scholarly journals Self‐Organization Principles of Cell Cycles and Gene Expressions in the Development of Cell Populations

2021 ◽  
pp. 2100005
Author(s):  
Xiaoliang Wang ◽  
Dongyun Bai
Author(s):  
T. G. Sarphie ◽  
C. R. Comer ◽  
D. J. Allen

Previous ultrastructural studies have characterized surface morphology during norma cell cycles in an attempt to associate specific changes with specific metabolic processes occurring within the cell. It is now known that during the synthetic ("S") stage of the cycle, when DNA and other nuclear components are synthesized, a cel undergoes a doubling in volume that is accompanied by an increase in surface area whereby its plasma membrane is elaborated into a variety of processes originally referred to as microvilli. In addition, changes in the normal distribution of glycoproteins and polysaccharides derived from cell surfaces have been reported as depreciating after cellular transformation by RNA or DNA viruses and have been associated with the state of growth, irregardless of the rate of proliferation. More specifically, examination of the surface carbohydrate content of synchronous KB cells were shown to be markedly reduced as the cell population approached division Comparison of hamster kidney fibroblasts inhibited by vinblastin sulfate while in metaphase with those not in metaphase demonstrated an appreciable decrease in surface carbohydrate in the former.


2016 ◽  
Vol 78 (11-3) ◽  
Author(s):  
Noor Hanis Abu Halim ◽  
Norashikin Zakaria ◽  
Badrul Hisham Yahaya

Purpose: This study was aimed to isolate the putative cancer stem cell (CSC) populations from A549 lung cancer cell line and to evaluate the difference of carcinogenesis-related genes expression within parental population (A549) and isolated CSC populations (A549 CD166+ /EpCAM+ and CD166+ /CD44+). Methods: We performed flow cytometry analysis to sort out cell positive for these markers; CD166+ /EpCAM + and CD166+ /CD44+ from A549 cancer cell line. The isolated cells were tested for multipotent capacities by clonogenic and differentiation assays. Quantitative real time PCR was performed for both isolated CSC population and parental population to test expression of ALDH1A1 and 6 other genes that known to contribute to carcinogenesis; RARβ CYP24A1, BIRC5, EDN1, IL1β and PTGS2. Result(s): Both CD166+ /EpCAM+ and CD166+ /CD44+ have ability to form colonies and able to differentiate into adipocytes and osteocyte. Expression of ALDH1A1 was downregulated in all three cell populations (parental A549, A549 CD166+ /EpCAM+ and A549 CD166+ /CD44+) whereas the other 6 carcinogenesis-related genes were upregulated in all three cancer cell populations. There are no significant differences of gene expressions were detected among all three populations (p > 0.05). Conclusion(s): Downregulation of ALDH1A1 in all three cancer populations up-regulate the expression of other 6 carcinogenesis-related genes. Gene regulations between parental cancer cell (A549) and both putative CSC populations show no significant difference suggesting the existence of various CSC subpopulations reside within parental A549 population


2017 ◽  
Vol 19 (11) ◽  
pp. 113024 ◽  
Author(s):  
Kaumudi H Prabhakara ◽  
Azam Gholami ◽  
Vladimir S Zykov ◽  
Eberhard Bodenschatz

2020 ◽  
Author(s):  
Jiayuan Zhong ◽  
Chongyin Han ◽  
Xuhang Zhang ◽  
Pei Chen ◽  
Rui Liu

AbstractCell fate commitment occurs during early embryonic development, that is, the embryonic differentiation sometimes undergoes a critical phase transition or “tipping point” of cell fate commitment, at which there is a drastic or qualitative shift of the cell populations. In this study, we presented a novel computational approach, the single-cell graph entropy (SGE), to explore the gene-gene associations among cell populations based on single-cell RNA sequencing (scRNA-seq) data. Specifically, by transforming the sparse and fluctuating gene expression data to the stable local network entropy, the SGE score quantitatively characterizes the criticality of gene regulatory networks among cell populations, and thus can be employed to predict the tipping point of cell fate or lineage commitment at the single cell level. The proposed SGE method was applied to five scRNA-seq datasets. For all these datasets of embryonic differentiation, SGE effectively captures the signal of the impending cell fate transitions, which cannot be detected by gene expressions. Some “dark” genes that are non-differential but sensitive to SGE values were revealed. The successful identification of critical transition for all five datasets demonstrates the effectiveness of our method in analyzing scRNA-seq data from a network perspective, and the potential of SGE to track the dynamics of cell differentiation.


2020 ◽  
Author(s):  
Pei Li ◽  
Ping Li ◽  
Yuanlin Liu ◽  
Weijiang Liu ◽  
Lanlan Zha ◽  
...  

