Mice that are engineered to block expression of the gene coding for telomerase protein age at a much faster rate than normal and have a decreased life span. The results of these mice experiments led researchers to propose that treatments that could lead to overexpression of the telomerase gene might serve as the “fountain of youth” leading to reversal of aging in humans. Why should we be very cautious about trying such treatments? Why it might be advantageous for multicellular organisms for most of their somatic cells not to express telomerase?

Mice that are engineered to block expression of the gene coding for telomerase protein age at a much faster rate than normal and have a decreased life span. The results of these mice experiments led researchers to propose that treatments that could lead to overexpression of the telomerase gene might serve as the “fountain of youth” leading to reversal of aging in humans. Why should we be very cautious about trying such treatments? Why it might be advantageous for multicellular organisms for most of their somatic cells not to express telomerase?

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Description: Mice that are engineered to block expression of the gene coding for telomerase protein age at a much faster rate than normal and have a decreased life span.The results of these mice experiments led researchers to propose that treatments that could le

Biology Today and Tomorrow without Physiology (MindTap Course List)

5th Edition

ISBN:9781305117396

Author:Cecie Starr, Christine Evers, Lisa Starr

Publisher:Cecie Starr, Christine Evers, Lisa Starr

Chapter6: Dna Structure And Function

Section: Chapter Questions

Problem 2CT

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n yeast cells, telomerase remains active and maintains telomeres of about 300 base pairs. Propose what would happen to the telomeres over time in a yeast lineage in which the following mutations were created. The gene encoding the catalytic subunit of the telomerase is deleted.
In yeast cells, telomerase remains active and maintains telomeres of about 300 base pairs. Describe how the telomeres would change over time in a yeast lineage after the following mutations were created. a. The gene encoding the catalytic subunit of the telomerase is inactivated. b. The template portion of the telomerase RNA is changed from 5’-ACACCCACA to 5’-ACAUCUACA.
In yeast cells, telomerase remains active and maintains telomeres of about 300 base pairs. Propose what would happen to the telomeres over time in a yeast lineage in which the following mutations were created. a) The gene encoding the catalytic subunit of the telomerase is deleted. b) The template portion of the telomerase RNA is changed from 5’-ACACCCACA to 5’-ACAUCUACA.
In yeast cells, telomerase remains active and maintains telomeres of about 300 base pairs. Propose what would happen to the telomeres over time in a yeast lineage in which the following mutations were created. a) The gene encoding the catalytic subunit of the telomerase is deleted. b) What happens to the yeast telomeres over time if the telomerase RNA retains the same anchor but is altered in its templating region?
If you knew the mRNA sequence for the human insulin gene could you know what size cDNA fragment you would find on your DNA gel when you ran it against a size standard (a “molecular ruler”)? Would you continue with your insulin cloning experiment, if the DNA from your PCR was very different in size from that predicted by the insulin mRNA? Why or why not? Primers can sometimes bind and target the wrong gene, especially if the primers are allowed to bind to the DNA strands at a low temperature. PCR also preferentially amplify short segments of DNA. Would it be important to actually run the cDNA after the PCR on a DNA gel in order to check for a PCR product of the predicted size for the insulin gene? Why or why not?
Rsearcher has discovered that one human promoter is responsible for producing two different proteins (Protein K and Protein B) from the same gene. In Kidney cells it is responsible for the production of Protein K, while in Brain cells it is responsible for the production of Protein B. How are these different proteins being produced from the same gene? Describe the mechanism
The enzyme telomerase is part protein and part RNA. What would be the most likely effect of a large deletion in the gene that encodes the RNA component of telomerase? How would the function of telomerase be affected?
Why do adult human cells (other than germ cells and stem cells) NOT express the enzyme telomerase? In other words what benefit does not having telomerase provide to these cells?
If you knew the mRNA sequence for the human insulin gene could you know what size cDNA fragment you would find on your DNA gel when you ran it against a size standard (a “molecular ruler”)? Would you continue with your insulin cloning experiment, if the DNA from your PCR was very different in size from that predicted by the insulin mRNA? Why or why not?
The amino acid asparagine is synthesized from aspartic acid by the enzyme asparagine synthetase (AS). In the previous problem you proposed a model for how this gene could be regulated. Suppose that you carry out an experiment to test your model. To do this you cut out the regulatory sequences upstream of the gene and fuse it to a gene for green fluorescent protein (GFP). Now you can visually observe when the gene is activated. You insert this engineered gene into a host cell and look for GFP expression. You discover some mutants that have different expression levels of GFP and call them GFP1- and GFP2-. The expression levels of GFP are given below. Cell GFP expression Wild type 100 GFP1- 50 GFP2- 0 Propose an explanation for these results based on your model. In other words, what was mutated and how? This answer should include whether the mutation is (view links for more information): dominant or recessive https://www.ncbi.nlm.nih.gov/books/NBK21578/#A1877 in a cis…
The amino acid asparagine is synthesized from aspartic acid by the enzyme asparagine synthetase (AS). In the previous problem you proposed a model for how this gene could be regulated. Suppose that you carry out an experiment to test your model. To do this you cut out the regulatory sequences upstream of the gene and fuse it to a gene for green fluorescent protein (GFP). Now you can visually observe when the gene is activated. You insert this engineered gene into a host cell and look for GFP expression. You discover some mutants that have different expression levels of GFP and call them GFP1- and GFP2-. The expression levels of GFP are given below. Cell GFP expression Wild type 100 GFP1- 50 GFP2- 0 Propose an explanation for these results based on your model. In other words, what was mutated and how? Your answer should include whether the mutation is (see links for more information): dominant or recessive https://www.ncbi.nlm.nih.gov/books/NBK21578/#A1877…
Woolly mammoths have been extinct for about 4,000 years, but we often find their well-preserved remains in Siberian permafrost. Research groups are now planning to use SCNT to resurrect these huge elephant-like mammals. No mammoth eggs have been recovered yet, so elephant eggs would be used instead. An elephant would also be the surrogate mother for the resulting embryo. The researchers may try a modified SCNT technique used to clone a mouse that had been dead and frozen for 16 years. Ice crystals that form during freezing break up cell membranes, so cells from the frozen mouse were in bad shape. Their DNA was transferred into donor mouse eggs, and cells from the resulting embryos were fused with undifferentiated mouse cells. Four healthy clones were born from the hybrid embryos. What are some of the pros and cons of cloning an extinct animal?