scholarly journals Highlight on fusing multiple chromosomes in yeast into a single chromosome

2019 ◽  
Author(s):  
Wenfa Ng
Keyword(s):  
Cell Viability ◽  
Genetic Information ◽  
Significant Loss ◽  
Cell Physiology ◽  
Chromosome Research ◽  
Single Chromosome ◽  
Biochemical Processes ◽  
Cellular Physiology ◽  
Physiology And Biochemistry ◽  
Chromosome Level

Multiple biological mysteries remain in the definition and organization of genetic information into different chromosomes. Up to now, genome architecture at the chromosome level remain enigmatic concerning the reasons why evolution and natural selection arranged genetic information in separate segments in eukaryotic cells as compared to the single chromosome in the prokaryotic world. Specifically, one important unresolved question has been the role of chromosomes in cellular physiology and biochemical processes. By deleting the centromere and telomere regions of different chromosomes in Saccharomyces cerevisiae and fusing the different chromosomes into one chromosome, research reported by Shao and coworkers in Nature revealed the technical possibility of concatenating all genetic information into one segment. Furthermore, cell viability assays revealed that there was no significant loss of cell viability after the fusing of 16 chromosomes into a single chromosome. This highlighted that centromere and telomere sequences were not critical to overall cellular function, physiology and biochemistry. More importantly, the results highlighted that genetic information and its organisation at the sub-chromosome level play a more important role in defining cellular biochemical processes and physiology such as metabolism and cell division processes. Collectively, the technical feasibility of fusing multiple chromosomes into a single chromosome has been shown in new research that deleted the centromere and telomere regions of different chromosomes for fusing the resulting genetic information into a single chromosome. Little loss of viability and function in cells with a single chromosome and the stability of replicating the chromosome revealed that centromere and telomere sequences may not play critical roles in defining cellular physiology and biochemistry. More importantly, genomic information and its regulation was shown indirectly to have a more direct influence on cell physiology and metabolism than chromosomal architecture.

scholarly journals Highlight on fusing multiple chromosomes in yeast into a single chromosome

2019 ◽  
Author(s):  
Wenfa Ng
Keyword(s):  
Cell Viability ◽  
Genetic Information ◽  
Significant Loss ◽  
Cell Physiology ◽  
Chromosome Research ◽  
Single Chromosome ◽  
Biochemical Processes ◽  
Cellular Physiology ◽  
Physiology And Biochemistry ◽  
Chromosome Level

Multiple biological mysteries remain in the definition and organization of genetic information into different chromosomes. Up to now, genome architecture at the chromosome level remain enigmatic concerning the reasons why evolution and natural selection arranged genetic information in separate segments in eukaryotic cells as compared to the single chromosome in the prokaryotic world. Specifically, one important unresolved question has been the role of chromosomes in cellular physiology and biochemical processes. By deleting the centromere and telomere regions of different chromosomes in Saccharomyces cerevisiae and fusing the different chromosomes into one chromosome, research reported by Shao and coworkers in Nature revealed the technical possibility of concatenating all genetic information into one segment. Furthermore, cell viability assays revealed that there was no significant loss of cell viability after the fusing of 16 chromosomes into a single chromosome. This highlighted that centromere and telomere sequences were not critical to overall cellular function, physiology and biochemistry. More importantly, the results highlighted that genetic information and its organisation at the sub-chromosome level play a more important role in defining cellular biochemical processes and physiology such as metabolism and cell division processes. Collectively, the technical feasibility of fusing multiple chromosomes into a single chromosome has been shown in new research that deleted the centromere and telomere regions of different chromosomes for fusing the resulting genetic information into a single chromosome. Little loss of viability and function in cells with a single chromosome and the stability of replicating the chromosome revealed that centromere and telomere sequences may not play critical roles in defining cellular physiology and biochemistry. More importantly, genomic information and its regulation was shown indirectly to have a more direct influence on cell physiology and metabolism than chromosomal architecture.

scholarly journals The Gut Microbiota and Human Health with an Emphasis on the Use of Microencapsulated Bacterial Cells

2011 ◽  
Vol 2011 ◽  
pp. 1-12 ◽  
Author(s):  
Satya Prakash ◽  
Catherine Tomaro-Duchesneau ◽  
Shyamali Saha ◽  
Arielle Cantor
Keyword(s):  
Gastrointestinal Tract ◽  
Gut Microbiota ◽  
Cell Viability ◽  
Crucial Role ◽  
Bacterial Population ◽  
Significant Loss ◽  
Bacterial Cells ◽  
Lower Gastrointestinal Tract ◽  
Viable Cells ◽  
Harsh Conditions

