From CellBiology

--Z3289558 15:13, 8 March 2012 (EST)

Lab Attendance (lab 1)

--Z3289558 15:29, 8 March 2012 (EST)


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Internal Link

Lab Two




Question 1.

Reference: <pubmed>21144999</pubmed>

Question 2.

Chemical synapses occur over pre and post synaptic terminals. Many proteins have been identified to facilitate the signal transmission over these terminals, most notably, those that anchor signalling molecules and neurotransmitter receptors. However, Proteomic studies suggest several hundred proteins may exist within the junction. Electron microscopy images have only enabled a small selection of these proteins to be identified. The introduction of 3D multicolour superresolution microscopy has allowed the detection of many more protein constituents localised within the chemical synapses of the brain. Dani et al. (2010), were not only able to observe the protein composition, but utilised the technology to further examine the morphological structure of such synapses.

Lab 3

--Z3289558 14:10, 22 March 2012 (EST) --Z3289558 10:25, 26 March 2012 (EST)

Homework Sources

1. <pubmed>11176375</pubmed> This article is a good source for an integrated history of testosterone.

2. <pubmed>12017541</pubmed> This article investigates the hormonal regulation of spermatogenesis and identifys testosterone as an essential component.

3. <pubmed>1425487</pubmed> This source provides a detailed explanation of the gene expression mechanisms of steriod hormones such as testosterone. This information can integrated with our knowledge of testosterone's hormonal regulation in spermatogenesis.

4.<pubmed>22421515</pubmed> This article provides a broad overview of the effects of testosterone deficiency and the pathological effects it has on the body.

Formalin (Formaldehyde)

Physical Properties

Appearance: Clear liquid

Odour: pungent odour.

Boiling Point: ~ 96 °C @ 760 mm Hg

Vapour Pressure: None Available.

Specific Gravity:1.1

Flash Point:64 - 85 °C

Lower Explosive Limits:7%

Upper Explosive Limits: 73%

Solubility in Water: Miscible

pH: 2.8-4.0


Hazard Category: Harmful, Corrosive

Swallowed: Toxic if swallowed. Will cause burns to the mouth, mucous membranes, throat, oesophagus and stomach. If sufficient quantities are ingested (swallowed) death may occur. The methanol stabilizer in solutions is a cause of visual impairment and possible permanent blindness.

Eye:Will cause burns to the eyes with effects including: Pain, tearing, conjunctivitis and if duration of exposure is long enough, blindness will occur.

Skin:Toxic by skin contact. Will cause burns to the skin, with effects including; Redness, blistering, localised pain and dermatitis. The material is capable of causing allergic skin reactions and may cause skin sensitisation. Toxic effects may result from skin absorption..

Inhaled:Toxic if inhaled. Will cause severe irritation to the nose, throat and respiratory system with effects including: Dizziness, headache, incoordination, chest pains, coughing, respiratory paralysis and or failure.

Chronic:Some long term animal test data suggests a carcinogenic potential for the formaldehyde contained in these solutions. This was found to occur at levels which caused chronic tissue irritation, and was well above the exposure standard. These particular data are not considered relevant to normal use because these high concentrations would not be voluntarily tolerated by humans, but do emphasise the need for care in handling. Chronic exposure to methanolfrom skin contact, inhalation and/or swallowing, at concentrations greater than 1000ppm can result in permanent blindness and central nervous system effects.

Formaldehyde: Reported fatal dose for hgumans: 60-90 mL Oral LD50 (rat): 800 mg/kg Inhalation LC50 (rat): 590 mg/m3

Methanol: Oral LD50 (rat): 5628 mg/kg Inhalation LC50 (rat): 64000 mg/kg / 4 hrs Repeated or prolonged exposure to methanol could result in visual impairment and central nervous system effects.

Lab 4

--Z3289558 14:02, 29 March 2012 (EST) --Z3289558 15:35, 29 March 2012 (EST)


Reference: <pubmed>22429745</pubmed> UniProt Data Base(Musashi)

Musashi is a conserved family of RNA-binding proteins identified in 1998. It is most commonly expressed in stem cells within the nervous system. Two mammalian homolog proteins have been identified. RNA-binding protein Musashi homolog 1 has been completly sequenced and contains 362 amino acids. It has been detected in fetal kidney, brain, liver and lung, and in adult brain and pancreas tissues. The protein regulates the expression of target mRNAs at a translation level, and has a role in the proliferation and maintenance of stem cells in the central nervous system.

