Talk:2016 Group 1 Project

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2016 Projects: Group 1 | Group 2 | Group 3 | Group 4 | Group 5 | Group 6 | Group 7
Group Projects - Blood Cell Biology - Updated 21 April  
This year's main topic is Blood Cell Biology. Each group should discuss with group members the specific sub-topic that will be covered by their project.

Here is a list of some of the cell types (Structure and Function)

PuMed citations PuMed Central citations PuMed Central note
Note - that while full publications are available online at PuMed Central, not all these publications allow reuse. You should still always identify the copyright statement within the actual article that allows reuse. Many research labs that receive government grants are required to make their published research available on PMC, this does not mean that the publicly available copy content can be used in your projects.

Remember - No easily identifiable statement usually means that you cannot reuse.

Examples from Megakaryocyte references on PubMed Central

Embryology - content cannot be reused but a useful resource about cell development.

Histology - images these can be reused in your projects.

Group Assessment Criteria  

Group Assessment Criteria

  1. The key points relating to the topic that your group allocated are clearly described.
  2. The choice of content, headings and sub-headings, diagrams, tables, graphs show a good understanding of the topic area.
  3. Content is correctly cited and referenced.
  4. The wiki has an element of teaching at a peer level using the student's own innovative diagrams, tables or figures and/or using interesting examples or explanations.
  5. Evidence of significant research relating to basic and applied sciences that goes beyond the formal teaching activities.
  6. Relates the topic and content of the Wiki entry to learning aims of cell biology.
  7. Clearly reflects on editing/feedback from group peers and articulates how the Wiki could be improved (or not) based on peer comments/feedback. Demonstrates an ability to review own work when criticised in an open edited wiki format. Reflects on what was learned from the process of editing a peer's wiki.
  8. Evaluates own performance and that of group peers to give a rounded summary of this wiki process in terms of group effort and achievement.
  9. The content of the wiki should demonstrate to the reader that your group has researched adequately on this topic and covered the key areas necessary to inform your peers in their learning.
  10. Develops and edits the wiki entries in accordance with the above guidelines.

Z5020175 (talk) 21:05, 22 March 2016 (AEDT) Hi Guys, my name is Matthew and I was wondering which blood cell type you would like to choose as a research topic? From the list, I actually find mast cells and megakaryocytes to be quite interesting, but we will work out which one is best for all of us. Also, it would be appreciated if you could write out your names so that we know who is in the group! Thankyou.

Z5020043 (talk) 00:53, 24 March 2016 (AEDT) Hey guys! I'm Jaclyn and I think choosing either mast cells or megakaryocytes as a research topic would be a good idea, I'm down with any option.

Z3489355 (talk) 11:04, 24 March 2016 (AEDT) Heya, I'm Kevin and I also think megakaryocytes may be an interesting topic to research.

Z3330991 (talk) 11:15, 24 March 2016 (AEDT) Hi guys, I'm Nadine and megakaryocytes sounds great! Key concepts that need to be addressed;

-how are they generated

- life expectancy

- why only located in bone marrow - function

- whats special about cell division

- diseases

- direction of research (currently )

- sub heading on Platelets (as they come from Megakaryocytes)

- internal structure and common structure

- function

- manufacture (made in bone marrow?)

- special features (surface receptors etc)

- history and who discovered them

- images, videos

- we are all about clarity!

Z5017493 (talk) 11:22, 24 March 2016 (AEDT) T here. Looking forward to it :)

Z5017493 (talk) 12:27, 24 March 2016 (AEDT) T: History and related diseases of cell for the week 4 individual assessment

Z3489355 (talk) 12:28, 24 March 2016 (AEDT) K: I will take the development and maturation process (manufacture as listed) if you guys don't mind :3

Z5020175 (talk) 12:27, 24 March 2016 (AEDT) M: Function and role of megakaryocytes for week 4 individual assessment!

Z5020043 (talk) 12:29, 24 March 2016 (AEDT) J: I'll research about special features such as surface receptors then

Z3330991 (talk) 12:32, 24 March 2016 (AEDT) N: I'm happy to do structure and i will have to work with the person who is doing special features

Z5020175 (talk) 19:24, 3 April 2016 (AEST) M: Lab 3 Individual Assessment

Paper 1: Ciovacco et al. [1] examined the complex interplay between megakaryocytes and bone development. They had done so through studying the effect of megakaryocyte (MK) maturation and numbers on osteoblast proliferation and osteoclast inhibition. Megakaryocytes from the wild type C57BL/6 mice were assorted into 3 sub - populations based on their increasing levels of maturity: megakaryoblasts, immature MK and mature MK. These cells were incubated with the same numbers of osteoblasts in separate cultures respectively. In conjunction, two other cultures were also made: osteoblasts alone and osteoblasts with BSA separated MKs. These were the negative and positive controls respectively. The same experiment was repeated with the use of osteoclasts instead. The numbers of bone cells within each experiment were recorded after 3 days of incubation and it was determined that megakaryoblasts do not exhibit a proliferative or inhibitory effect on osteoblasts and osteoclasts respectively. However, this was not the case for immature and mature MKs, as they were able to enhance the proliferation of osteoblasts and inhibit the formation of osteoclasts at virtually identical levels. This study was also able to demonstrate that as the numbers of megakaryocytes increase, so does the level of osteoblast proliferation. Overall, it was illustrated that the effect of megakaryocytes on bone growth is complex and determined by multiple factors such as their level of maturity and population numbers. This article is therefore relevant to the 'function and roles' subsection as one of the main functions of megakaryocytes is the regulation of skeletal homeostasis.

