BIO 181 Lab Instructions: Cell Biology Act II Mission Memo

Lab Instructions: Cell Biology Act II Mission Memo Greetings Fellow Explorer: What an incredible medical discovery we have made together! A contagious cancer is one of the rarest diseases throughout the galaxy. If left untreated, the cancer will not only spread from the lungs to other organs, but will spread from sick gliders to healthy gliders. Fortunately, we have collected data needed to determine how the tumor cells differ from healthy cells. The elevated concentration of Growth Factor L in the blood of spotted gliders provides a clue to the mutations responsible for the cancer. We may be able to use this information to devise a treatment that targets tumor cells. Use the following questions to guide your work: ● Which receptors in the cell membrane bind Growth Factor L? (Appendix 1) ● Which proteins in the cytoplasm are activated when a receptor binds Growth Factor L? (Appendix 2) ● Should we treat the cancer of spotted gliders with a drug or a virus? (Appendix 3) Universally in your debt, The AI Note: You will be using the program Microsoft Excel for this assignment. We have provided links to Excel tutorials and transcripts where applicable, to help you answer the questions. Appendix 1 Which receptors in the cell membrane bind to Growth Factor L? Cancer—the uncontrolled growth of abnormal cells—results from a malfunction in a signaling pathway. The figure below shows a signaling pathway that regulates cell division in spotted gliders. When the signaling pathway is in the inactive state, a protein called CDI2 is in its active form and prevents the cell from dividing. All other proteins (R1, KR1, KR2, KR3, and CDP1) are in their inactive form. When the signaling pathway is in the active state, the following steps occur: 1) A signal (SR1) binds to a receptor (R1), activating this receptor through phosphorylation. 2) The active form of R1 binds and phosphorylates a kinase (KR1). 3) The active form of KR1 binds and phosphorylates a second kinase (KR2). 4) The active form of KR2 binds and phosphorylates a third kinase (KR3). 5) The active form of KR3 interacts directly with two proteins, CDP1 and CDI2. KR3 activates CDP1, which enables CDP1 to promote cell division. KR3 inactivates CDI2, preventing CDI2 from inhibiting cell division—thus enabling cell division to occur. Figure 1. The signaling pathway that regulates cell division in spotted gliders. Upper left: The signaling molecule (SR1) binds to the receptor (R1). Center: When no signaling molecule is bound to the receptor, most proteins in the signaling pathway are inactive, but a protein that represses cell division (CDI2) is active. Right: When a signaling molecule is bound to the receptor, most proteins in the signaling pathway become active. The first three proteins in the pathway (KR1-KR3) are activated by phosphorylation. The protein KR3 inactivates CDI2, which prevents CDI2 from inhibiting cell division. KR3 also activates CDP1, which directly promotes cell division. When examining the spotted gliders, we discovered an elevated concentration of a second type of signal, which Phygaran scientists called Growth Factor L (abbreviated as GF-L). According to my database, GF-L only reaches these concentrations during the embryonic stage early in the development of spotted gliders, when cells are rapidly dividing. By experimenting with some cells from a spotted glider, you discovered that GF-L binds to receptors in the membrane of a tumor cell. We might presume that these receptors are the same as R1, which would explain how GF-L promotes cell division (see Fig. 1). However, after you left the Intergalactic Wildlife Sanctuary, I analyzed the membrane of tumor cells and discovered a second type of receptor, R2, that has a similar structure to R1. According to research conducted on Phygaris, spotted gliders usually produce R2 as embryos when rapid cell division creates new tissues and organs. R2 is not usually expressed in adult gliders. We need to understand the role that GF-L plays in the cancer of spotted gliders. To begin, let’s determine whether GF-L binds to R1 or R2. This knowledge would help us identify the cause of the cancer. We will follow two steps to answer the question “Is Growth Factor L binding to Receptor 1 or Receptor 2?” Step 1: Anticipate your analysis: Determine what you should observe if GF-L binds to R1, R2, both receptors, or neither receptor. This step will help us identify the evidence needed to build an argument in Step 3. Step 2: Model the effects of GF-L on the activity of R1 and the activity of R2: Determine how the presence of GF-L affects the activity of R1 and the activity of R2. This step gives us the evidence needed to build an argument in Step 3, when we will conclude whether GF-L binds to R1, R2, both receptors, or neither receptor. Step 3: Weigh the evidence and conclude if GF-L binds to R1, R2, both receptors, or neither receptor: Construct an argument to answer the question “Does GF-L bind only to R1, only to R2, both receptors, or neither receptor?” Your argument should draw on your answers in Steps 1 and 2.