Anti-Musashi-1 Monoclonal Antibody from eBIOSCIENCE INC, is a primary antibody specific for Musashi-1 proteins. This monoclonal antibody is derived from rats. Reactive species to this antibody include Humans, mice and rats. The isotype of this antibody is IgG2a and can be used at a concentration less than or equal to 10 μg/ml. Reported applications include Immunohistochemical Staining of Formalin-Fixed Paraffin Embedded Tissue Sections, Immunocytochemistry and Western Blotting. Anti-Musashi-1 Antibody information

Secondary Anti-rat IgG Information Alexa Fluor® 488 Goat Anti-Rat IgG can be used as a secondary antibody against Anti-Musashi-1 Monoclonal Antibody from eBIOSCIENCE INC.

Lab 5

--Z3289558 16:35, 5 April 2012 (EST)

Lab 6

--Z3289558 14:06, 19 April 2012 (EST)



A)Do you see a difference in the phenotype (morphology) between Tm4 overexpressing and control cells?

When comparing the cells in group A(Tm4 overexpressing neuroepithelial cells) to those in B (Control neuroepithelial cells), it is evident that they can be phenotypically distinguished from each other. The cells in group A characteristically exhibited longer cell extensions that were thinner and showed more branching than those in group B. This phenotypic difference is reflected statistically in the above graph. The most prevalent phenotypes in group A were stumped (27%), pronged (25%) and stringed phenotype (24%). Whereas those in group B commonly presented as stumped (30&), pronged (22%), and broken fan (20%). The increased incidence of the stumped phenotype in both groups may be a reflection of a classification bias brought on by inexperience in defining each phenotype.

B) If so, how could Tm4 overexpression lead to this difference?

The protein Tropomyosin binds to actin polymers and is a fundamental component of actin microfilaments(1). Therefore, the phenotypic alterations between those in group A and B is a reflection of this interaction between the Tm4 isoform and the actin filaments of the B35 neuroepithelial cells. Tm4 has been identified to be localised primarily in the growth cone of neurons(2). Furthermore, studies have implicated tropomyosins as stabilisers of the actin cytoskeleton(3,4). The suggested mechanism of action is shielding the microfilaments from both cleavage by gelosolin(3) or depolymerisation by ADF/ cofilin(4). Therefore, through regulation of the organisation of actin filaments, overexpression of Tm4 in B35 cells would lead to increased actin filaments and consequently, increased budding of processes/elongation of existing processes. This is consistent with the phenotypic observations reported above.

Part 2:

A)Induced differentiation of the cells can also be seen to have an effect on the phenotype of both the overexpressed Tm4 and control cells. Overall there can be seen an increase in the incidence of the “stringed” phenotype. Before induction with db cAMP, the “stringed” phenotype was rare in group B cells. Furthermore, the induced cells from group A exhibited significantly more branching when compared to the induced group B cells. There is also evidence of increased filopodia and growth cone size and the induced group A cells.

B) If so, how could Tm4 overexpression lead to this difference?

The main distinguishable phenotype between the induced cells in group A and B is the level of branching, whereas both groups illustrated longer processes characteristic of the “stringed” phenotype. Therefore, it can be concluded that the branching of neurites in cAMP induced cells is differentially controlled by Tm4. The mechanism by which Tm4 manipulates branching is unclear, however due to its association with actin filaments it can be hypothesised that an increase in Tm4 leads to an increase in Actin and therefore branching of the neurites. This branching correlates with our current knowledge suggesting that Tm4 is localized in the growth cones of neurons(2).


1. Phillips, G. N., et al. (1979). Crystal structure and molecular interactions of tropomyosin. Nature 278, 413–417

2. Had, L., Faivre-Sarrailh, C., Legrand, C., Mery, J., Brugidou, J., and Rabie, A. (1994). Tropomyosin isoforms in rat neurons: the different developmental profiles and distributions of TM-4 and TMBr-3 are consistent with different functions. J. Cell Sci. 107, 2961–2973

3. Ishikawa, R., Yamashiro, S., and Matsumura, F. (1989). Differential modulation of actin-severing activity of gelsolin by multiple isoforms of cultured rat cell tropomyosin. Potentiation of protective ability of tropomyosins by 83-kDa nonmuscle caldesmon. J. Biol. Chem. 264, 7490–7497

4. Bernstein, B. W., and Bamburg, J. R. (1982). Tropomyosin binding to F-actin protects the F-actin from disassembly by brain actin-depolymerizing factor (ADF). Cell Motil.