Paper 2: Uchiyama et al. [2] studies the role of growth differentiation factor 15 (GDF15) in the pathogenesis of primary myelofibrosis (PMF) which is a severe disorder that involves bone marrow fibrosis. The serum of patients with PMF were analysed within this study and nearly all patients demonstrated abnormally high levels of GDF15. This led the researchers to determine the source of this cytokine and it was found to be megakaryocytes within the bone marrow. Relative to other cell populations within the bone marrow of patients with PMF, megakaryocytes demonstrated greater haematoxylin and eosin staining and this means that the expression of GDF15 predominantly occurs in megakaryocytes. The numbers of these precursor cells are also known to be elevated in PMF and GDF15 was shown to be upregulated in megakaryocytes of patients with PMF when compared to expression levels in normally healthy individuals. The study had further found that GDF15 was responsible for the abnormal proliferation of fibroblasts and osteoblasts in the bone marrow of PMF patients. These two cells are known to cause the fibrosis of the bone marrow in PMF which leads to an inability to generate cells of the blood. Hence, megakaryocytes appear to play a regulatory role in the biogenesis of fibroblasts and osteoblasts in the bone marrow, through signalling molecules such as GDF15. This undoubtingly highlights the relevance of this article to both our 'disease' and 'function/roles' subsections as it explores the complex interaction between megakaryocytes and the cells that lead to fibrosis in PMF.

Paper 3: Within this study, Nishimura et al. [3] has identified an alternative pathway that involves megakaryocyte rupture and thereby enhanced platelet release in response to acute platelet needs mediated by Interlukin-1α (IL-1α). The main mode of platelet production is regulated by the molecule 'thrombopoietin' (TPO) which promotes a "microtubule - dependent extension of elongated pseudopodal structures" that eventually break off from the megakaryocyte as platelets. The process of generating these megakaryocyte projections is known as 'proplatelet formation' (PPF). The results of this study illustrate that PPF alone is not sufficient in producing the rapid platelet turnover required to meet acute platelet needs in inflammatory reactions. They demonstrate that there is an additional pathway of platelet production (thrombopoesis) mediated by IL-1α. Using a screening assay, it was determined that IL-1α is able to increase platelet production from megakaryocytes to a greater degree than TPO. By studying the effects of exogenous IL-1α on bone marrow megakaryocytes in vivo, it was found that IL-1α significantly enhanced megakaryocyte rupture but notably reduced PPF without altering the serum levels of TPO. The loss of PPF was due to the impairment of microtubule assembly and weakening of the plasma membrane by the IL-1α signalling pathway. The platelets from this cytokine mediated rupture were larger in size than those produced by PPF but demonstrated the same aggregation and thrombotic functions. This article evidently related to the 'function and roles' subsection as it illustrates the importance of megakaryocytes in platelet production under both physiologically normal and stress conditions.

Paper 4: Zhao et al. [4] sets out to illustrate the dual role of megakaryocytes (MKs) in maintaining HSC quiescence during homeostasis and promoting the repletion of haematopoietic stem cells (HSCs) following chemotherapeutic stress. Many cell types in the bone marrow stroma have been identified as HSC-regulating niche cells. However, whether a HSC progeny is recruited as a HSC niche cell is not clearly known and is thought to be regulated by megakaryocyte secretions. The results of this study show that MKs have physical interactions with HSCs in mice bone marrow and that a deficiency of MKs will lead quiescent HSCs to become activated and thereby proliferate rapidly. In comparison to other stromal niche cells, MKs were revealed to express higher levels of biologically active transforming growth factor β1 (TGF-β1 ) through analysing RNA sequencing data. When MKs are removed from the bone marrow, the levels of functional TGF-β1 protein and nuclear-localized phosphorylated SMAD2/3 (pSMAD2/3) is significantly lowered in the resident HSCs. This insinuates that the HSCs are kept in the quiescent state through the TGF-β-SMAD signalling pathway triggered by megakaryocyte secretions. In order to prove this further, the researchers had injected TGF-β1 into mice with MK ablation and this had reverted the actively proliferating HSCs into a quiescent state. When this injection was depleted, the quiescent HSCs became activated and there was an increase in their proliferative activity. Thus, it is apparent that TGF-β1 which is primarily expressed by MKs, is the key signal in maintaining HSC quiescence. Moreover, there was a significant impairment in the expansion of HSCs when the test mice were under chemotherapy. During this stress phase, megakaryocytes were observed to release fibroblast growth factor 1 (FGF1) which had appeared to override the inhibitory signal induced by TGF-β1. This had temporarily enabled the quiescent HSCs to become activated and clonally expand. On the whole, the data produced in this article is relevant to the 'function and roles' subsection as it highlights the importance of megakaryocytes in maintaining HSC homeostasis through the secretion of signalling molecules.