AbstractRecently, many epidemiological and animal studies have indicated that obesity have their origin in the early stages of life including the inappropriate balance of some nutrients, the objective of this study is to determine the risk of obesity in male mice offspring as a consequence of maternal VD deficiency-mediated disordering of the immune response. Four-week-old C57BL/6J female mice were fed VD-deficient or normal reproductive diets during pregnancy and lactation. Their male offspring were weighted and euthanized after being fed control and high-fat diets (HFD) for 16 weeks starting at the weaning. The serum was collected for biochemical analyses. Epididymal (eWAT) and inguinal (iWAT) white adipose tissues were excised for histological examination, immunohistochemistry, gene expressions of inflammatory factors, and for determining the proportions of immune cells by flow cytometry. Insufficient maternal VD intake exacerbated the development of obesity both in non-obese and obese male offspring as evidenced by larger adipose cells and abnormal glucose and lipid metabolisms. Also, the expression of proinflammatory cytokine genes was increased and that of anti-inflammatory cytokines was decreased in maternal VD-deficient groups in the eWAT and/or iWAT. This was accompanied by higher levels of TNF-α or/and INF-β, and lower levels of IL-4 and IL-10. Insufficient maternal VD intake was also observed to induce a shift in the profiles of immune cells in the eWAT and/or iWAT, resulting in increased percentages of M1 macrophage, ATDCs, and CD4+ and CD8+ T cells, but caused a significant decrease in the percentage of M2 macrophages, both in non-obese and obese male offspring. All these changes in the immune cell profile were more obvious in the eWAT than in the iWAT. These results indicated that insufficient maternal VD intake promoted the development of obesity in male offspring by modulating the immune cell populations and causing a polarization in the adipose depots.ImportanceEvidence in this study has indicated that insufficient maternal VD intake promotes the development of obesity in the male offspring by modulating the recruitment of immune cell populations and their polarization as well as the expression and secretion of proinflammatory adipokines in the adipose depots in a weight-independent manner, which is more obvious in eWAT than that in the iWAT.


eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Sriram Varahan ◽  
Adhish Walvekar ◽  
Vaibhhav Sinha ◽  
Sandeep Krishna ◽  
Sunil Laxman

How phenotypically distinct states in isogenic cell populations appear and stably co-exist remains unresolved. We find that within a mature, clonal yeast colony developing in low glucose, cells arrange into metabolically disparate cell groups. Using this system, we model and experimentally identify metabolic constraints sufficient to drive such self-assembly. Beginning in a uniformly gluconeogenic state, cells exhibiting a contrary, high pentose phosphate pathway activity state, spontaneously appear and proliferate, in a spatially constrained manner. Gluconeogenic cells in the colony produce and provide a resource, which we identify as trehalose. Above threshold concentrations of external trehalose, cells switch to the new metabolic state and proliferate. A self-organized system establishes, where cells in this new state are sustained by trehalose consumption, which thereby restrains other cells in the trehalose producing, gluconeogenic state. Our work suggests simple physico-chemical principles that determine how isogenic cells spontaneously self-organize into structured assemblies in complimentary, specialized states.


2019 ◽  
Author(s):  
Sriram Varahan ◽  
Adhish Walvekar ◽  
Vaibhhav Sinha ◽  
Sandeep Krishna ◽  
Sunil Laxman

AbstractHow phenotypically distinct states in isogenic cell populations appear and stably co-exist remains an unresolved question. We find that within a clonal yeast colony developing in low glucose, cells arrange into metabolically disparate cell groups. Using this system, we model and experimentally identify metabolic constraints sufficient to drive such assembly. Beginning in a gluconeogenic state, cells in a contrary state, exhibiting high pentose phosphate pathway activity, spontaneously appear and proliferate, in a spatially constrained manner. The gluconeogenic cells in the developing colony produce a resource, which we identify as trehalose. At threshold concentrations of trehalose, cells in the new metabolic state emerge and proliferate. A self-organized system establishes, where cells in this new state are sustained by trehalose consumption, which thereby restrains other cells in the trehalose producing, gluconeogenic state. Our work suggests simple physico-chemical principles that determine how isogenic cells spontaneously self-organize into structured assemblies in complimentary, specialized states.


2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Xiaodong Mu ◽  
Daniel Brynien ◽  
Kurt R. Weiss

Osteosarcoma (OS) is the most common primary malignancy of bone and affects patients in the first two decades of life. The greatest determinant of survival is the presence of pulmonary metastatic disease. The role of epigenetic regulation in OS, specifically the biology of metastases, is unknown. Our previous study with the murine OS cell populations K7M2 and K12 demonstrated a significant correlation of metastatic potential with the DNA methylation level of tumor suppressor genes. In the current study, we investigated if the histone deacetylase (HDAC) inhibitor, vorinostat, could regulate the metastatic potential of highly metastatic OS cells. Our results revealed that vorinostat treatment of highly metastatic K7M2 OS cells was able to greatly reduce the proliferation and metastatic potential of the cells. Morphological features related to cell motility and invasion were changed by vorinostat treatment. In addition, the gene expressions of mTOR, ALDH1, and PGC-1 were downregulated by vorinostat treatment. These data suggest that vorinostat may be an effective modulator of OS cell metastatic potential and should be studied in preclinical models of metastatic OS.


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