Test Bank For Biotechnology 2nd Edition by David P. Clark, Nanette J. Pozdernik

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Clark: Biotechnology, 2nd Edition

 

Chapter 1: Basics of Biotechnology

 

 

1. Which of the following statements has no bearing on cancer?
   1. As cancer develops, at least two mutations are required.

*b. Mutations on embryonic development are very deleterious.

1. For microtumors to continue growing, angiogenesis is required.
2. Somatic mutations after the organism reaches maturity may be involved in cancer.

 

2. Which of the following statements about causes of cancer is NOT true?
   1. Cancer-causing agents are called carcinogens.
   2. Cancers occur more often in tissues that have growing, dividing cells.

*c. Nerves and muscles grow quickly and account for more than half of all cancers.

1. Cigarettes, harmful chemicals, and nuclear radiation may all contribute to cancer.
2. Carcinogens are also usually mutagen

 

3. Which of the following happens during the G1 phase of the cell cycle?
   1. Externals factors that bind to receptors and promote synthesis of cyclin D
   2. The phase of cell cycle when DNA is replicated and chromosomes are duplicated.

*c. During this phase of cell cycle, the cell increases in size.

1. G1 factors prevent the ending of M phase

 

4. Which of the following happen during the S phase of the cell cycle?
   1. Externals factors that bind to receptors and promote synthesis of cyclin D

*b. The phase of cell cycle when DNA is replicated and chromosomes are duplicated.

1. During this phase of cell cycle, the cell increases in size.
2. G1 factors prevent the ending of M phase

 

5. Cyclin-dependent kinases are

*a. Factors that bind to cyclin, and then phosphorylate other proteins to initiate the next phase of the cell cycle

1. External factors that bind to receptors and promote synthesis of cyclin D
2. Proteins that removes phosphates from cyclins and prevents the cell cycle from progressing
3. All of the above are correct

 

6. Growth factors are
   1. Factors that bind to cyclin and then phosphorylate other proteins to initiate the next phase of the cell cycle

*b. External factors that bind to receptors and promote synthesis of cyclin D

1. Proteins that remove phosphates from cyclins and prevent the cell cycle from progressing
2. A and B are correct

 

7. Which of the following domains are not part of a growth factor receptor?
   1. Extracellular binding site
   2. Transmitter region
   3. Tyrosine kinase domain

*d. Oncogene domain

 

8. The extracellular binding site of a growth factor receptor

*a. Is the portion of the protein that receives its specific signal molecule or growth factor

1. Is the hydrophobic portion of the receptor
2. Dimerizes and initiates a phosphorylation cascade
3. Only attaches to the cell via integrins

 

9. The tyrosine kinase domain of a growth factor receptor
   1. Is the portion of the protein that receives its specific signal molecule or growth factor
   2. Is the hydrophobic portion of the receptor

*c. Dimerizes and initiates a phosphorylation cascade after a signal is received

1. Only attaches to the cell via integrins

 

10. Susceptibility genes are
    1. Genes involved in suppressing the growth of cancer
    2. Genes that cause cancer with a dominant phenotype

*c. Genes passed from one generation to the next that lead to hereditary increased incidence of cancer

1. Genes that make you more susceptible to viral infections

 

11. Oncogenes are
    1. Genes involved in suppressing the growth of cancer

*b. Genes that cause cancer with a dominant phenotype

1. Genes passed from one generation to the next that lead to hereditary increased incidence of cancer
2. Genes that make you more susceptible to viral infections

 

12. Anti-oncogenes are

*a. Genes involved in suppressing the growth of cancer

1. Genes that cause cancer with a dominant phenotype
2. Genes passed from one generation to the next that lead to hereditary increased incidence of cancer
3. Genes that make you more susceptible to viral infections

 

13. With respect to the growth of cells in culture, which of the following statements is NOT true?
    1. Healthy cells that pick up DNA from cancerous cells are said to be transformed.

*b. Normal cultured cells grow on top of each other and aggregate into heaps.

1. Transformed cell in culture can be injected into mice and tumors will form.
2. Cancerous cells exhibit anchorage independence in which they can move around and proliferate in an “incorrect” position in the body.

 

14. Which of the following are NOT factors involved in the control of cell division of specific tissues.
    1. Transcription factors
    2. Cell surface receptors

*c. Transport proteins

1. Growth factors
2. Signal transduction proteins

 

15. Which of the following is NOT true of the oncogenic form of RAS protein?
    1. It receives signals from outside the cell.
    2. It binds GTP to turn itself on but cannot split the GTP to turn itself off.