Z3489355 (talk) 22:05, 6 April 2016 (AEST)

Lab 3 Assessment

1. Xie, X. (2002). Thrombopoietin promotes mixed lineage and megakaryocytic colony-forming cell growth but inhibits primitive and definitive erythropoiesis in cells isolated from early murine yolk sacs. Blood, 101(4), pp.1329-1335.

This article tested the effects of thrombopoietin to early embryonic cells (E6.5-7.5) which includes hematopoietic stem cells and erythroid cells in an assay. While thrombopoietin alone failed to give any effect, when added alongside growth factors, erythroid growth was inhibited and megakaryopoiesis was enhanced. This showed that thrombopoietin and growth / transcription factors have significant role in regulating differentiation of hematopoietic stem cells to different types of circulatory cells. [5]

2. Ono-Uruga, Y., Tozawa, K., Horiuchi, T., Murata, M., Okamoto, S., Ikeda, Y., Suda, T. and Matsubara, Y. (2016). Human adipose tissue-derived stromal cells can differentiate into megakaryocytes and platelets by secreting endogenous thrombopoietin. J Thromb Haemost

Ono-Uruga et al. discovered that adipose tissue-derived stromal cells (ASC) can differentiate into megakaryocytes under the effects of endogenous thrombopoietin. It is also found that CD71, a transferrin receptor is a main contributor for thrombopoietin endogenous release in MK progenitor cells among human ASCs. In the experiment, CD71-positive ASC cells induced a higher levels of thrombopoietin endogenesis compared to CD71-negative cells. Therefore, higher levels of CD71-positive cells act as a significant sign to the process of megakaryopoiesis in humans. [6]

3. Carow, C., Fox, N. and Kaushansky, K. (2001). Kinetics of endomitosis in primary murine megakaryocytes. J. Cell. Physiol., 188(3), pp.291-303.

Megakaryocytes are differentiated from diploid megakaryocyte progenitor cells via endomitosis (EnM), continuous synthesis of genetic materials (ie. DNA) without undergoing cellular division (mitosis). S-phase length in EnM Megakaryocytes is the same as in other blood-cell cycles, with G1 and G2 slightly shortened. However the M-Phase (mitotic phase), is significantly shortened or even nonexistent in some observed cells. The research showed decomposing of spindle fibres at metaphase, which prevented the chromosomes from being pulled by the fibres and migrating to opposite poles of the cells, leading to incomplete mitosis. [7]

4. Suzuki, A., Shin, J., Wang, Y., Min, S., Poncz, M., Choi, J., Discher, D., Carpenter, C., Lian, L., Zhao, L., Wang, Y. and Abrams, C. (2013). RhoA Is Essential for Maintaining Normal Megakaryocyte Ploidy and Platelet Generation. PLoS ONE, 8(7), p.e69315.

RhoA, an intracellular signaling protein, was proved to play important role in the development of megakaryocytes. In the experiment, it was found that RhoA-negative megakaryocytes were larger, contained higher numbers of chromosomes (ploidy), and were rapidly releasing immature, unstable platelets which were immediately discarded by the circulation system. RhoA-positive cells (control) showed normal maturation speed and completed development of platelets before their release. [8]

Z5020043 (talk) 08:05, 7 April 2016 (AEST) J

Lab 3 Assessment

Paper 1 Ng et al[9]. investigated the actions of Thrombopoietin (TPO) on megakaryocytes via the Mpl receptor. It was discovered that TPO binding onto the Mpl receptors causes dimerization of the receptors and a targeted cell response to stabilize megakaryocyte cell numbers. However, it was also discovered that TPO action on Mpl receptors led to the stimulation and production of proplatelets. Ng et al., employed techniques involving the use of green fluorescent protein expressed on mice Mpl alleles to more accurately observe the actions of the Mpl locus. It was then concluded that the presence of Mpl receptors on megakaryocytes was crucial for the regulating the megakaryocyte population.

Paper 2

Khetawat et al.[10] examined the expression of estrogen receptor (ER), estrogen receptor (ER ), progesterone receptor (PR) and androgen receptor (AR) within the megakaryocytic lineage. Samples of megakaryocytes were obtained and generated ex vivo from human donor stem cells. It was discovered that these samples contained ER, RNA and AR. The seconda major finding showed that both “ER and AR transcripts are up-regulated during megakaryocyte differentiation”(Khetawat et al., 2000). Hormonal influence also played a part in the expresseion of AR. ER protein was shown to be greatest in the cytoplasm in glycoprotein llb+ megakaryocytes through immunofluorescence microscopy. The occurrence of AR and ER was observed in platelets via western immunoblotting.

