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Microinjection of the active form of PKN inhibits cell division of the Xenopus embryo. (A) Effects of microinjection of the active form of PKN on cell division of Xenopus embryos. Control buffer, 0.75 ng per embryo of GST/PKN () or 4 ng per embryo of GST/PKN ()-K644E, was injected into one blastomere at the two-cell stage. Embryos were photographed 5 h after fertilization. Arrows indicate the position of injection. GST/PKN () and GST/PKN ()-K644E are indicated as PKN and PKN(KN), respectively. (B) Dose dependency of the active form of PKN for cleavage arrest of Xenopus embryos. The indicated amounts of GST/PKN () were microinjected as in A. A typical result of three independent experiments is shown.
 
Microinjection of the active form of PKN inhibits cell division of the Xenopus embryo. (A) Effects of microinjection of the active form of PKN on cell division of Xenopus embryos. Control buffer, 0.75 ng per embryo of GST/PKN () or 4 ng per embryo of GST/PKN ()-K644E, was injected into one blastomere at the two-cell stage. Embryos were photographed 5 h after fertilization. Arrows indicate the position of injection. GST/PKN () and GST/PKN ()-K644E are indicated as PKN and PKN(KN), respectively. (B) Dose dependency of the active form of PKN for cleavage arrest of Xenopus embryos. The indicated amounts of GST/PKN () were microinjected as in A. A typical result of three independent experiments is shown.
  

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Lab attendance

--Z3331321 (talk) 15:54, 14 March 2013 (EST)


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Individual Assessments

Lab 1

Tubular Structures in Cells.jpg

Tubular structures found in tissues and cultures. Naturally occurring and stress induced tubular structures from mammalian cells, a survival mechanism Yonnie Wu, Richard C Laughlin, David C Henry, Darryl E Krueger, JoAn S Hudson, Cheng-Yi Kuan, Jian He, Jason Reppert, Jeffrey P Tomkins BMC Cell Biology 2007, 8:36 (16 August 2007) © 2007 Wu et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Lab 2

[1] <pubmed>16971509</pubmed>

The aim of the experiment in this research article was to demonstrate the fundamental role of the membrane-bound metalloproteinase MT1-MMP catalyst in preparing collagen fibrils for phagocytic degradation of collagen in adult tissues. Confocal laser microscopy has been utilized in this experiment to show that human fibroblasts do in fact initiate degradation of collagen through the collagenase activity of the membrane-bound metalloproteinase MT1-MMP. And examination of the collagen degradation under a confocal microscope revealed that cell surface MT1-MMP was in fact associated with degrading collagen fibrils therefore satisyfing the aim of the experiment.

Lab 3

Extracellular Regulation of Cell Division

[2] <pubmed>2259205</pubmed> This article puts forward a model that hypothesizes that extracellular regulation of cell division and differentiation acts through only two communication channels. They consist of a “series of redundant components: extracellular messenger hormones; these hormones' receptors; cytoplasmic proteins activated by the hormone-receptor complex; and trans-activating nuclear regulatory proteins.” The channels in this model are labeled as such: "D" ("differentiate"), includes transforming growth factor-beta as one of its hormones; the other, labeled "G'" ("growth") includes epidermal growth factor. The article uses a cell type in an adult mammal capable of either division or differentiation, which in this case is a stem cell from an epithelium. The principal prediction of this hypothesis is that when appropriate experimental conditions are implemented the addition of various ratios of D- and G-class growth factors will lead to different consequences.


[3] <pubmed>11134534</pubmed> Protein phosphorylation/dephosphorylation reaction is an important factor in the regulation of cell division. Entry into mitosis in dividing eukaryotic cells is controlled by the M phase-promoting factor. Cdc2 protein kinase and cyclin B are the main constituents of this factor and acts by phosphorylating substrates that are essential for the completion of mitotic processes. This article explores the effects of PKN in the control of mitotic timing by inhibition of Cdc25C on Xenopus egg extracts. The results of this experiment suggest that PKN does in fact efficiently phosphorylate Cdc25C in vitro, demonstrating that PKN directly inhibits Cdc25C activity by phosphorylation. The results also showed that microinjections of the active form of PKN inhibit cell division of the Xenopus Embryo, therefore having an effect on the regulation of cell division.


[4] <pubmed>20133808</pubmed> This article focuses on the morphogenesis of plant cells. According to this article a fundamental factor of regulation of cell shape and division in plants are the mechanics of cell expansion. (Not sure if relevant to this assignment…)


[5] <pubmed>11134534</pubmed> This article also focuses on plant cell division. (Not sure if relevant)


Microinjection of active PKN.jpg

Microinjection of the active form of PKN inhibits cell division of the Xenopus embryo. (A) Effects of microinjection of the active form of PKN on cell division of Xenopus embryos. Control buffer, 0.75 ng per embryo of GST/PKN () or 4 ng per embryo of GST/PKN ()-K644E, was injected into one blastomere at the two-cell stage. Embryos were photographed 5 h after fertilization. Arrows indicate the position of injection. GST/PKN () and GST/PKN ()-K644E are indicated as PKN and PKN(KN), respectively. (B) Dose dependency of the active form of PKN for cleavage arrest of Xenopus embryos. The indicated amounts of GST/PKN () were microinjected as in A. A typical result of three independent experiments is shown.

Reference

[6] <pubmed>11134534</pubmed>

Copyright

Copyright © 2001, The National Academy of Sciences

  1. <pubmed>16971509</pubmed>
  2. <pubmed>2259205</pubmed>
  3. <pubmed>11134534</pubmed>
  4. <pubmed>20133808</pubmed>
  5. <pubmed>11134534</pubmed>
  6. <pubmed>11134534</pubmed>