The gut microbiota plays a crucial role in maintaining health. Alterations of the gut bacterial population have been associated with a number of diseases. Past and recent studies suggest that one can positively modify the contents of the gut microbiota by introducing prebiotics, probiotics, synbiotics, and other therapeutics. This paper focuses on probiotic modulation of the gut microbiota by their delivery to the lower gastrointestinal tract (GIT). There are numerous obstacles to overcome before microorganisms can be utilized as therapeutics. One important limitation is the delivery of viable cells to the lower GIT without a significant loss of cell viability and metabolic features through the harsh conditions of the upper GIT. Microencapsulation has been shown to overcome this, with various types of microcapsules available for resolving this limitation. This paper discusses the gut microbiota and its role in disease, with a focus on microencapsulated probiotics and their potentials and limitations.

scholarly journals Micropatterned Macrophage Analysis Reveals Global Cytoskeleton Constraints Induced by Bacillus anthracis Edema Toxin

2015 ◽  
Vol 83 (8) ◽  
pp. 3114-3125 ◽  
Author(s):  
Yannick Trescos ◽  
Emilie Tessier ◽  
Clémence Rougeaux ◽  
Pierre L. Goossens ◽  
Jean-Nicolas Tournier
Keyword(s):  
Bacillus Anthracis ◽  
Immune Cells ◽  
Adherens Junction ◽  
Peritoneal Macrophages ◽  
Cell Physiology ◽  
Actin Reorganization ◽  
Content Type ◽  
Cellular Physiology ◽  
Edema Toxin ◽  
Polar Organization

Bacillus anthracissecretes the edema toxin (ET) that disrupts the cellular physiology of endothelial and immune cells, ultimately affecting the adherens junction integrity of blood vessels that in turn leads to edema. The effects of ET on the cytoskeleton, which is critical in cell physiology, have not been described thus far on macrophages. In this study, we have developed different adhesive micropatterned surfaces (L and crossbow) to control the shape of bone marrow-derived macrophages (BMDMs) and primary peritoneal macrophages. We found that macrophage F-actin cytoskeleton adopts a specific polar organization slightly different from classical human HeLa cells on the micropatterns. Moreover, ET induced a major quantitative reorganization of F-actin within 16 h with a collapse at the nonadhesive side of BMDMs along the nucleus. There was an increase in size and deformation into a kidney-like shape, followed by a decrease in size that correlates with a global cellular collapse. The collapse of F-actin was correlated with a release of focal adhesion on the patterns and decreased cell size. Finally, the cell nucleus was affected by actin reorganization. By using this technology, we could describe many previously unknown macrophage cellular dysfunctions induced by ET. This novel tool could be used to analyze more broadly the effects of toxins and other virulence factors that target the cytoskeleton.

Can Genetic Instability Be Studied at the Single Chromosome Level in Cancer Cells?

1999 ◽  
Vol 109 (1) ◽  
pp. 51-57 ◽  
Author(s):  
Sanjay A Pai ◽  
Mie-Chi P Cheung ◽  
Marvin M Romsdahl ◽  
Asha S Multani ◽  
Sen Pathak
Keyword(s):  
Cancer Cells ◽  
Genetic Instability ◽  
Single Chromosome ◽  
Chromosome Level

scholarly journals Who's really in control: microbial regulation of protein trafficking in the epithelium

2014 ◽  
Vol 306 (3) ◽  
pp. C187-C197 ◽  
Author(s):  
Matthew R. Hendricks ◽  
Jennifer M. Bomberger
Keyword(s):  
Epithelial Cell ◽  
Protein Trafficking ◽  
Host Cells ◽  
Eukaryotic Cells ◽  
Cell Physiology ◽  
Cellular Physiology ◽  
Cellular Processes ◽  
Complex Interactions ◽  
Host Pathogen ◽  
Host Tissues

Due to evolutionary pressure, there are many complex interactions at the interface between pathogens and eukaryotic host cells wherein host cells attempt to clear invading microorganisms and pathogens counter these mechanisms to colonize and invade host tissues. One striking observation from studies focused on this interface is that pathogens have multiple mechanisms to modulate and disrupt normal cellular physiology to establish replication niches and avoid clearance. The precision by which pathogens exert their effects on host cells makes them excellent tools to answer questions about cell physiology of eukaryotic cells. Furthermore, an understanding of these mechanisms at the host-pathogen interface will benefit our understanding of how pathogens cause disease. In this review, we describe a few examples of how pathogens disrupt normal cellular physiology and protein trafficking at epithelial cell barriers to underscore how pathogens modulate cellular processes to cause disease and how this knowledge has been utilized to learn about cellular physiology.