Paper 3

Rozmyslowicz et al. [11] studied platelets and megakaryocyte- derived microparticles (MP) to determine whether the expression or abesnce of receptors led to HIV infection. It was discovered that cells expressing CD4 and virus co-receptors were susceptible to infection. It was also discovered that it may be due to other mechanisms played a role in infection such as the transfer of HIV entry receptors between cells by MP.

Paper 4

Bender et al. [12] observed the role dynamin played relating to vesicle transport and endocytosis in human thrombocytes. Bender et al. studied the megakaryocytes of mice lacking DNM2. It was discovered that a lack of DMN2 was lethal as megakaryocyte membrane formation and thrombopoiesis as dependent on DMN2 shown by high-resolution immunofluorescence confocal microscopy.

Z5020175 (talk) 19:58, 11 April 2016 (AEST) Guys, we need to start working on this project! For the functions and roles, I will be writing about:

  • Regulatation of skeletal homoeostasis by megakaryocyte secretions
  • HSC quiescence in the bone marrow due to megakaryocytes
  • Production of platelets from megakaryocytes
  • Platelet roles such as thrombus formation

Z3330991 (talk) 11:22, 14 April 2016 (AEST) N;

Models of mammalian adult hematopoiesis with respect to the megakaryocytic-erythroid compartment[13]

Article 1

<pubmed>26557683</pubmed> Due to the great similarities between erythroid and thrombocytic, this article seeks to demonstrate the differentiation between the erythroid and thrombocytic as they evolved overtime from a single ancestral linage. This article compares the thousands of platelets per one megakaryocyte that is in the mammalian as opposed to nonmammalian thrombocytes which are much smaller and more flexible. Hematopoiesis suggests that mammalian megakaryocytic and erythrocytic cells probably evolved to increase their biological performance such as oxygen transport and homostasis, ultimately being an improvement of their ancestral cells. There is evidence found that the megakaryocytes are likely evolved as thrombocytic improvement. This is derived from the characteristics of the relationships between the zebrafish hamatopoietic progenitors and the mapping of their proliferation kinetics. Additionally despite the striking phenotypic differences between the megakaryocytes of the mammalian and nonmammalian thrombocytes, there is a distinct link between mammalian and nonmammalian erythroid and thrombocytic cells in terms of their molecular control and their proliferation potential.

This article can be used in describing the development of the megakaryocyte and how it evolved and the similarities it has to nonmammalian thrombocytes. [14]

Article 2

<pubmed>11012198</pubmed> This paper highlights the structure and function of megakaryocytes (MK) and platelets and how they are not identical. MK is unique for its enormous size and polyploidy. MK cells also produce their progeny cells called platelets via a mechanism called cytoplasmic fragmentation. It should be noted that platelets have no nucleus and usually lack ribosomes however they have a well defined structure. MK cells undergo endomitoses where the chromosomal DNA reduplicates to an average ploidy of 16 N while the cytoplasm never divides. During this process the nuclear membrane disappear, thus allowing for free exchange between nucleoplasm and cytoplasm. Further this article tackles the important concepts of when a MK matures and what happens; the platelet territories become separated within the MK cytoplasm, the separated membrane system is made up of a blend of membranes that are from different sources, before fragmentation happens the peripheral zone of the cell is absent of organelles, the organelles- free peripheral zone may unpremeditatedly form large veils or blebs and finally the fragmentation of MK is best observed when the cells are fixed in suspension. It is imperative to note that although the platelet membrane is demarcated within the cytoplasm of the MK cell, it is wrong to assume that the surface membrane of the platelet is identical. Additionally it can be seen that antigenic epitopes found on platelets may not be found on MK even though it stands to reason that there is a considerable antigenic cross-reactivity.

This article has proven to be important in the structure and function sub heading in the group research as it highlights the characteristics of a MK cell while addressing the similarities and the link it has to platelets. [15]

Article 3

<pubmed>10468153</pubmed> The article demonstrates the understanding of the structure and the function of a megakaryocyte. It explains that MK cells are known to be large polyploidy cells that are mostly located in the bone marrow. The main role of the Mk cell is to maintain normal blood platelet count by releasing platelets from the mature MK cells. Mk cells can be divided into highly proliferative MK burst forming cells or MK colony- forming cells. Through evidence it can be seen that at the end of the proliferative phase the Mk precursors undergo transformation in the cell due to the increase in ploidy thanks to the process of endomitosis. Endomitotic division is characterized by DNA replication and nuclear segmentation. The maturation of MK cells is driven by the emergence and appearance in MK’s cytoplasm which contains specific organelles and the precursors of important platelet structures. The knock out mouse models have shown to be extensively functional in the delineation in the capacity of growth factors, their receptors, and transcription factors in Mk differentiation. P45-NFE2 is a transcription factor that has proven to be essential for MK cytoplasmic development due to NFE2-/- mice fail to produce platelets even though the present MK cells are normally located in the bone marrow.