*c. It floods the cell with cell division signals for short periods of time.

61. The oncogenic RAS differs from the normal protein at position 12, 13, or 61.
62. Oncogenic RAS is frequently detected in cancer of the lung, colon, and thyroid.

 

16. Myc can become an oncogene by which of the following mechanisms?
    1. A single base change is involved in converting the protein to a form that is always active.
    2. The myc gene is mistakenly duplicated 50-100 times.
    3. A chromosomal translocation leaves the gene under control of a much more highly active promoter.
    4. All of the above.

*e. Some of the above.

 

17. Which of the following statement regarding anti-oncogenes or tumor-suppressor genes is NOT true?
    1. Both copies must be mutated in order for cancer to initiate,
    2. The Rb gene has been named for the rare cancer of the retina.
    3. Mutations in these genes are recessive.
    4. Some anti-oncogenes are very tumor specific.

*e. Wild-type anti-oncogene products act directly on oncogene products to suppress cancer.

 

18. The protein, p53, is
    1. An anti-oncogene activated by another and blocks the action of all cyclins.

*b. An anti-oncogene that gives a dominant negative phenotype.

1. An anti-oncogene located on chromosome 16 and blocks the action of cyclin A.
2. An anti-oncogene blocks cyclin E, stopping cell cycle just before S phase.

 

19. The protein, p21, is

*a. An anti-oncogene activated by another and blocks the action of all cyclins.

1. An anti-oncogene that gives a dominant negative phenotype.
2. An anti-oncogene located on chromosome 16 and blocks the action of cyclin A.
3. An anti-oncogene blocks cyclin E, stopping cell cycle just before S phase.

 

20. The protein, p16, is
    1. An anti-oncogene activated by another and blocks the action of all cyclins.
    2. An anti-oncogene that gives a dominant negative phenotype.
    3. An anti-oncogene located on chromosome 16 and blocks the action of cyclin A.

*d. An anti-oncogene that blocks cyclin E, stopping cell cycle just before S phase.

 

21. Which of the following is NOT a step in the formation of most colon cancers?
    1. Mutation in one copy of the p53

*b. Mutation in the Rb anti-oncogene.

1. Inactivation of both APC anti-oncogenes.
2. Activation of the Ras oncogene.
3. Mutations of both DCC anti-oncogenes.

 

22. With respect to inherited susceptibility to cancer, which of the following is NOT true?
    1. Genes that affect the rate of mutation are inherited and are associated with cancer.
    2. Inheriting one defective copy of an anti-oncogene is associated with cancer.

*c. 25% of cancers are due to inherited defects.

1. BRCA1 and BRCA2 are examples of mutator genes.
2. Inheriting 2 defective copies of an anti-oncogene is lethal.

 

23. HTLV-1 can cause which of the following types of cancer?
    1. Karposi’s sarcoma
    2. Burkitt’s lymphoma
    3. Liver cancer
    4. Cervical cancer, skin cancer

*e. Adult T-cell leukemia

 

24. Hepatitis B can cause which of the following types of cancer?
    1. Karposi’s sarcoma
    2. Burkitt’s lymphoma

*c. Liver cancer

1. Cervical cancer, skin cancer
2. Adult T-cell leukemia

 

25. Epstein-Barr virus can cause which of the following types of cancer?
    1. Karposi’s sarcoma

*b. Burkitt’s lymphoma

1. Liver cancer
2. Cervical cancer, skin cancer
3. Adult T-cell leukemia

 

26. Human herpesvirus 8 can cause which of the following types of cancer?

*a. Karposi’s sarcoma

1. Burkitt’s lymphoma
2. Liver cancer
3. Cervical cancer, skin cancer
4. Adult T-cell leukemia

 

27. Human papillomavirus can cause which of the following types of cancer?
    1. Karposi’s sarcoma
    2. Burkitt’s lymphoma
    3. Liver cancer

*d. Cervical cancer, skin cancer

1. Adult T-cell leukemia

 

28. Which of the following is a method for generating an oncolytic virus?
    53. Change the recognition protein of mumps virus so it will bind to p53.
    54. Change the recognition protein of measles virus so it will bind to p53.

*c. Change the recognition protein of measles virus so it will bind to CD38 or EGFR.

1. Change the recognition protein of measles virus so it inhibits cyclin E.
2. Change the recognition proteins of mumps virus so it will bind to CD38 or EGFR.

