BIO 1140 Study Guide - Midterm Guide: Troponin, Protein Isoform, Alternative Splicing

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6 Apr 2018

School

University of Ottawa

Department

Biology

Course

BIO 1140

Professor

Caroline Petit- Turcotte

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Document Summary

Discuss what advantages alternative splicing confers to eukaryotes, with particular attention to how this advantageous mechanism is used across various cell types or cellular locations. This involves the formation of various mature mrna sequences from a single pre mrna transcript. This is advantageous because it allows the cells to express different characteristics depending on where they are in the body and their specific function. This makes them more or less susceptible to calcium concentrations, therefore affecting the rate of muscle contraction. One isoform is more sensitive to rises in intracellular calcium and will allow for faster muscle contraction; thereby being located in muscle groups that contain fast twitch fibers. Another advantage of alternative splicing is that is allows for the genome to maintain its current length but still allow for more variety of proteins to be transcribed. The major consequence of not having this mechanism would mean that either the number.

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True / False Questions

01. _____ Antibody is composed of 2identical long heavy chains and 2 identical shorter lightchains.

02. _____ Variable (V) and constant(C) regions are part of both heavy and light chains.

03. _____ Variable regions for heavyand light chains from the same antibody molecule are alwaysidentical.

04. _____ Variable region of lightchains are encoded by the DNA sequences that contain rearranged V,D, and J segments.

05. _____ Fc part of the antibody isnot important, F(abâ)₂ fragment has the same binding andeffector capacity.

06. _____ Fab fragments are generatedby alternative splicing.

07. _____ J chain is used as asurrogate light chain during pre-B cell receptor testing forsuccessful V(D)J rearrangement.

08. _____ Binding of the antigen byantibody is stabilized by disulfide bonds.

09. _____ RAG1/2 are always expressedin B cells at high level, because B cells need RAG1/2 to constantlyrearrange their V regions.

10. _____ âNâ (non template)nucleotides are added by TdT.

11. _____ The 12/23 rule is appliedduring class switching.

12. _____ For B cells, V(D)Jrecombination occurs only in the bone marrow.

13. _____ The process of somatichypermutation helps to improve specificity of the antibody.

14. _____ In late pro-B cells, Vsegment is rearranged with DJ segments.

15. _____ Failure to eliminateself-reactive B cells may lead to serious autoimmune diseases.

16. _____ Mature, naÃ¯ve B cellsexpress IgD and any of the other classes of antibody (IgM, IgG,IgA, or IgE) on their surfaces.

17. _____ B1 cells are present in theperitoneal cavity, pleural spaces and brain.

18. _____ AID (activation inducedcytidine deaminase) is expressed only in B cells and it canintroduce breaks in double stranded DNA.

19. _____ Different classes (isotypes)of antibodies have different effector functions, which aretriggered by special receptors expressed by a variety of cells.

20. _____ Plasma cells are terminallydifferentiated cells that produce large quantities ofantibodies.

21. _____ Repeated exposure to thesame antigen eventually leads to immunological exhaustion and lackof immunity, because there is no room for new plasma cells in thebone marrow.

22. _____ Germinal centers arespecialized sites within the bone marrow where Ig genes ofactivated B cells undergo affinity maturation.

23. _____ B cells can present antigensto T helper cells.

24. _____ Co-stimulatory molecules arerequired for efficient generation of memory B cells.

25. _____ Lymphocytes migrate to thelymphoid tissues in response to chemokines.

26. _____ Class switching duringgerminal center reaction is a random process.

27. _____ T cell independent responsescan generate strong and long lasting B cell memory.

28. _____ Fc receptors that arepresent on many different cell types are crucial for removal of thepathogens.

29. _____ The ideal vaccine should bedesigned to mimic the natural course of infection without causingsymptoms of the disease.

30. _____ The protective immunity canbe generated against any pathogen because there is virtuallyunlimited number of possible V regions, thus any antigen can berecognize by an antibody.

oliverhinoceros960

Chapter 10

1.Outline the history of our knowledge on DNA up to Watson and Crick. What were the main contributions made by each researcherâs key experiment?

2.Explain the setup of the Hershey and Chase experiment, what would the results have been if protein was the genetic material?

3.Draw the structure of a DNA nucleotide, labeling each main component correctly. How does an RNA nucleotide differ?

4.If a section of double stranded DNA contains 19% Adenine, how much Thymine is present?

5.You are a researcher studying the genetic basis of heart attacks and have been working to determine the expression levels of different genes that might contribute to cancer formation. You obtain the DNA methylation status of five genes of interest (the data are shown in the table below). The plus (+) sign indicates the level of DNA methylation; more plus signs correlates with increased methylation levels.Based on this information which genes would you predict to have the highest rate of transcription?

Gene	Methylation levels
1	++
2	+++++
3	+++
4	++
5	+

What are the characteristics of the 3 main DNA forms?

Chapter 11

What are the different types of chromatin?

What are the structures and important roles for telomeres and centromeres?

What are the differences found between eukaryotic chromosomes and mitochondrial?

Chapter 12

Explain each of the different models of replication.

If you grow a culture of bacteria in media with radioactive nucleotides so that all DNA in the cells include radioactive nucleotides and then place the bacteria in new non radioactive media. After two rounds of replication what proportion of the DNA molecules will contain radioactivity?

Summarize the similarities and differences between rolling-circle replication, theta replication and linear eukaryotic replication.

