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Lab Attendance:

--Z3375878 (talk) 15:54, 14 March 2013 (EST)

--Z3375878 (talk) 15:31, 21 March 2013 (EST)

--Z3375878 (talk) 15:11, 28 March 2013 (EST)

--Z3375878 (talk) 15:09, 11 April 2013 (EST)

--Z3375878 (talk) 15:19, 18 April 2013 (EST)

--Z3375878 (talk) 15:07, 2 May 2013 (EST)




Red White Blood cells 01.jpg

They're cells maaaaaaan! Checkit!


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  • Three

Individual Assessments

Lab 1

Bacterial beta barrel OMP.jpg

Planar lipid bilayer experiments revealed that the evolutionarily conserved assembly factor Omp85 recognizes the signature motif present at the C termini of bacterial OMPs. doi:10.1371/journal.pbio.0040399.g001

Hoff M (2006) Picking the Right Parts at the Beta Barrel Factory. PLoS Biol 4(11): e399. doi:10.1371/journal.pbio.0040399

© 2006 Public Library of Science. 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


Lab 1 image[1]

Intravital observation of Plasmodium berghei sporozoite infection of the liver.[2]

In this study, confocal laser scanning microscopy was used to determine the location of green fluorescent protein (GFP) in the sinusoidal endothelia of a mouse which had been infected with green fluorescent Plasmodium berghei Sporozoites. This research was carried out in order to seek to understand more about the Plasmodium sporozite invasion of hepatic cells, known from secondary observations to pass through Kupffer cells; therefore the aim was to directly observe the process of infection. Confocal laser scanning microscopy allowed for a view of the internal microscopic structure of the mice livers who were then examined for the presence of the GFP-expressing sporozites.

--Mark Hill (talk) 13:59, 11 April 2013 (EST) References are formatted correctly. The research article does use CLSM (Immunofluorescence-labeled frozen liver sections were examined with a Zeiss LSM 510 laser scanning microscope) that is critical to the papers findings and you have explained correctly here. I prefer the reference to sit within the paragraph, as you would see in a research article or your project page, rather than within the heading, I have not penalised you for this.

Lab 3

- If the chromosome tips are damaged during anaphase then cytokinesis cannot occur[3] and therefore the cell cannot divide into two daughter cells, not sure if this is in relation to both mitosis and meiosis but should be interesting to further research. The experimental removal of chromosomal tips shows cell division being delayed, the furrow itself being delayed or even regressing from its ready to divide state.

- Anaphase-Promoting-Complex mutants of C. elegans demonstrate defects in germline proliferation, the development of the female vulva and male tail and the metaphase to anaphase transition in meiosis I. Therefore irregularities in the APC contribute to physical deformities in this species[4].

- The Anaphase-Promoting-Complex has many important roles in the development, function and survival of the nervous system[5]. Incorrect ACP activity leads to some neurological and psychiatric disorders. Research into the APC's role in neurobiology may grant us ways to use the APC to manage neurological disorders such as mental retardation and autism to even neurodegenerative disorders.

- When the chromosomes do not separate properly in Anaphase, referred to as "nondisjunction" aneuploidy results[6]. This refers to an abnormal number of chromosomes. A well known one is Trisomy 21 or Down's syndrome in which there are three copies of the 21st chromosome[7].

- Anaphase bridges can cause mutations such as the structural rearrangement of chromosomes which usually lead to the formation of isochromosomes (chromosomes which, after losing one of their arms are replaced with a copy of another arm) and whole-arm translocations, the loss of the entire chromosome through mitotic spindle detachment or faulty cytokinesis in which the failure to divide results in polyploidy (more than 2 copies of a chromosome) and additional centrosomes which may lead to multipolar spindle formations in future mitosis[8]. The presence of chromatin bridges in Anaphase is also linked to chromosomal instability which may contribute to cancer[9].

Lab 4

[Rabbit N Cadherin polyclonal antibody manufacturer website]

Name: N Cadherin Antibody, CD325, CDHN, CDw325, NCAD, N-cadherin 1; cadherin 2, N-cadherin (neuronal); cadherin-2; calcium-dependent adhesion protein, neuronal; neural cadherin; neural-cadherin

Type of antibody: Polyclonal

Type of Immunoglobulin: IgG

Species grown in: Rabbit

Species recognized: Xenopus laevis (Xl) Human (Hu) Mouse (Ms) Rat (Rt)

Applications: immunoprecipitation, immunofluorescence, immunohistochemistry (paraffin, frozen), Western blot, and flow cytometry

Paper: A potential role for N-cadherin in mediating endothelial cell-smooth muscle cell interactions in the rat vasculature[10]

Lab 5

- Hand in

Lab 6

Phenotypic changes in overexpressing Tm4 B35 cells.jpg

Group A: Tm4 overexpressing Group B: Control

Questions: 1. Do you see any change in the phenotypes between group A and group B?

According to my results in the counting exercise I do notice a shift between the phenotypes. Group A (the Tm4 overexpressing group) are mostly pronged, with a circa 7% increase in percentage and a 10% increase in stringed phenotypes. There is a large drop of around 15% in the stumped phenotype while group B (the control) have roughly equal numbers of stumped and pronged, with 15% less stringed phenotypes and small increases in the percentages of both broken fans and pygnotic types. There is also a little decrease in the presence of fans.

2. If you see a difference, speculate about a potential molecular mechanism that has lead to this change, if you don't see a change, speculate why that could be.

Tropomyosin (of which there are >40 isoforms) are proteins associated with Actin whose function it is to strengthen and stabilise filaments, they are one of the important binding proteins whom influence Actin structure. I propose that since each type of Tropomyosin is intended for different purposes in the body then maybe some sort of stress stimulated a shifting of Tropomyosin types. A possible molecular mechanism could be that since there is a shift towards pronged/stringed phenotypes, then Troponin 4 act as a cytoplasmic/membrane stabiliser for Actin in B35 cells allowing for longer chains of Actin to be be formed and in turn demonstrating the phenotypic change. The cytoplasm/membrane extends, even forming fibrils because of longer Actin chains resulting from greater numbers of Actin monomers polymerising, made possible due to its newfound stability from Tropomyosin 4.


  1. <pubmed>20076495</pubmed>
  2. <pubmed>15901208</pubmed>
  3. <pubmed>20811641</pubmed>
  4. <pubmed>12620985</pubmed>
  5. <pubmed>21439392</pubmed>
  6. <pubmed>18369452</pubmed>
  7. <pubmed>15262983</pubmed>
  8. <pubmed>16082199</pubmed>
  9. <pubmed>15156327</pubmed>
  10. <pubmed>8350598</pubmed>