Lab 7

--Z3289558 14:15, 26 April 2012 (EST)

Homework: In addition to the work posted below, I have continually contributed to the disscussion page and set up the reference formatting for our project thus far.


1767 John Hunter performed the first intention testicular transplantation, however physiological effects were not studied as he was more interested in the techniques of tissue transplantation. [1]
1849 Arnold Berthold postulated that the physiological and behavioural changes of castration were due to a substance secreted by the testes, and further determined that this substance must interact with the body through transmission in the blood stream. [1]
1889 Charles Edouard Brown-Séquard prepared a solution of testicular extracts that he subcutaneously injected. After 3 weeks he reported an increase in strength and a decrease in memory loss, insomnia and other signs of aging. This extract become known as “the elixir of life”, and although other scientists were sceptical of its effects, this research promoted much more experimentation within the field of orgnotherapy. [2]
1902 William Bayliss and Ernest Starling recovered an extract from duodenal mucosa which they named secretin. They observed secretins physiological effect and postulated that the extract was a blood borne chemical messenger which acted on a target tissue to elicit the observed effect. William B. Hardy later proposed the term hormone for these chemical messages and in 1905 the name was first published in an article submitted by Starling in the lancet. [1]
1929 Adolf Butenandt isolated estrone-the first pure sex hormone, followed by androstenone. In 1934 Leopold Ruzicka synthesized androstenone. The work by Butenandt and Ruzicka not only proved that hormones could be isolated, but that they could be synthesized and therefore easily implemented in modern medicine. [1]
1935 Kàroly Gyula David, E. Dingemanse, J. Freud and Ernst Laqueur first isolated and named Tesosterone and published a paper titled: “On Crystalline Male Hormone from Testicles (Testosterone),” [3]. Later in that year, Adolf Butenandt synthesized testosterone and published “A Method for Preparing Testosterone from Cholesterol”. A week after Butenandts paper was published Ruzicka and A. Wettstein published their own article describing the synthesis of testosterone and therefore, in 1939 both Ruzicka and Butenandt were offered the Nobel prize for chemistry. Butenandt however, was forced to decline the award due to the Nazi government. [1]
1944 Heller and Myers report that the symptoms of Andropause (male climacteric) may be reversed by treatment with testosterone. [4]
1948 First clinical studies suggesting testosterone replacement therapy can be used as an effective antidepressant. [5]
1951 Charles D Kochakian published “Recent Studies on the Vivo and in Vitro Effect of Hormones on Enzymes” indentifying androgens as stimulators of the protein anabolic processes. Following the publication of this article, many scientists have looked into the use of androgen therapy to restore protein and stimulate growth in patients suffering from a number of diseases. [6]
1950’s Anabolic steroids such as testosterone become widely used by athletes to increase muscle mass. [7]
1960 Invention of the Radioimmunoassay allowed researches to efficiently measure the endogenous levels of testosterone. Shortly after this, methods were developed to measure testosterone through saliva samples. Saliva radioimmunoassays made research on humans simpler by avoiding blood assays for testosterone. [8]
1990’s Effective routes of administering testosterone alternative to injection are developed. These methods include patches, gels and buccal systems. [9]
1993 Morley reports that Testosterone replacement therapy in older men (over a short trial period) decreases cholesterol and increases hematocrit and muscle strength. [10]
1994 Department of Medicine at Columbia University reported that low levels of free testosterone correlate directly with an increased incidence of coronary artery disease. They also identified low testosterone and a risk factor for hypotension and obesity. [11]

Current Research

Since testosterones isolation in 1935[12], it has been the subject of many scientific studies. Consequently, numerous clinical uses of testosterone have been identified.

Testosterone is administered clinically via testosterone replacement therapy, which aims to increase the level of “free” testosterone in the blood. The most reported use of this therapy is for treatment of hypogonadism; a condition in which the body’s concentration of testosterone is severely reduced[13].Testosterone replacement therapy in hypogonadal men has been associated with increased: bone density, muscle strength, mood elevation, sexual function, and some aspects of cognitive function.[10]

As implied above, testosterone is a promoter of protein restoration and tissue growth[14]. This principle has been utilised in testosterone based treatments of “wasting conditions” such as HIV, in which participants show an increase is lean body mass prior to treatment.[15]

Testosterones ability to increase bone density has also made it a suitable tool for treatment of osteoporosis. The mechanism by which testosterone achieves this is by slowing down bone reabsorption, rather than increasing bone formation.[16]