This article has proven to be effective enough to include in the subheading Structure and function as it addresses both headings in detail and includes pathology. It describes cytokine effect on MK development, proplatelet formation and transendothelial migration of MK cells. [16]

Article 4

<pubmed>11012205</pubmed> This article address some studies that report a hierarchy of hematopietic cells that are competent of producing MKs cloned from both Adult bone marrow (ABM) and fetal bone marrow (FBM). The studies of in vitro megakaryocytopoiesis helped produce a hierarchy of MK progenitor cells. The hierarchy begins with the hematopoietic stem cells due to the presence of thromboproietin (TPO) alone produce MKs. The BFU-MK is a primative progenitor cell committed to the megakaryocytic linage. The properties of the BFU-MK allow it to be readily distinguished from the more differentiatied MK progenitor cell, the colony-forming unit- megakaryocyte (CFU-MK). The primitive HPPC-MK, BFU-MK and the highly differentiated CFU-MK cells are known as MK progenitor cells that’s are lineage- restricted. In the FBM a significant number of oligopotent hematopoietic progentitor cells are cabale in vitro of producing colonies composed of many hematopoietic linages including a subpopulation of MKs. It is still unknown the contributions of these mixed lineages progentior cells to megakayocyopiesis and the growth factors responsible for their in vivo development. It can be seen in the experiment that human bone marrow cells showed to express CD34 but not HLA-DR (which is known to contain a high amounts of hematopoiectic stem cells) was competent in developing MK progenitors cells for 10 weeks in the presence of various cytokine combinations.

This article fits under the subheading structure as it targets the structure of the MK cells and the factors and the lineages associated with MK cells. Further this article tackles the commitment of pluripotent hematopoietic stem cells to the Lineage of MK cells and the changes in the MK progenitor cells. [17]

Z3489355 (talk) 20:10, 14 April 2016 (AEST) I'm currently working on megakaryopoiesis. The articles related to it are much scarcer than those about production of platelets, unfortunately. So I think it will take a bit more time to find the appropriate references.

Z5020043 (talk) 22:51, 20 April 2016 (AEST) J: Hey guys, so for the "Special Features" part, since I will be researching mainly about the receptors found on megakaryocytes, should I research info and briefly write about a few different receptors or just mainly focus on one type of receptor e.g. the Mpl receptor and talk about the consequences in relation to abnormal TPO levels?

Z3489355 (talk) 09:34, 21 April 2016 (AEST) Heya, I think you can briefly list and describe a few receptors, and then focus on the ones which have the biggest roles or unique to megakaryocytes.

Z5020175 (talk) 12:59, 21 April 2016 (AEST) M: Hi guys, Mark has suggested that a timeline is good for the history, for structure we should: include picture showing size and morphology, for development: Histological slides that show the different stages of MK development

Z5017493 (talk) 13:04, 21 April 2016 (AEST) T: I have done work on history and pathology. Will upload when I get access to the document. I have to convert my paragraphs into a timeline for history and will discuss with Jaclyn the two main diseases of MK/platelets

Z5020043 (talk) 21:27, 23 April 2016 (AEST) J: Okay then I will research briefly about the receptors and I think this information can be placed with under the structures heading.

Z3330991 (talk) 15:48, 24 April 2016 (AEST) Nadine;

the link above is for a book that i think is great, you guys can use it as a resource for our group project. you'll find that on page 292-305 of the text book it focuses on MEGAKARYOCYTES

Z3330991 (talk) 21:45, 25 April 2016 (AEST) Nadine; Guys this week i'd like for us to have all information up on the page before this time next week. Doesn't have to be the finished product, it can be dot points and just copy and paste parts of articles that you will use with reference and that way you can reword it and have the reference already there. I will edit my section tomorrow morning hopefully. Also as i was reading papers and websites i just added two sentences to the intro section. Doesn't have to be used but its there now, we can delete or include it , up to you guys. Let me know how everything on your end is going.

Z3489355 (talk) 23:05, 27 April 2016 (AEST) Hi guys, I've added most of the main points in megakaryocyte development. I still feel I can expand it further though, so I will add more in pretty soon. I actually also feel our figure/image about the development uploaded by Matthew should be put in this section as well, to give a better flow to the page, rather than jumping to the next section and revisit the same information previously detailed. But let me know if you guys have any other ideas :)

Group 1: User:Z5017493 | User:Z3330991 | User:Z5020043 | User:Z5020175 | User:Z3489355

Z5017493 (talk) 08:59, 28 April 2016 (AEST) T: I will upload my portion of the history once I get to university as the wifi is awful where I live. Only portions are uploading and it's skipping on entire sections.

