Golgi Maturation. The way that proteins move through the golgi has long been a source of contention. Two major models have been proposed. One is a cisternal maturation model, and the other is a model of stable cisternae and mostly vesicular transport. In this paper they set out to try and differentiate these models using a modified Golgi resident protein.

In this paper they talk a bit about Golgi Tubules, these are like vesicles but form as long tubes rather then little circles… don’t worry too much about this issue.

Intro Questions (from last weeks panopto’s and the intro of the paper)

1) What is the main role of the golgi? How do the processes that are occurring differ from one stack to another (in other words, why have different stacks) – what is happening to proteins in these stacks?

2) What are the two main models of Golgi maturation? What is the different between Golgi resident proteins, and proteins moving through the endomembrane system? How would you expect the paths of these two protein types to be different?

Figure Questions:

Figure 1: What is Mani? How is Mani-FM different, and what is happening to Mani-FM when they add AP what about when AP is absent? What is the pellet vs supernatant test telling them?

Figure 2: What is Figure 2 showing them? Why did they do this test?

Figure 3: What are the main findings of figure 3?

Figure 4 a-i : What do they find about the localization of MANI-FM with and without AP within the golgi? Which of the two mechanisms of golgi maturation does this support?

Figure 4 j&k – what does this tell them about Mani-Fm with and without AP?

Figure 5: How is what they are doing in this figure different from what they did in Figure 4? What is this showing them? What did the washout tell them that the initial application did not? Given your knowledge of golgi trafficking, what kind of vesicles would you expect to fine Mani-FM in?

Conclusion Questions: What are the overall conclusions from the paper? Which model of Golgi trafficking does this support? Why is this interesting to us?

More Challenging questions: How are there findings different from previous work? What did they show that no-one has showed about this model before?

Be sure to include a bibliography of your sources.

Golgi Maturation

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Biology. Please read it carefully and answer the questions:

Q1: Each Student must find two types of differentiated cells- (1 animal, 1 plant)

(No repeats so first come first serve)

· Post

· An image of the cell,

· A quick description of the cell

· Answer this question “what makes that type of cell unique”.

· Include a source link to your where you found your type of cell & information.

· Present

· To start the next class period each student will have 1 minute to present their cells.

As a class we will have a comprehensive list of differentiated cells.

Q2: How many genes do we have written into our DNA?

Q3: DNA Helicase is the blue donut shaped protein that does what?

Q4: Because DNA is antiparellel one strand must be copied backwards. As DNA polymerase creates loops of DNA and copies these sections called okazaki fragments. A specific molecular machine or enzyme called DNA ligase joins these fragmented sections of DNA together to a complete strand of DNA? Google to find they type of bond DNA ligase catalyzes.

Q5: DNA is only about 2 nanometers thick, but DNA is about 30 to 40 million nanometers long. How long is DNA in centimeters?

Q6: To keep the DNA organized and regulate access to the genetic code DNA is wrapped around what purple colored proteins?

Q7: There are approximately 37.2 trillion cells in a human body. Drew Berry says that roughly how many cells are undergoing the process of mitosis right now? (Dozens, Thousands, or Billions of cells).

Q8: What is the wisker like dynamic scaffolding that pulls the duplicated chromosomes to the opposite sides of the cell during cell division?

Q9: How can can errors in, or damage to your DNA (f not repaired) cause premature aging?

Q10: Why are some DNA mutations beneficial?

Q11: Defects in DNA repair are associated with many kinds of cancer. Cancer is when a cell loses control of its replication. How can a mistake in DNA cause cancer?

Q12: What was the goal of the Human Genome Project?

Q13: What makes you, you? Where do the instructions that make you, you come from? What are these instructions stored on?

Q14: What are the 4 main chemicals or nucleotide bases of DNA?

Q15: How many base pairs are in the human genome?

Q16: Nutritional experts say that eating 1/2 lb of meat a week is healthy but the average American eats 1/2 lb a day. How does this lead to micro-nutrient malnutrition?

Q17: Use this video to dig a bit deeper into Mitosis- and answer the below.

On a blank sheet of paper-

1- Sketch out the cell cycle- G1, G0, S, G2, M

2-sketch the phases of mitosis- interphase, prophase, metaphase, anaphase, telophase, cytokinesis (include the nuclear envelope, nuclear envelope fragments, the accurate number of chromosomes through all the stages, spindle fibers, spindle poles,

Biology

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