What information did the study of the crown gall disease provide that was critical for plant genetic engineering? Discovery of a plasmid that can integrate within the genome of plants Understanding the role of plant hormones in growth promotion Understanding the role of opine synthesis enzymes in tumor progression Knowledge of plant tumor inducing genes
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What information did the study of the crown gall disease provide that was critical for plant genetic engineering?
- Discovery of a plasmid that can integrate within the genome of plants
- Understanding the role of plant hormones in growth promotion
- Understanding the role of opine synthesis enzymes in tumor progression
- Knowledge of plant tumor inducing genes
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- One example of innovation from an unexpected source came from the study of tumor-like plant growths caused by Agrobacterium tumefaciens. What information did the study of the plant tumors provide that was critical for plant genetic engineering? O learning that metastasis is critical for tumor progression Olearning how A. tumefaciens uses plant pathways to synthesize beta carotene Oknowledge of plant tumor suppressor genes and their role in tumor development Othe ability of A. tumefaciens to integrate its genes into the plant genomeIs it correct to say that the palladin gene causes cancer?The introduction of genes into plants is a common practice that has generated not only a host of genetically modified foodstuffs, but also significant worldwide controversy. Interestingly, a tumor-inducing plasmid is often used to produce genetically modified plants. Is the use of a tumor-inducing plasmid the source of such controversy?
- One hallmark of cancer cells is their ability to divideindefinitely, in contrast with most normal somaticcells that undergo senescence after 30 to 50 generations of divisions. We saw in this chapter that one reason for this difference is that many cancer cellsexpress the telomerase enzyme that can mediate telomere lengthening.Interestingly, about 15% of tumors do not expresstelomerase. Instead, they lengthen their telomeres byan alternative pathway. Tumor cells of this class appear to have telomeres that are highly heterogenous inlength; some telomeres have many more TTAGGGrepeats than others.a. Diagram an event involving homologous recombination that would allow some telomeres in thesecells to become longer. What feature(s) of telomeresmake(s) such homologous recombination possible?b. Does this recombination need to occur between homologous telomeres (that is, telomeres of the samearm of the same chromosome)? If such recombination could occur between nonhomologous telomeres, how might…Part A and B A. What below would be likely to lead to cancer development? A) Overexpression of a cell cycle checkpoint inhibitor B) Loss of expression of a growth factor that promotes cell cycle entry C) Overexpression of a receptor tyrosine kinase that promotes cell cycle entry D) Overexpression of a DNA damage repair enzyme E) Loss of expression of a regulatory transcription factor that activates transcription of a cyclin B. Taxols inhibit the proper function of microtubules and are frequently used as chemotherapy drugs. What is the function of microtubules during the cell cycle? A) They promote the G1 to S checkpoint B) They normally inhibit M phase from being completed C) They form the mitotic spindle E) They mediate DNA replication F) They form the cleavage furrow during cytokinesisYou are a developmental geneticist studying flowering time variation in Arabidopsis. You perform a mutagenesis screen to identify mutants in the photoperiod pathway. Given what you know about photoperiodism in Arabidopsis, what phenotype are you looking for and under what photoperiodic conditions would you perform the experiment? delayed flowering in long days delayed flowering in short days same flowering in short days early flowering in short days same flowering in long days early flowering in long days
- Personalized cancer treatments involve identifying specific pathways in an individual tumor and selecting drugs that are effective for the modified pathways. One way to do this is to take culture cells from a biopsy of a specific paient and test the effects of a battery of drugs on the patiets cells in culture. How might heterotypic interactions complicate this strategy? How might cells be cultured differently to minimize these complications (limit 5-6 sentences)?Why is it important to model cancer through the generation of induced pluripotent stem cells ? Explain in detail the main findings. Please sort as a list.To identify genes controlling the cell cycle in budding yeast, a genetic screen was carried out. In this screen, haploid yeast cells were exposed to a DNA damaging agent to introduce random mutations in the genome. By culturing cells at an elevated temperature (e.g. 37 degrees), where many mutated genes lose their function, scientists identified yeast mutants that showed growth defects and arrest at specific stages of the cell cycle (e.g. in mitosis with large buds). In this screen, mutants of the cyclin-dependent kinase were identified, but not mutants of cyclins. Explain the reason for this outcome.
- Describe how Ras and p53 can alter the simplified genetic pathway controlling cell division shown below. For each of the two genes, would uncontrolled cell division result from a loss-of-function or a gain-of-function mutation? growth factors - receptors - cyclins - cyclin-dependent kinases - cell divisionIn roses, the synthesis of red pigment is by two steps ina pathway, as follows:colorless intermediate gene Pmagenta intermediate red pigment gene Qa. What would the phenotype be of a plant homozygousfor a null mutation of gene P?b. What would the phenotype be of a plant homozygousfor a null mutation of gene Q?c. What would the phenotype be of a plant homozygousfor null mutations of genes P and Q?d. Write the genotypes of the three strains in parts a, b,and c.e. What F2 ratio is expected from crossing plants fromparts a and b? (Assume independent assortment.)Why is it important to model cancer through the generation of induced pluripotent stem cells ? Please list item by item. Explain in detail the main findings.