A study conducted at Rockerfeller University in New York determined that testosterone is actively involved in reducing the neuronal secretion of beta-amyloid peptides[17]. Alzheimer’s disease is caused by the deposition of beta-amyloid peptides in susceptible brain regions. Treatment of Alzheimers patients with testosterone has been shown to successfully increase spatial memory, constructional abilities and verbal memory.[18]

Still need to elaborate on testosterone treatment of:



1970’s used as a male contraception through inhibition via feedback mechanisms Cardiovascular disease- reduces cholesterol


  1. 1.0 1.1 1.2 1.3 1.4 <pubmed>11176375</pubmed>
  2. <pubmed> 21434249 </pubmed>
  3. David KG., Dingemanse E, Freud J. Laqueur E (May 1935). "Über krystallinisches mannliches Hormon aus Hoden (Testosteron) wirksamer als aus harn oder aus Cholesterin bereitetes Androsteron [On crystalline male hormone from testicles (testosterone) effective as from urine or from cholesterol]" (in German). Hoppe Seylers Z Physiol Chem 233 (5–6): 281. doi:10.1515/bchm2.1935.233.5-6.281.
  4. Heller CG, Myers GB. The male climacteric: its symptomatology, diagnosis and treatment. The Journal of the American Medical Association: 1944, 126;472-477.doi:10.1001/jama.1944.02850430006003
  5. Snyder, PJ. Clinical use of Androgens. Annual Review of Medicine:1984,35:207-17.
  6. <pubmed>14903797</pubmed>
  7. Hoberman, Y. The History of Synthetic Testosterone. Scientific American Magazine:1995,76-81
  8. <pubmed>3581474</pubmed>
  9. Kanayama, G., Amiaz, R., Seidman, S., Pope, HG. Testosterone Supplementation for Depressed Men: Current Research and Suggested Treatment Guidelines. Experimental and Clinical Psychopharmacology:2007, 15(6), 529-538.
  10. 10.0 10.1 <pubmed>8426037</pubmed>
  11. <pubmed>11545281</pubmed>
  12. David KG., Dingemanse E, Freud J. Laqueur E (May 1935). "Über krystallinisches mannliches Hormon aus Hoden (Testosteron) wirksamer als aus harn oder aus Cholesterin bereitetes Androsteron [On crystalline male hormone from testicles (testosterone) effective as from urine or from cholesterol]" (in German). Hoppe Seylers Z Physiol Chem 233 (5–6): 281. doi:10.1515/bchm2.1935.233.5-6.281.
  13. <pubmed>6777395</pubmed>
  14. <pubmed>14903797</pubmed>
  15. <pubmed>12409050</pubmed>
  16. <pubmed>8833211</pubmed>
  17. <pubmed>10655508</pubmed>
  18. <pubmed>15985573 </pubmed>
  19. <pubmed>22265242 </pubmed>
  20. <pubmed>18772488</pubmed>

Lab 8

Tissue Culture

1. NCTC clone 929 (L cell, L-929, derivative of Strain L) ATCC Catalogue

2. Organism: Mus musculus (House Mouse) Tissue of origin: subcutaneous connective tissue; areolar and adipose

3. Isolation date: March, 1948. [1]


  1. <pubmed>18105872</pubmed>

Lab 9

Group 2

  • Good use of images, I like the clear descriptions used to describe what processes are occurring.
  • History section is a bit vague. Is there a more specific date for the discovery of tumor-secreted protein that potently increased microvascular permeability to plasma proteins other than late 1970’s? Or if it was a collection of works maybe reference some of those.
  • Hormone section in regular function looks incomplete, but I would prefer brief descriptions of how each hormone induces VEGF production. Citations also need to be included for the oncogenesis section.
  • The table used in the signalling pathway is good as it provides a clear summary of the role of each receptor. However the subheadings below do not provide much more info. I suspect VEGFR-3 may be incomplete but if it is not I think more information is needed here. Also the references for VEGF receptors 1 and 2 are not present. Also i think this section could be supplemented with information about the regulation of this pathway for a more thorough representation of knowledge in this field.
  • The abnormal function section is very extensive and the pictures make it very engaging.
  • Images are referenced correctly but I believe there are too many Wikipedia references, also as of yet there is no student drawn image
  • Format is good and engaging.