Z5020175 (talk) 11:55, 28 April 2016 (AEST) M: Hi guys, so here is a lot of list things we should do for our page:

  • Banner Image
  • Table for structure - comparing megakaryocytes to platelets
  • Drawing for TPO signalling
  • Brainstorm of megakaryocyte functions
  • Drawing for platelet plug formation
  • Add in a few more diseases: Maybe add in 1 more bone disorder
  • Add in histological slides
  • Add in references
  • Please put down which aspects you are doing! I will be doing the Brainstorm & Drawing for platelet plug

Z5017493 (talk) 12:00, 28 April 2016 (AEST) T: I will be designing the Banner image and upload it for K to add to the page. I will also be doing the overall editing of the page to ensure everything flows and is unified. (We're doing great stuff but I feel like its somewhat stilted just because we're different people) I will be doing a GlossIary/Definitions list I will also be adding some external links about pathology and history for people to do further readings if they wish it. I suggest you guys add some too.

Z5020043 (talk) 12:06, 28 April 2016 (AEST) J: I've put some info for the receptors, right now they're just dot points but as I research more I'll make proper paragraphs out of them. I will also be drawing a diagram for TPO:MPL signalling as well as forming a table about the different types of secretions and mediators involved with megkaryocytes. Lastly, I will also add on to what we already have for the future of megakaryocytes.

Z3489355 (talk) 22:47, 1 May 2016 (AEST) I've roughly finished putting all the essential information for my section, I will keep expanding them as soon as I find any relevant information

Z3330991 (talk) 12:10, 4 May 2016 (AEST)Nadine; hi guys, I've dramatically cut out and left the relevant information on my section. However in saying that i know i need to add an image or get a drawing of the structure of megakaryocytes or platelets to help with the understanding of the content. Also I'm hoping to somehow format the structure part into a table that allows for easier understanding of the structure of both plateles and MK cells while addressing the similarities and the differences.

Z5020043 (talk) 12:26, 4 May 2016 (AEST) J: So far I've finalised the info for CAMT and the TPO:c-Mpl signalling pathway. I have also drawn a diagram that explains this pathway and inserted it on the page. I will now gather information about the future of megakaryocytes and put it on the page later tonight. I will also try to insert a collapsable table for mediators formed and involved with megakaryocytes.

Z5017493 (talk) 14:32, 4 May 2016 (AEST) T: Hey guys, I'll be putting up the banner tonight, editing before tomorrow's lab, and adding my work thus far. I'll also e adding some images, for the sake of aesthetics and to give our peer reviewers a greater visual aspect to improve the understanding of the visual learners here. Glossary is being worked on as I speak/type!

Z5020043 (talk) 22:22, 4 May 2016 (AEST) J: As of now I have uploaded a diagram a drew of haemostasis and vascular. Tomorrow I'll decide whether its necessary or not to put in a table for the mediators formed and involved with megakaryocytes.

Z5017493 (talk) 09:29, 5 May 2016 (AEST) T: Just to clarify, the glossary will consist of the abbreviations and definitions of jargon.

Z5020043 (talk) 10:56, 5 May 2016 (AEST) J: I have updated the banner for our wiki page with an original image I made.

Z3489355 (talk) 11:26, 5 May 2016 (AEST) I've checked and fixed some referencing errors around the page. Please make sure all of the references are from a primary article :)

Z5020175 (talk) 11:39, 5 May 2016 (AEST) M: Hi guys, good job on what we have so far! So last night Jaclyn and I had discussed redoing the banner & we have decided to add a signalling bit. I also edited the wording of different sections. Here are a list of things that I feel our page should add:

  • Tables - Structure and signalling
  • Graphs - Possibily in Pathology
  • More diseases

Z3330991 (talk) 10:00, 10 May 2016 (AEST) guys once out section is unlocked i need to work on two things;

  • table for the structure
  • image for structure

Z3330991 (talk) 10:44, 10 May 2016 (AEST) Also i need to go back to my review article and gather all of the primary references that where used from that paper and reference accordingly.

Z3330991 (talk) 13:50, 10 May 2016 (AEST) guys i really like group 6 layout, when you're free have a look at it.

Peer Reviews

Please put your peer reviews here

Group 1 peer review

Introduction: Gives a really nice overview however, it would be good to know what megakaryocytes actually do straight away rather than later in the introduction.

History: I found this section really long and also lacked references, not being the main focus of the assignment I think cutting down to the major events or making it collapsible so if someone is interested they can click to read it.

Structure: I think it has a good amount of content and is structured well. It would be nice to have a couple of pictures to show the different zones though.

Development and maturation: This section was really easy to read however, I had to go back and forth a little to figure out where RhoA fitted in, so maybe mention that in development section and have the elaboration as well below (which was also good).

Signaling: The JAK/STAT signaling section could be worded a little better but I liked the signaling section. The TPR explained well.

Function and role: Platelet production section is great! However, I think all the platelet stuff should be together (platelet function is later on – I feel like it jumps back and forward). In the regulation of skeletal homeostasis I’m left with the question is there another functioning life stage other immature and mature that isn’t involved in this regulation process? A concern in maintenance of hematopoietic stem cells is that it is mentions studies – but only one reference.

Pathology: The second last paragraph on essential thrombocytosis is quite poorly worded and a bit hard to understand. The referencing for this section is also not to format. CAMT section is nice and I assume that the osteoporosis section is not yet complete.

Future: Good, gave me something to think about and was relevant.