What are the functions of the different DNA polymerases found in eukaryotic cells?

Draw a replication fork and include all key components and orientations. (Leading/lagging strands, DNA helicase, RNA primer and DNA gyrase)

What is the Holliday model of recombination and what are the necessary steps?

Chapter 13

What are the different types of RNA and what roles do they play?

Describe the properties and functions of each of the RNA polymerases and how they differ depending on the organism.

Describe in detail the process and mechanisms of transcription in both prokaryotes and eukaryotes.

Chapter 14

What are the primary purposes of each of the three post transcriptional modifications that occur in eukaryotic cells.

What is alternative splicing and what role does it play in the cell?

How is ribosomal RNA processed after transcription?

How do siRNA and miRNA work, describe/draw out the process in detail.

paraphrase the review in your own words?

The tumor suppressor PTEN (phosphatase and tensin homolog deleted from chromosome 10), is a lipid phosphatase that converts phosphatidylinositol-3, 4, 5- triphosphate (PIP3) into phosphatidylinositol (4, 5)- diphosphate (PIP2). PTEN is well-known as the most highly mutated tumor suppressor gene in the p53-post era [66, 67]. Recently, three papers by Nadav Bar and Rivka Dikstein, Linhua Liu and colleagues, and Laura Poliseno and colleagues, have demonstrated that PTEN was a bona fide target of miR-22 in a small cohort of cancer cell lines that are driven from breast cancer, cervical cancer, prostate cancer, and bronchial epithelial cancer. These studies contradict a uniform role of miR-22, indicating that under certain circumstances, miR-22 may function as an oncogene because of its antagonistic effects on tumor suppressive PTEN signaling [26, 68, 69] (Fig. 3). Using various miRNA target prediction programs and/or RNAhybrid program for evaluating the minimum free energy hybridization, these three groups all found that miR-22-PTEN was a high scoring miRNA-target pair. Enforced or reduced expression of miR-22 in human HEK293T, cervical cancer HeLa and breast cancer MCF-7 cell lines (Nadav Bar and Rivka Dikstein), anti-benzo[a]pyrene-7, 8-diol-9, 10-epoxide (anti-BPDE)-induced transformed human bronchial epithelial cancer cell line 16HBE-T (Linhua Liu and colleagues) and prostate cancer cell line DU145 (Laura Poliseno and colleagues), revealed that miR-22 negatively regulated PTEN protein expression. Intriguingly, an inverse correlation between miR-22 and PTEN mRNA expression has been presented by Poliseno et al., while Liu et al. found that there was no change of PTEN mRNA expression regardless of miR- 22 levels. A similarly inverse association of miR-22 and J. Xiong PTEN protein levels was observed in 16HBE-T and its parental normal cell line16HBE (Linhua Liu and colleagues), and in several prostate cancer cell lines, prostate cell lines and a prostate tumor tissue microarray (Laura Poliseno and colleagues). Furthermore, the mature levels of miR-22 were significantly increased in these tumor cells versus their normal counterparts. In line with this result, a direct correlation between miR-22 expression and phosphorylated AKT or between the expression of miR- 22 and that of DICER was also identified by Laura Poliseno and colleagues. These three groups all showed that an intact binding site at the 3âUTR of PTEN mRNA was required for miR-22 targeting. Functional analyses showed that miR-22 could induce apoptosis, inhibited colony formation and suppressed motility of bronchial epithelial cancer cells (Linhua Liu and colleagues), and intrinsically promote prostate cancer cell growth and tumorigenesis in tumor-bearing nude mice (Laura Poliseno and colleagues). Subsequently, the influence of miR-22 on the downstream signaling of PTEN was tested. Bar et al. showed that miR-22 could stimulate AKT activity, and in turn, AKT significantly upregulated miR-22 expression, suggesting a regulatory loop comprising miR-22, PTEN and AKT. Analogously, Poliseno et al. showed that miR-22-mediated oncogenic activity was dependent on decreased PTEN expression and increased phosphorylated AKT [26, 68, 69]. Surprisingly, the conclusion presented by these three papers is challenged by a more recent study that argues against the downregulation of PTEN by miR-22 [70]. The cytotoxicity of paclitaxel, a featured anti-tumor activity, can induce apoptosis, and inhibit proliferation and survival of p53 wild-type colon cancer cells, rather than chemoresistant p53-mutated colon cancer cells. Chemoresistance assay showed that overexpression of miR-22 prevented the chemoresistance to paclitaxel and induced apoptosis, and inhibited proliferation and survival of p53-mutated colon cancer cells. Finally, Li et al. pinpointed that tumor-suppressive miR-22 decreased AKT activity and MTDH expression, and subsequently increased Bax and active caspase-3 expression through upregulation of PTEN expression. These studies emphasize the complex of miR-22 function in tumor pathways, and provide another good example identical to miR-17-92 cluster that functions as either tumor suppressors or oncogenes due to cell types and expression profiles of miRNA-target pairs [71]. Paradoxically, contrary to the conventional view that different target repertoire of one miRNA contributes to its distinct functional role, miR-22 leads to the opposite effects on the regulation of the same target gene PTEN and the acquisition of tumor cell phenotypes. Further investigations will be required to elucidate this cellular context-dependent role of miR-22 as a key negative or positive regulator of PTEN, and as a tumor suppressor or an oncogene.

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BIO 1140 Study Guide - Midterm Guide: Troponin, Protein Isoform, Alternative Splicing

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