BIO 181 - General Biology I Mod2 Act2_Student Version Lab Instructions: Cell
Biology Act II Mission Memo 2025 Arizona State University
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 inactive.
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 rapidly divide.
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 GFL’s role 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.
Biology Act II Mission Memo 2025 Arizona State University
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 inactive.
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 rapidly divide.
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 GFL’s role 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.
