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You work for a biotech company that is designing genetic regulatory circuits that could be used to combat cancer. The company aims to one day introduce controllable genetic constructs that would express BAX, a protein that initiates apoptosis (cell death), specifically in cancer cells in order to eradicate tumors. a) One colleague suggests the system below as a way to test some genetic 'circuitry' in a cell. TetR is a transcriptional repressor protein that binds to TetR binding sites and represses the expression of promoters (arrows) directly downstream of the binding site. Lacl is a repressor that binds to Lacl binding sites, but will fail to bind DNA in the presence of the drug IPTG. Assume all indicated promoters are active in this cell type unless repressed. If this construct was introduced into a cell, what set of growth conditions would be required to induce cell death via BAX? Lacl binding site Lac! BAX b) Realizing that the scheme above may not be a clinically viable, you instead consider a modified design consisting of the set of two different genetic constructs below. Here, a new site (labeled sRNA binding) is added which is complimentary to a small RNA that is highly expressed only in cancer cells; all other pieces function as above. Would this design theoretically be able to induce apoptosis specifically in human cancer cells? Why or why not? Your answer should briefly describe the sequence of regulatory events that would occur in both a normal and a cancerous cell. TetR

You work for a biotech company that is designing genetic regulatory circuits that could be used to combat cancer. The company aims to one day introduce controllable genetic constructs that would express BAX, a protein that initiates apoptosis (cell death), specifically in cancer cells in order to eradicate tumors. a) One colleague suggests the system below as a way to test some genetic 'circuitry' in a cell. TetR is a transcriptional repressor protein that binds to TetR binding sites and represses the expression of promoters (arrows) directly downstream of the binding site. Lacl is a repressor that binds to Lacl binding sites, but will fail to bind DNA in the presence of the drug IPTG. Assume all indicated promoters are active in this cell type unless repressed. If this construct was introduced into a cell, what set of growth conditions would be required to induce cell death via BAX? Lacl binding site Lac! BAX b) Realizing that the scheme above may not be a clinically viable, you instead consider a modified design consisting of the set of two different genetic constructs below. Here, a new site (labeled sRNA binding) is added which is complimentary to a small RNA that is highly expressed only in cancer cells; all other pieces function as above. Would this design theoretically be able to induce apoptosis specifically in human cancer cells? Why or why not? Your answer should briefly describe the sequence of regulatory events that would occur in both a normal and a cancerous cell. TetR

Human Anatomy & Physiology (11th Edition)
Human Anatomy & Physiology (11th Edition)
11th Edition
ISBN:9780134580999
Author:Elaine N. Marieb, Katja N. Hoehn
Publisher:Elaine N. Marieb, Katja N. Hoehn
Chapter1: The Human Body: An Orientation
Section: Chapter Questions
Problem 1RQ: The correct sequence of levels forming the structural hierarchy is A. (a) organ, organ system,...
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You work for a biotech company that is designing genetic regulatory circuits that could be used to combat cancer. The company aims to one day introduce controllable genetic constructs that would express BAX, a protein that initiates apoptosis (cell death), specifically in cancer cells in order to eradicate tumors. a) One colleague suggests the system below as a way to test some genetic 'circuitry' in a cell. TetR is a transcriptional repressor protein that binds to TetR binding sites and represses the expression of promoters (arrows) directly downstream of the binding site. Lacl is a repressor that binds to Lacl binding sites, but will fail to bind DNA in the presence of the drug IPTG. Assume all indicated promoters are active in this cell type unless repressed. If this construct was introduced into a cell, what set of growth conditions would be required to induce cell death via BAX? Lacl binding site TetR SRNA binding Lacl TetR binding site TetR binding site b) Realizing that the scheme above may not be a clinically viable, you instead consider a modified design consisting of the set of two different genetic constructs below. Here, a new site (labeled sRNA binding) is added which is complimentary to a small RNA that is highly expressed only in cancer cells; all other pieces function as above. Would this design theoretically be able to induce apoptosis specifically in human cancer cells? Why or why not? Your answer should briefly describe the sequence of regulatory events that would occur in both a normal and a cancerous cell. TetR BAX BAX
Transcribed Image Text:You work for a biotech company that is designing genetic regulatory circuits that could be used to combat cancer. The company aims to one day introduce controllable genetic constructs that would express BAX, a protein that initiates apoptosis (cell death), specifically in cancer cells in order to eradicate tumors. a) One colleague suggests the system below as a way to test some genetic 'circuitry' in a cell. TetR is a transcriptional repressor protein that binds to TetR binding sites and represses the expression of promoters (arrows) directly downstream of the binding site. Lacl is a repressor that binds to Lacl binding sites, but will fail to bind DNA in the presence of the drug IPTG. Assume all indicated promoters are active in this cell type unless repressed. If this construct was introduced into a cell, what set of growth conditions would be required to induce cell death via BAX? Lacl binding site TetR SRNA binding Lacl TetR binding site TetR binding site b) Realizing that the scheme above may not be a clinically viable, you instead consider a modified design consisting of the set of two different genetic constructs below. Here, a new site (labeled sRNA binding) is added which is complimentary to a small RNA that is highly expressed only in cancer cells; all other pieces function as above. Would this design theoretically be able to induce apoptosis specifically in human cancer cells? Why or why not? Your answer should briefly describe the sequence of regulatory events that would occur in both a normal and a cancerous cell. TetR BAX BAX
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