 

29. An anti-cancer therapy targeting PARP would cause .
30. an accumulation of poly(ADP-ribose) chains
31. activation of base excision repair pathways
32. decreased apoptosis
33. mitotic spindle malformation

*e. an increased incidence of double-strand breaks in the DNA

 

30. Which of the following is a small molecule anti-cancer agent that targets microtubules of the mitotic spindle?

*a. colchicine

1. alvocidib
2. seliciclib
3. anthracycline
4. cis-platin

 

31. The  is an example of a tumor-suppressor miRNA.
32. myc
33. p53

*c. miR-34

1. miR-21
2. STAT3

 

Clark: Biotechnology, 2nd Edition

 

Chapter 5: RNA-Based Technologies

 

 

1. Antisense RNA is a
2. RNA that can be found in the ribosome that can carry out catalysis.

*b. RNA with sequence complementary to an mRNA, this RNA will prevent translation.

1. Small non-coding RNA molecules that modulate gene expression
2. Small non-coding RNA that identifies an mRNA and triggers degradation

 

2. Short-interfering RNA (siRNA) are
3. RNAs that can be found in the ribosome that can carry out catalysis.
4. RNAs with sequence complementary to an mRNA, this RNA will prevent translation.
5. Small non-coding RNA molecules that modulate gene expression

*d. Small non-coding RNAs that identify an mRNA and trigger its degradation

 

3. MicroRNAs are
4. RNAs that can be found in the ribosome that can carry out catalysis.
5. RNAs with sequence complementary to an mRNA, this RNA will prevent translation.

*c. Small non-coding RNA molecules that modulate gene expression

1. Small non-coding RNAs that identify an mRNA and trigger its degradation

 

4. Ribozymes are

*a. RNAs that can be found in the ribosome that can carry out catalysis.

1. RNAs with sequence complementary to an mRNA, this RNA will prevent translation.
2. Small non-coding RNA molecules that modulate gene expression
3. Small non-coding RNAs that identify an mRNA and trigger its degradation

 

5. RNAI and RNAII are sense and antisense partners controlling this process.
6. Control of HIV gene expression
7. Developmental control of nFGF

*c. Control of ColE1 replication

1. Control of Neurospora circadian rhythm
2. Control of X-chromosome inactivation

 

6. Antisense mRNA binds to cellular mRNA during development of Xenopus laevis and degrades the message.
7. Control of HIV gene expression

*b. Developmental control of nFGF

1. Control of ColE1 replication
2. Control of Neurospora circadian rhythm
3. Control of X-chromosome inactivation

 

7. Involves the use of xist
8. Control of HIV gene expression
9. Developmental control of nFGF
10. Control of ColE1 replication
11. Control of Neurospora circadian rhythm

*e. Control of X-chromosome inactivation

 

8. Antisense env mRNA binds to the Rev response element, blocking production of protein.

*a. Control of HIV gene expression

1. Developmental control of nFGF
2. Control of ColE1 replication
3. Control of Neurospora circadian rhythm
4. Control of X-chromosome inactivation

 

9. Regulated by antisense and sense mRNA for the frq
10. Control of HIV gene expression
11. Developmental control of nFGF
12. Control of ColE1 replication

*d. Control of Neurospora circadian rhythm

1. Control of X-chromosome inactivation
2. Regulated by antisense and sense mRNA for the frq gene.

 

10. Antisense oligonucleotides may alter aberrant splicing. Which two of the following are examples of human diseases and the gene involved with aberrant splicing.
11. The env mRNA in HIV and the antisense oligonucleotides for splice site in beta-globin gene.

*b. The antisense oligonucleotide for Bcl-x splice sites in cancer and the antisense oligonucleotides for splice site in beta-globin gene.

1. The antisense oligonucleotide for Bcl-x splice sites in cancer and the antisense oligonucleotide for the env MRNA in HIV.
2. None of the above.

 

11. Major challenges to studying the use of antisense technology in the lab include all of the following EXCEPT:
12. Nonspecific interactions with other molecules in the cells.

*b. The sensitivity to of dsRNA to RNase H.

1. Targeting regions of mRNA that may fold back on themselves.
2. The decision to synthesize the oligonucleotides chemically or to clone antisense genes.

 

12. Which of the following delivery methods are used to deliver antisense RNA to cells:
13. Liposomes
14. Cationic polymers
15. Streptolysin
16. Scrape loading

*e. All of the above

13. Fill-in: With RNA interference (RNAi), ______ triggers _______ to degrade the mRNA into short interfering RNA or siRNA.
14. siRNA, dicer
15. antisense RNA, slicer

*c. dsRNA, dicer

1. miRNA, drosha

 

14. RNAi has been observed in many organisms and given many names prior to the elucidation of the mechanism. Which of the following terms has NOT been a name for RNAi?
15. Quelling.

