated using the monoclonal antibody NV1. NV1+ sensory nerve cells form specific complexes with battery cells in tentacles. NV1+ cells can only be formed by differentiation from interstitial cell precursors. These precursors complete a terminal cell cycle in the distal gastric region at the base of tentacles; differentiation from the S/G2 boundary to expression of the NV1 antigen requires 30h. During this time, precursors move from the distal gastric region into the tentacles, differentiate to morphologically fully formed nerve cells and then begin expressing NV1 antigen. The neuropeptide head activator stimulates NV1+ differentiation in S-phase of the precursor's cell cycle.


2021 ◽  
Vol 22 (5) ◽  
pp. 2472
Author(s):  
Carl Randall Harrell ◽  
Valentin Djonov ◽  
Vladislav Volarevic

Mesenchymal stem cells (MSCs) are self-renewable, rapidly proliferating, multipotent stem cells which reside in almost all post-natal tissues. MSCs possess potent immunoregulatory properties and, in juxtacrine and paracrine manner, modulate phenotype and function of all immune cells that participate in tissue repair and regeneration. Additionally, MSCs produce various pro-angiogenic factors and promote neo-vascularization in healing tissues, contributing to their enhanced repair and regeneration. In this review article, we summarized current knowledge about molecular mechanisms that regulate the crosstalk between MSCs and immune cells in tissue repair and regeneration.


2020 ◽  
Vol 11 ◽  
Author(s):  
Courtney B. Johnson ◽  
Jizhou Zhang ◽  
Daniel Lucas

Hematopoiesis in the bone marrow (BM) is the primary source of immune cells. Hematopoiesis is regulated by a diverse cellular microenvironment that supports stepwise differentiation of multipotent stem cells and progenitors into mature blood cells. Blood cell production is not static and the bone marrow has evolved to sense and respond to infection by rapidly generating immune cells that are quickly released into the circulation to replenish those that are consumed in the periphery. Unfortunately, infection also has deleterious effects injuring hematopoietic stem cells (HSC), inefficient hematopoiesis, and remodeling and destruction of the microenvironment. Despite its central role in immunity, the role of the microenvironment in the response to infection has not been systematically investigated. Here we summarize the key experimental evidence demonstrating a critical role of the bone marrow microenvironment in orchestrating the bone marrow response to infection and discuss areas of future research.


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