scholarly journals Titration of SF3B1 Activity Reveals Distinct Effects on the Transcriptome and Cell Physiology

2020 ◽  
Vol 21 (24) ◽  
pp. 9641
Author(s):  
Karen S. Kim Guisbert ◽  
Isiah Mossiah ◽  
Eric Guisbert
Keyword(s):  
Gene Expression ◽  
Protein Folding ◽  
Mrna Splicing ◽  
Differential Sensitivity ◽  
Cell Physiology ◽  
Nonsense Mediated Decay ◽  
Cellular Physiology ◽  
Pladienolide B ◽  
Expression Pathways ◽  
Different Levels

SF3B1 is a core component of the U2 spliceosome that is frequently mutated in cancer. We have previously shown that titrating the activity of SF3B1, using the inhibitor pladienolide B (PB), affects distinct steps of the heat shock response (HSR). Here, we identify other genes that are sensitive to different levels of SF3B1 (5 vs. 100 nM PB) using RNA sequencing. Significant changes to mRNA splicing were identified at both low PB and high PB concentrations. Changes in expression were also identified in the absence of alternative splicing, suggesting that SF3B1 influences other gene expression pathways. Surprisingly, gene expression changes identified in low PB are not predictive of changes in high PB. Specific pathways were identified with differential sensitivity to PB concentration, including nonsense-mediated decay and protein-folding homeostasis, both of which were validated using independent reporter constructs. Strikingly, cells exposed to low PB displayed enhanced protein-folding capacity relative to untreated cells. These data reveal that the transcriptome is exquisitely sensitive to SF3B1 and suggests that the activity of SF3B1 is finely regulated to coordinate mRNA splicing, gene expression and cellular physiology.

Biochemical topology: From vectorial metabolism to morphogenesis

1991 ◽  
Vol 11 (6) ◽  
pp. 347-385 ◽  
Author(s):  
Franklin M. Harold
Keyword(s):  
Living Cells ◽  
Energy Transduction ◽  
Self Organization ◽  
Cellular Space ◽  
Biochemical Processes ◽  
Cellular Physiology ◽  
Cytoplasmic Transport ◽  
Fungal Hyphae ◽  
Vectorial Metabolism ◽  
Point Of Departure

In living cells, many biochemical processes are spatially organized: they have a location, and often a direction, in cellular space. In the hands of Peter Mitchell and Jennifer Moyle, the chemiosmotic formulation of this principle proved to be the key to understanding biological energy transduction and related aspects of cellular physiology. For H. E. Huxley and A. F. Huxley, it provided the basis for unravelling the mechanism of muscle contraction; and vectorial biochemistry continues to reverberate through research on cytoplasmic transport, motility and organization. The spatial deployment of biochemical processes serves here as a point of departure for an inquiry into morphogenesis and self-organization during the apical growth of fungal hyphae.

scholarly journals Differential Cytotoxicity of Different Sizes of Graphene Oxide Nanoparticles in Leydig (TM3) and Sertoli (TM4) Cells

Nanomaterials ◽  
2019 ◽  
Vol 9 (2) ◽  
pp. 139 ◽  
Author(s):  
Sangiliyandi Gurunathan ◽  
Min-Hee Kang ◽  
Muniyandi Jeyaraj ◽  
Jin-Hoi Kim
Keyword(s):  
Graphene Oxide ◽  
Cell Viability ◽  
Graphene Nanosheets ◽  
Critical Factor ◽  
Biological Properties ◽  
Significant Loss ◽  
Toxic Effects ◽  
Biological Behavior ◽  
Ros Generation ◽  
Size Dependent

