Difference between revisions of "User:Z3376548"

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--[[User:Z3376548|Z3376548]] ([[User talk:Z3376548|talk]]) 15:06, 11 April 2013 (EST)
 
--[[User:Z3376548|Z3376548]] ([[User talk:Z3376548|talk]]) 15:06, 11 April 2013 (EST)
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--[[User:Z3376548|Z3376548]] ([[User talk:Z3376548|talk]]) 15:06, 18 April 2013 (EST)
  
 
==Individual Assessments==
 
==Individual Assessments==

Revision as of 15:07, 18 April 2013

Attendance

--Z3376548 (talk) 15:57, 14 March 2013 (EST)

I was in the lab on 21 March but forgot to mark myself off for this lab, have talked about the issue with Mark and got his consent.

--Z3376548 (talk) 15:14, 28 March 2013 (EST)

--Z3376548 (talk) 15:06, 11 April 2013 (EST)

--Z3376548 (talk) 15:06, 18 April 2013 (EST)

Individual Assessments

Lab 1

Transporters' differences in cells

Citation: Ren Q, Paulsen IT (2005) Comparative Analyses of Fundamental Differences in Membrane Transport Capabilities in Prokaryotes and Eukaryotes. PLoS Comput Biol 1(3): e27. doi:10.1371/journal.pcbi.0010027

Editor: Peer Bork, EMBL Heidelberg, Germany

Received: March 24, 2005; Accepted: July 8, 2005; Published: August 19, 2005

Copyright: © 2005 Ren and Paulsen. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Lab 2

1st task

PMID 16118665

<pubmed>16118665</pubmed>

[1]

2nd task

The researcher of the article "Biofilm Matrix Regulation by Candida albicans Zap1" found a specific gene ZAP 1 that controls the formation of biofilm from the organism called Candida albicans. They manipulate this gene in order to see how the production of biofilm changes. However, the researcher need to precisely observe the biomass or thickness of the biofilm and this could not be done by using the normal microscope. Therefore, they used confocal microscopy which contribute to this experiment process that it enables the 3D image of the biofilm to be observed thus helps the researcher to understand more about how the ZAP 1 gene regulate the appearance of the biofilm.

PMID 19529758

<pubmed>19529758</pubmed>

[2]


--Mark Hill (talk) 10:25, 11 April 2013 (EST) Referencing is formatted correctly, but not positioned correctly. The research article does also use CLSM in its findings, as you have described here.

Lab 3

1st task

Article 1: This article searches the roles of actin filaments (F-actin) and F-actin-based motors (myosins) which are required components of mitotic spindles. In their research, they found out that myosin-10 (Myo10) is important for assembly of meiotic spindles. In more detail, Myo10 set themselves to mitotic spindle poles and is very important for proper spindle anchoring, normal spindle length, spindle pole integrity as well as progression through metaphase. They also found out the antagonistic relationship between F-actin and Myo10 in maintenance of spindle length and that they work independently.[3] Actin filaments (F-actin) and F-actin-based motors (myosins) are essential components in the proper functioning of spindle apparatus. They are required for correct positioning of the spindle towards the anchor point.

<pubmed>18606852</pubmed>

Article 2: Their finding found out the function of the long-tailed class-1 myosin myosin-1C from Dictyostelium discoideum during mitosis. They use the data obtained as back up, suggested that myosin-1C binds to microtubules and play parts in maintenance of spindle stability during chromosome separation and that the association of myosin-1C with microtubules is mediated through the tail domain. Further data has leaded to another suggestion that myosin-1C tail can inhibit kinesin motor activity, strengthen the stability of microtubules as well as forming crosslinks between microtubules and F-actin. [4] Myosin-1C motor and tail-domain-mediated MT-F-actin are required for the relocalization of certain protein from the cell periphery to the spindle. Therefore, both contribute to the formation and stability of spindle apparatus in considerable amount.

<pubmed>21712373</pubmed>

Article 3: This article states thoroughly for the process of spindle assembly, spindle positioning and separation of the nascent spindle poles in relation to cortical dynein-based pulling on astral microtubules, and kinesin-based sliding of polar microtubules. They talked about the motors and microtubule binding proteins at kinetochores which provide attachment sites for microtubule to the chromosomes. They also states that there is a complicated mechanism that which perform pushing and pulling action to chromosomes that puts them in metaphase plate position. Kinetochore motors and microtubule binding proteins can also give signal to the cell cycle regulatory machinery for on time advance passing the cell cycle phrases. [5] Dynein-based pulling and kinesin-based sliding of microtubules is very important in spindle assembly and positioning. Motors and microtubule binding proteins will aid spindle for its function to separate sister chromatids.

<pubmed>21920311</pubmed>

Article 4: By combine the use of force-calibrated needles, high-resolution microscopy, and biochemical perturbations, the researcher analyze the vertebrate metaphase spindle and found that spindle viscosity is dependent on microtubule density and cross-linking. Spindle elasticity are said to be relating to kinetochore and non-kinetochore microtubule rigidity, and also to spindle pole organization by kinesin-5 and dynein. [6] The data obtain in their research provides micromechanics modal insight of this cytoskeletal architecture and provide insight into how structural and functional stability is maintained for proper control of spindle function.

<pubmed>21703450</pubmed>

2nd task

Knockdown of Myo10 leads to mitotic spindle defects

Description: The researcher use combination of Western blot and Confocal microscopy determine the cause of spindle defects has strong relation to Myo10 malfunction.

Citation: Sarah Woolner, Lori L O'Brien, Christiane Wiese, William M Bement Myosin-10 and actin filaments are essential for mitotic spindle function. J. Cell Biol.: 2008, 182(1);77-88 PMID:18606852

Copyright: Copyright © 2008 Woolner et al.

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jcb.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

Note - This image was originally uploaded as part of a student project and may contain inaccuracies in either description or acknowledgements. Please contact the site coordinator if the uploaded content does not meet the original copyright permission or requirements, for immediate removal.

Lab 4

http://www.pierce-antibodies.com/Catenin-beta-antibody-clone-6F9-Monoclonal--MA1300.html

Beta catenin takes partin in cell-cell communication and adhesion junction. Furthermore, beta Catenin can also activate a family of Lef/Tcf transcription factors which stimulate transcription of the genes that encode cyclin D and c-myc. Cyclin D and c-myc do the job to promote cell proliferation. Therefore, the protein is important for both cell adhesion as well as interacting with tumorgenesis.

The antibody, Catenin beta Antibody, is able to recognise and bind to this protein. Catenin beta Antibody, according to the data sheet, is raised in mouse and it can react against human as well as non-human primate. It is a monoclonal antibody. It can be used in Western Blot, Immunohistochemistry as well as Immunofluorescence.

References

  1. <pubmed>16118665</pubmed>
  2. <pubmed>19529758</pubmed>
  3. <pubmed>18606852</pubmed>
  4. <pubmed>21712373</pubmed>
  5. <pubmed>21920311</pubmed>
  6. <pubmed>21703450</pubmed>

links

First Lecture

SMH