Group 3

  • The introduction is set out very well. I can tell that the person writing it has understood the information and therefore they convey it in a manner which is understandable to those unfamiliar with apoptosis. I am impressed that you justified why certain aspects of apoptosis were excluded and it helps me understand the final information presented in your project. This section however lacks citations and towards the end you can tell it is still being edited due to the brackets.
  • History section provides knowledge that is evenly represented throughout the decades. However, as there is only one reference at the bottom I can see that extensive research has not been done into possible discoveries that were not mentioned in the paper. I would also prefer to see references to the original papers where possible rather than to this one review. Also a table would make this section more engaging to the reader.
  • The signalling pathway section is good, it is well written but it would be easier to understand if some terms were linked to the glossary section and images would be useful in helper the reader understand the complex processes described in this section. Also, I can see this section has been cited but not in the wiki format required for this project.
  • Function section was detailed however I think more information should be included in regards to the role of extrinsic apoptosis rather than caspases. Formatting this section would help readers understand the complex information. Instead of uses dashes you could use dot points (formatted by the* key if you are unsure how to generate them).
  • The current research section is very interesting however the work in cardiovascular disease still needs expanding. Also referencing needs to be formatted according to the wiki format.
  • Overall I feel more information should be included, even though you justified what you were not including in the introduction. Perhaps you could include a section looking at Regulation? Or include more information about implication in disease, as I did like what you provided in the current research section. Also as of yet there is no student drawn image.

Group 4

  • Introduction is well written but very brief. Perhaps you could mention that it is a signalling pathway important in cell to cell communication here and expand on that a bit and provide a picture (such as the structure of the ligand binding region on the NOTCH receptor) to make it more appealing to the reader.
  • I like the formatting of the history section. The use of a coloured table makes it very attractive to the reader. However the information in this section is very brief and does not provide a thorough representation across the decades since its discovery. You could provide information on current research like you have at the end of your assignment as it will indicate what is currently being done in this field.
  • An image could help readers understand the pathway section, however the information presented here is well written and synthesised nicely.
  • I really enjoyed both the Proteins and receptors and Normal functions sections. The information was well written and the subheadings helped unclutter the information. However there were no references for the Proteins and Receptors section. Also the image in the protein and receptors section does not have the copyright info pasted in, just a reference.
  • The future research section could be improved a brief description of what is being investigated in each study mentioned.
  • The external links were very helpful and I enjoyed your video. Additionally, a student drawn image still needs to be uploaded. One group provided external links in the text to the definitions of the words listed in the glossary, you could use this idea also. Finally, you still need to add the title of your page.

Group 5

  • I really like the picture at the top of the project, makes me interested in the topic.
  • Intro was good as there was a good selection of relevant background information only. I also liked the justifications for what was going to be discussed in the project.
  • History was detailed and drew information from a wide variety of sources. And the picture made the section interesting.
  • There was extremely thorough work in the mechanism of action section which is evident in the referencing of this section as they cover a wide range of sources. Your understanding of the topic in this section is excellent and the inclusion of the external link to the movie was nice.
  • Disease section was also well written. The information was summarised nicely and the two pictures complement the information presented.
  • The embryonic development section was very interesting and overall you covered a wide variety of subtopics which was nice.
  • I appreciated that the project had a style that was consistent throughout even though it was edited by different people. Only improvements I could suggest are including a student drawn image and providing internal links in the text to the terms listed in the glossary. Also you may want to check you are formatting your references correctly so they don’t double up. References 73 and 74 are the same.

Overall, very good project.

Group 6

  • Introduction was very informative but I’m not sure if all the information provided should be placed under the introduction heading. Especially the information provided about the signalling pathway as it is addressed later on. Also there is only one reference provided for this entire section.
  • The inclusion of the structure of insulin was a nice touch and it was very well described however there is no copyright information for the picture provided.
  • The history section provided a good coverage of the decades and I especially liked the use of external links in this section.
  • The insulin receptor image was very good as it was simple yet informative and drawn by a student? However, it isn’t very clear why you introduce both a beta and alpha subunit yet only continue on to describe the beta subunit. Perhaps you could add a sentence justifying the exclusion of the alpha subunit or the inclusion of more detail for the beta subunit.
  • Signalling pathway, abnormal and normal function sections are very good. I like that you broke them up into subheadings. In the Abnormal function section, it is clear that very extensive research was done, however the signalling pathway picture does not have copyright information provided.
  • The current research section was very well organised however, if they have websites, it might be nice to add external links to the Wilson Research Institute and the Mediterranean Research Centre. Also the glossary section needs expanding

Good work.