Graphene oxide (GO) is an common nanomaterial and has attracted unlimited interest in academia and industry due to its physical, chemical, and biological properties, as well as for its tremendous potential in applications in various fields, including nanomedicine. Whereas studies have evaluated the size-dependent cytotoxicity of GO in cancer cells, there have been no studies on the biological behavior of ultra-small graphene nanosheets in germ cells. To investigate, for the first time, the cyto- and geno- toxic effects of different sizes of GO in two different cell types, Leydig (TM3) and Sertoli (TM4) cells, we synthesized different sized GO nanosheets with an average size of 100 and 20 nm by a modification of Hummers’ method, and characterized them by various analytical techniques. Cell viability and proliferation assays showed significant size- and dose-dependent toxicity with GO-20 and GO-100. Interestingly, GO-20 induced significant loss of cell viability and cell proliferation, higher levels of leakage of lactate dehydrogenase (LDH) and reactive oxygen species (ROS) generation compared to GO-100. Both GO-100 and GO-20 induced significant loss of mitochondrial membrane potential (MMP) in TM3 and TM4 cells, which is a critical factor for ROS generation. Furthermore, GO-100 and GO-20 caused oxidative damage to DNA by increasing the levels of 8-oxo-dG, which is formed by direct attack of ROS on DNA; GO-100 and GO-20 upregulate various genes responsible for DNA damage and apoptosis. We found that phosphorylation levels of EGFR/AKT signaling molecules, which are related to cell survival and apoptosis, were significantly altered after GO-100 and GO-20 exposure. Our results showed that GO-20 has more potent toxic effects than GO-100, and that the loss of MMP and apoptosis are the main toxicity responses to GO-100 and GO-20 treatments, which likely occur due to EGFR/AKT pathway regulation. Collectively, our results suggest that both GO-100 and GO-20 exhibit size-dependent germ cell toxicity in male somatic cells, particularly TM3 cells, which seem to be more sensitive compared to TM4, which strongly suggests that applications of GO in commercial products must be carefully evaluated.

scholarly journals This Is a Title in Title Case: Prediction of CML Evolution By Telomere Length Analysis at the Single-Chromosome Level

Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. 2937-2937
Author(s):  
Jingyuan Lu ◽  
Yingxing Zhou ◽  
Xiaomei Yan ◽  
Quanyi Lu
Keyword(s):  
Cell Division ◽  
Telomere Length ◽  
Conflicts Of Interest ◽  
Critical Length ◽  
M Cell ◽  
Single Chromosome ◽  
Healthy Donors ◽  
Fluorescent Peptide ◽  
Length Analysis ◽  
Chromosome Level

Telomeresplay a vital role in DNA repair activities and protecting chromosomes from degradation[1]. Telomeres are shortened during each cell division because of the end replication problem. After several cell division, telomeres are shortened to a critical length (< 3 kb), and eventually lead to overall genomic instability and triggering the DNA damage response[2-3], which is related to the cancerization of numerous cancers. The commonly used method to estimate telomere length isterminal restriction fragment (TRF) basedon southern blot, which requires thousands of cells and provides only a crude estimate of the average telomere length of all cells analyzed. However, it is believed that the frequency of critically short telomeres, rather than the mean telomere length, is a crucial factor for telomere dysfunction. Therefore, analysis of telomere length at the single-chromosome level is necessary to determine the frequency of critically short telomeres. Here, we describe the development of a high-throughput method for telomere length analysis at the single-chromosome level by using a laboratory-built high-sensitivity flow cytometer (HSFCM)[4] combined with targeted fluorescent peptide nucleic acid (PNA) probes. The unambiguous detection of the telomere signalsfrom a single chromosome was achieved via HSFCM analysis. The fluorescence intensity of single chromosome was converted to the probe number by a calibration curve, and was further transformed to the base pair number of the telomere. Five representative cell lines were analyzed to compare their telomere length and the ratio of critically short telomeres at the single-chromosome level. The potential of using frequency of short telomere for disease treatment monitoring is examined by analyzing the telomere length in lymphocyte of leukemia patients. The abundance of short telomeres was compared between healthy donors and patients with chronic myeloid leukemia (CML) to see whether it can be used to predict the efficacy of therapeutics. Moreover, the quantity of short telomeres was compared among patients with acute leukemia, patients in different phases of CML and healthy donors to see whether it can be used as a marker for disease progression prediction in CML. Reference [1] Blackburn E. H., Epel E. S., Lin J., Science,2015, 350, 1193-1198. [2]Collado M., Blasco M. A., Serrano M., Cell, 2007, 130, 223-233. [3] Deng Y., Chan S. S., Chang S., Nat. Rev. Cancer, 2008, 8, 450-458. [4] Yang LL, Zhu SB, Hang W, Wu LN, Yan XM, Anal. Chem., 2009, 81, 2555-2563. Figure 1 Disclosures No relevant conflicts of interest to declare.

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