*b. Attenuation.

1. Posttranscriptional Gene Silencing.
2. Transcriptional Gene Silencing.
3. All of the above ARE names for RNAi.

 

15. MicroRNAs (miRNAs) are small RNAs that modulate gene expression by
16. Cutting stem loops.
17. Binding to target RNA and blocking translation.
18. Blocking to the 3’UTR.
19. All of the above.

*e. Some of the above.

 

16. Methods are developed to deliver dsRNA into cells in order to study gene expression. In elegans, which of the following methods is used.
17. Feeding them E. coli that is expressing the RNA
18. Bathing C. elegans in RNA which they then take up into their bodies.
19. Inject the RNA into the worms.

*d. All of the above work to deliver dsRNA to C. elegans.

1. Some of the above will work to deliver RNA to C. elegans.

 

17. Studying RNAi is more problematic in human cell culture than in Drosophila or elegans because:
18. dsRNA cannot get into the cells
19. Interferon is produced triggering RNA degradation.
20. A potent antiviral response is triggered to the dsRNA
21. All of the above are correct.

*e. Some of the above are correct.

 

18. Ribozymes have been found to carry out which of the following processes.
19. Removal of group I introns from other mRNA.
20. Degrade RNA, especially the 5′ end of pre-tRNA
21. Participate in the replication of viroids and satellite viruses.

*d. All of the above.

1. Some of the above.
2. Antisense combined with an engineered ribozyme would work in which of the following ways.
3. Antisense RNA regions on the ends of the RNA find the target and then RNAse H cleaves it. The product is degraded by the ribozyme.
4. Antisense RNA region in the middle of the RNA finds the target and then the ribozymes cleave it.

*c. Antisense RNA regions on the ends of the RNA find the target and then the ribozyme cleaves it.

1. All of the above are mechanisms for ribozyme and antisense RNA function.
2. None of the above are mechanisms for Ribozyme and antisense RNA function.

 

20. Ribozymes can be evolved in vitro and have gained which of the following activities EXCEPT.
21. Catalyzing ligations.
22. Adding metal ions.
23. Carry out nucleophilic attack at phosphoryl, carbonyl, and alkyl halides.
24. Conversion of deoxyribonucleotides to ribonucleotides.

*e. All of the above are activities that evolved ribozymes have gained.

 

21. Riboswitches work by alternating between different RNA secondary structures in an mRNA. Which of the following is NOT true of riboswitch examples
22. Many are found in biosynthetic operons of bacteria

*b. With the thiamine riboswitch, the presence of thiamine is required for the production of mRNA.

1. There are both attenuator mechanisms affecting transcription and translational mechanisms preventing translation off a full length mRNA
2. Riboswitches can be affected by temperature (thermal stress).
3. All of the above are true.

 

22. Regulation of miRNA abundance in eukaryotes is aided with the help of       .
23. miRNA
24. snoRNA
25. gRNA
26. crRNA

*e. circRNA

 

23. ________ rescues stalled ribosomes in bacteria.
24. Xist

*b. tmRNA

1. piRNA
2. snoRNA

 

24. Which of the following RNAs are involved in splicing?
25. TERC

*b. snRNA

1. gRNA
2. miRNA

 

25. ____________ is responsible for transposon silencing in germ lines.
26. tmRNA
27. circRNA
28. tRNA

*d. piRNA

 

26. Dyskeratosis congenital results from a deletion in the protein or RNA portion of telomerase. The RNA portion of telomerase is called and functions                               .
27. TERT; to shorten the telomeres in aging cells

*b. TERC; as a template to increase the length of telomeres

1. Xist; to inactive one X chromosome in mammalian females
2. piRNA; to silence transposons in germ line cells
3. lncRNA; to maintain genome stability

 

27. All of the following statements about the CRISPR system is true except       .
28. The CRISPR system is not found in eukaryotes.
29. CRISPR protects against viruses having either RNA or DNA genomes, hostile plasmids, and transposons.
30. CRISPR is based upon memory of short sequences of nucleic acid that are stored on the bacterial chromosome.

*d. CRISPR targets specific sequences on double-stranded RNA.

1. Stored sequences within the bacterial genome are transcribed and processed into crRNA that are then used by CAS nucleases as guides to seek and destroy foreign nucleic acid.

 

28. Concerning PTEN expression, which non-coding RNA functions to convert the PTEN genome region into heterochromatin to prevent transcription?

*a. PTENpg1 antisense ?

1. PTENpg1 antisense ?
2. PTENpg1 sense
3. DNMT3A
4. EZH2