Group 7

  • The title is a bit complicated. Maybe you could simplify it like it is on the web page to just G-protein (Beta adrenergic). Also the introduction contains too much information, although all well written. This information can be supplemented elsewhere nicely. A brief summary would be better in this section. Also the references should be integrated throughout the text not just listed at the end.
  • History section is very good. A picture or table may make it more appealing to the reader.
  • The subheadings of you project all reflected very interesting insight into your topic. I liked the description of the genes and I especially liked the colour used for the receptor agonists section.
  • The justification at the beginning of the receptor structure section was good and the pictures in this section were well referenced and helped me understand the complicated information presented in the text.
  • The pathway/normal function section was very detailed and you could tell the writer had a comprehensive understanding of what they were presenting. I was very impressed with the student drawn images in this section. However, I think the regulatory mechanisms could have their own subheading just to break the information up a bit.
  • The abnormal function section was very impressive and elaborate. I am glad you provided a summary table to supplement the text which illustrates that extensive research has been done.
  • The glossary is very good, as are the references however check 7 and 8 as they are just websites.

Group 8

  • Introduction presents a nice summary of relevant information however it is not referenced.
  • History section has not been completed yet
  • The pathway section is very nicely summarised although references are missing. I also like the use of the picture to supplement the text however I’m not sure if this is the student drawn image or if it just lacks referencing.
  • Normal function section is very informative however it needs to be proof read because there are some small grammatical errors, e.g be instead of by. Also the references need to be formatted in the correct wiki format. I do however like the use of subheadings in this section.
  • The abnormal function section is very informative however the layout should be uniform throughout. LAD 2 and 3 are followed by symptom and treatment subheadings but LAD 1 is only supplemented by a symptoms subheading even though the treatment information is there.
  • Protein section is good. It might be better to name what the four families are in the introductory sentence and then progress with the subheadings but it is not vital.
  • New or current research is not done yet. However you can use this section as an opportunity to introduce some external links into your project.
  • The referencing of the pictures is excellent. However there seems to be a problem with reference number 5.

Group 9

  • Pathway section has some small grammatical errors but is otherwise informative.
  • The receptor and protein sections still need doing
  • The history section is very well done. I like the layout and colours used. Also the references show extensive research.
  • What is under current research is a good start. More information about other studies would improve this section.
  • Normal Function section is also very well researched and well worded. Perhaps you could put this section into a table though to break up the information a bit and make it easier to read.
  • Abnormal function section also needs expanding and to be written in own words rather than a quote. Also the formatting of the references for this section needs to be fixed. However the image in this section compliments it nicely.
  • Dont forget to include a student drawn image and perhaps some external links. Also additional pictures would make the project more engaging for the reader. However once the missing sections are completed I believe the project will provide a comprehensive overview of p53

--Mark Hill 13:08, 17 May 2012 (EST) Your analysis has shown that you have worked through each project and applied a critical assessment with specific comments included.

Lab 10

--Z3289558 15:25, 17 May 2012 (EST)

Lab 11

--Z3289558 14:24, 24 May 2012 (EST)

Lab 12

--Z3289558 14:12, 31 May 2012 (EST) 1.Identify a current technique used in gene sequencing.

Next Generation Gene sequencing is at the foreground of current sequencing technology. Illumina has created sequencing by synthesis technology that allows reads of up to 15,000 nucleotides, is very succesfull and an excellent example of this next generation sequencing.

2.Identify a recent cell biology research paper that has used microarray technology.

Wei, J., Shi, Y., Zheng, L., Zhou, B., Inose, H., Wang, J., Guo, E. X., Grosschedl, R., & Karsenty, G. (2012) miR-34s inhibit osteoblast proliferation and differentiation in the mouse by targeting SATB2. Journal of Cell Biology, 197(4), 509-521, doi. 10.1083/jcb.201201057

Link to article on JCB

3.What aspect of the research findings were contributed by the microarray technique.

This paper looked into the specific genes of the miR-34 family, and the mechanism by which they inhibit osteoblast proliferation and differentiation. To identify which genes were expressed and their subsequent expression profile throughout the various stages of osteoblast differentiation, microarray analysis was used. Osteoblasts were cultured from mouse calvaria in either the presence or absence of a differentiating medium. Microarray analysis of the two cultures then allowed the researchers to observe an increase in the expression of miR-34 genes throughout osteoblast differentiation. The researchers used this information to justify their subsequent analysis of the function of miR-43 in vivo.