Overall I really like this project page! It was well written and easy to understand, with the more complex concepts where explained in a comprehensible manner. The paragraphs broken up so it wasn’t too overwhelming and links were made back to structures covered in the course.


General pointers :

  • A few grammatical and tense errors
  • the flow is a bit stuttered
  • Attempt to not use colloquial language, try to write like how wikipedia pages write
  • Proof read before final submission.

A few more specific pointers:

  • If possible try find a few references for the history of megakaryocytes
  • Do not need the small intro at the beginning of structure subheading. That can be fitted into the introduction.
  • Several Images can be inserted into the Structure subheading to visualise the different zones
  • Would be good to provide a brief explanation of functions of secretions when mentioned e.g alpha granules in the "Outer (Marginal) Zone" section
  • In "Common Myeloid Progenitor Cells", the first sentence is a bit long. Maybe split it up
  • Hide the youtube video in Pathology subheading like how the glossary is hidden.
  • A bit self explanatory but finish osteoporosis and also maybe add in another disease involving malfunctioning platelets if you have time.


  • Each section clearly set out with appropriate subsection headings that cover a good range of topics
  • Logical flow, easy to read and understand, little grammatical/spelling errors
  • Good use of images however they could be a little bigger on page and more images are needed especially for the section on structure (cartoon or drawn). Apart from the histological images, a better image of a megakaryocyte is needed as well as one for platelets. This will also help break up the blocks of information.
  • A table that sets out the different surface markers present on megakaryocytes could be included, although some signalling pathways have been mentioned, this would be a good summary.
  • Introduction, good overview of what megakaryocytes are and what they do
  • History probably a bit too detailed, some points are not as important as others, focus more on the major discoveries.
  • Great use of video for pathology, however could probably written on the page itself (brief overview of pathogenesis for each disorder)
  • Development/ maturation and function are well explained
  • The inclusion of current research and glossary are clever


The page is good, but the main problem is a consistent misuse or no use of proper referencing. Here are my observations: - Unreferenced statements thrombopoetin section - ET references box is not technically referred to so it’s a bibliography not a reference - Glossary is unfinished - History is fully unreferenced - “Megakaryocytes have been shown to maintain HSC quiescence during homeostasis “ i think this would read better if it was written "in homeostatic conditions" - I like the figures but they have very little text information. Figure 4 could discuss in more detail the 4 branches of the mind map of MK functions. - Good job inserting the essential thrombocytosis video but I would put it under the Essential thrombocyte title not the “pathology” title seeing as it’s specific to one pathology. - For consistency I would ensure that all acronyms are uppercase (in CAMT subsection of pathology some acronyms aren’t in uppercase. Also you use the acronym TPO several times and describe it several times. You could reduce the wordiness by just doing this once. - Needs a reread through for minor spelling checks as well

Group 1 peer review

The introduction provides a solid basic overview of megakaryocytes and the history section is very comprehensive. The structure section is detailed and informative, however it doesn't seem to provide any details of the cytoskeleton or the cell membrane of a megakaryocyte. An electron micrograph or diagram of a megakaryocyte and a platelet should also be in this section (although there is a histological image later). Furthermore, the entire structure section only cites one article which is rather old; references to more recent articles are needed and the reference tag should be placed before a period (e.g. [1].). In your developmental section I would also place a note to refer to figure 3 as a summary of the developmental stages of the megakaryocyte. The section on the TPO receptor doesn't appear to have any references at all. The numbering of your figures is out of order, and two of your figures have the same number. If you say "Many studies have illustrated that" or "Megakaryocytes have been shown to" then perhaps you should link to these articles immediately following the statement, or say that "authors et al. have shown" (this particularly applies to a couple of the function sections). The osteoporosis section doesn't seem to be completed although I'm sure it will be later.

Overall I think it's a good page: the images that are there are useful, the current research section was nice and brief, and the glossary is a nice touch. I felt that the developmental section and the platelet function sections were the strongest. However some of the earlier sections are in desperate need of revision of spelling and grammar.

Group 1

Over all I think this is a great page and you guys have done a great job! All the sections are really well writing and explain the concepts in appropriate language and enough detail to provide a sound understanding.

  • The history section again is really well written and provides a lot of detail but there are no references. References for each year would be great and would also add another level of depth to the assignment so students could undertake further reading if necessary.
  • The structure section provides awesome detail, especially the information on platelets which was really interesting and actually taught me something I didn't know. Some pictures or diagrams for this section would be really helpful in visualising the information.
  • One of the criteria set by Mark was to have one student generated or drawn image and I think that the development section; specifically the explanation of the hematopoietic stages of development is a great opportunity for you guys to draw a nice diagram or flow chart of the stages.
  • One area of concern is that the Essential Thrombocytosis section has no references at all. Even if you used only one source, it's super important to include it. It also provides an opportunity for further research for students if they're interested.
  • The glossary section is insane! I was really impressed, especially with the acronyms table- AMAZING!!

Great job guys!



  • The introduction is very clear and provides a good overview of the project as a whole, with valuable insight into the important basic information about megakaryocytes.


  • The history section is too long, and i would recommend cutting it down to increase its clarity. Removing the references to history other than those specific to MK cells and platelets, and only including those discoveries which a highly significant to our current understanding of these cells would make this section clearer and the reader more inclined to read the whole table. The information within the table is good, and relevant, there is just too much of it. It would also be useful to put in some references for this section to show where your information came from.


  • The structure section is informative and clear, however it might be helpful to go into more detail of the overall structure of megakaryocytes as well as each zone individually, and how the zones interact with each other. It would also be helpful to include a diagram/image here, showing the different zones, to help the reader visualise the information you are providing.

Development and maturation

  • This section flows well between the steps of maturation, however the sentence structure could be improved to make it easier to read. There are a lot of new terms that a reader may not have seen before, so breaking this up with simpler language would help it to be more easily understood


  • Signalling could be better linked in with the rest of the information on the page. I wasn’t really sure how and where it fit in to megakaryocytes as a whole. What is the purpose of the signalling and under what circumstances does it occur?


  • Clear and well structured
  • The images nicely draw together the information presented, and summarise the cells functions as a whole, as well as providing detailed information on their main role in platelet production


  • Im assuming the the osteoporosis section is not finished, but it requires an explanation on how the condition is linked to megakaryocytes


  • Provides valuable insight into future research involving megakaryocytes. Although each subheading only has a small amount of information, it sums it up well

Overall tips

  • Have a check through the whole page for spelling and grammatical errors
  • Make sure all information is referenced correctly
  • More images, perhaps EMs would reinforce the information you’re presenting and help the readers overall understanding of megakaryocytes. Keep up the good work, really nice page so far!

group 1

1. key points are addressed throughout with good subheadings and headings

2. Content is brilliant and love the original diagrams they show a deep understanding of the topic.

3. Nothing in the history section is cited, seems like random information without any references. I don’t know why the references for ET are in a collapsible table at the end rather than the regular reference list just because you found the reference through a different resource doesn’t mean it doesn’t exist on pubmed eg. Rumi et al. resource from “blood” has a pubmed ID; 24366362

4. Diagrams are brilliant I feel like a diagram in the structure would be a really good idea just to illustrate what you’re talking about

5. Significant research has been undertaken as seen through the 34 references I feel like more than one reference however could be used for structure.

6. You have successfully taught the learning aims of cell biology with an informative and interesting wiki page.

Group 1

This page is well detailed and provides comprehensive information about megakaryocytes and their structure and function. The introduction and history are well detailed, providing a good overview of the basic information regarding the cell, and the table format of the history allows the information to be presented in an organised and easy to follow manner. While the structure of the cell is well detailed, the majority of this section only uses one source, and I believe it may be able to be improved by using additional articles (which are perhaps a more recent). The development section is thoroughly done, with the information presented in an organised, easy to understand manner. The histological image is also very useful in supplementing the information, as was the image regarding the maturation of the megakaryocyte. However, the section regarding thrombopoietin receptors under the signaling topic does not appear to have any references, and this should be fixed whenever possible. The function and role section is well detailed, with clear subheadings organising the information into distinct sections, and the images also help to substantiate this information. The video in the pathology section is a useful tool of providing an overview of the topic. However, the references for the essential thrombocytosis section appear to be separate, and not within the standard reference list at the end of the page.  This seems to be a little disorganised, as the drop down table showcasing the references doesn’t allow for the specific citations/ reference numbers to be used within the body of information like the rest of the page. In addition, the osteoporosis section doesn’t appear to be complete, but this can be fixed in the near future. The future of megakaryocytes section was well detailed, with well structured information about each of the different areas of research. In addition to this, while this is a minor point, I found that the numbering of the images throughout the page is out of order, with some numbers doubling up (such as there being more than one figure 4), and this can cause some confusion on the page. Overall, I found this page to be quite informative and education regarding megakaryocytes. The information is well presented, with distinct sections showcasing different aspects of the cell. The images are also well chosen, and supplement the information very well. Some areas require a little more work in terms of referencing and providing more substantial information, as well as the formatting of the images. However, on the whole this is a good page that is very educational regarding megakaryocytes.


  1. <pubmed>20052670</pubmed>
  2. <pubmed>26276681</pubmed>
  3. <pubmed>25963822</pubmed>
  4. <pubmed>25326798</pubmed>
  5. <pubmed>12393382</pubmed>
  6. <pubmed>26990635</pubmed>
  7. <pubmed>11473355</pubmed>
  8. <pubmed>23935982</pubmed>
  9. <pubmed>24711413</pubmed>
  10. <pubmed>10733498</pubmed>
  11. <pubmed>12478067</pubmed>
  12. <pubmed>25468568</pubmed>
  13. <pubmed> 26557683 </pubmed>
  14. <pubmed> 26557683 </pubmed>
  15. <pubmed>11012198</pubmed>
  16. <pubmed>10468153</pubmed>
  17. <pubmed>11012205</pubmed>