BIO 1140 Lecture Notes - Lecture 8: Deoxyribonuclease, Intermediate Filament, Ryanodine

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peardinosaur3

28 Dec 2017

School

University of Ottawa

Department

Biology

Course

BIO 1140

Professor

Caroline Petit- Turcotte

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Document Summary

The caspases are proteototic enzymes so they specifically look for certain combinations in protein and are involved in both pathways that lead to apoptosis but those two pathways are very important both occur in cells: Intrinsic pathway: we will focus on this one. 1000 cells or so and every time it goes through its developing process to become an adult nematode it loses 131 cells, the exaxct same 131 cells. In the nematode these are called c. elegans death genes. And the homologue were identified in mammals as well, they were called apaf1, caspase3, bcl2. Proteases are enzymes that digest proteins, and when we look at the features of apoptosis we sa(cid:449) that the (cid:272)(cid:455)toskeleto(cid:374) shri(cid:374)ks, ho(cid:449) is that possi(cid:271)le, gotta start (cid:271)reaki(cid:374)g it do(cid:449)(cid:374), it"s (cid:373)ade of proteins. Nuclear envelope dissolving has lots of proteins involved, as you break those bonds it becomes easier to break the envelope down. Porteinsn kinases that are involved in maintain cell adhesions, kinases phosphorylate.

Related Questions

Class 6: Viruses (and Cells, continued)

Making connections: viruses and microbes Match the cell biology concept (on page 1) with an important application of that concept (on page 2). Then answer the follow-up questions at the bottom of page 2.

Cell Biology concepts
1. Bacteria that cannot construct new cell wall material become fragile and break down.
2. During influenza infection, the viral enzyme neuraminidase is required to release new viruses from the host cell in which they were made. Once released, the new viruses can infect many additional cells.
3. Thermus aquaticus is a bacterium found in hot springs and can live at temperatures up to ~80Â°C (175Â°F). It has adapted so that its enzymes are most functional at the elevated temperatures, compared with many organismsâ enzymes that function best ~37Â°C (98Â°F).
4. Until the isolation and investigation of retroviruses, scientists thought that RNA could be copied from DNA, but DNA could not be copied from RNA. Research on this class of viruses led to an update to this âCentral Dogmaâ of biology.
5. Some bacteria have adapted, so that the enzymes involved in making cell wall materials have a slightly different shape and can no longer be bound by certain drugs.
6. Rhizobia are bacteria that colonize the roots of certain plants (legumes, including beans and peas). The host plant benefits from the prokaryotesâ ability to âfixâ nitrogen, converting N2 from the atmosphere into a form that is usable by the plant.
7. Many species of bacteria contain the enzyme cellulase. More than 10 billion such bacteria and other symbiotic microbes may be found in a single milliliter of material from inside the digestive system of ruminant mammals.
8. Fungi, including those that cause athleteâs foot, use ergosterol to maintain healthy membranes. Animal cells do not make ergosterol, they use a similar lipid â cholesterol.
9. During retrovirus infection, a DNA copy is made of the virusâs RNA genome. A cut is made in the host cellâs DNA and the DNA copy of the viral genome is pasted into the host chromosome by a viral enzyme called integrase.
10. Prokaryotic cells contain smaller ribosomes (â70Sâ ribosomes) than eukaryotic cells (â80Sâ ribosomes). Both types of ribosomes synthesize proteins, but the macromolecules they use to do it are somewhat different.

2
Applications
_______ Oseltamivir, also called Tamiflu, binds and inhibits the viral protein neuraminidase.
_______ Clotrimazole is a drug that is used to treat certain infections. It interferes with synthesis of ergosterol, a lipid involved in phospholipid membranes.
_______ Penicillin is a drug that interferes with synthesis of peptidoglycans (these are biological molecules that are part protein and part carbohydrate) that are present in certain cell walls.
_______ HIV is often treated with several drugs that inhibit different parts of the viral replicative cycle. Raltegravir is an example of a drug that interferes with the integration of viral genes into the host cellâs chromosome.
_______ Cows, like other vertebrates, lack the ability to breakdown cellulose. Yet they are able to live on a diet of grass and other vegetation high in cellulose.
_______ Enzymes isolated from extremophiles have been very useful in laboratory research. For example, Taq polymerase facilitates PCR, a revolutionary technique for production of DNAs of particular sequences, which requires cycling reactions through high temperatures.
_______ Plants and animals require nitrogen to make biological macromolecules, however theyâre unable to convert atmospheric nitrogen (N2) into a biologically useful form.
_______ Azithromycin is a drug that binds to 70S ribosomes and blocks synthesis of any new proteins.
_______ Methicillin-Resistant Staphylococcus aureus (MRSA) can cause life-threatening infections of the skin and bloodstream. One of the reasons MRSA infections are so serious is that they are resistant to treatment by many antibiotics, including methicillin and penicillin.
_______ The enzyme reverse transcriptase, isolated from retroviruses, is an important tool in molecular biology research. Scientists interested in learning what genes are turned on in particular cells use it to make DNA copies of RNAs they are studying (The DNA copies are useful because they are more stable).

When you have completed the matching activity, answer these follow-up questions:
â¢ What types of infections can be treated with the following drugs?
o Penicillin
o Clotrimazole
o Azithromycin
o Tamiflu
o Raltegravir
â¢ Why are these drugs (above) safe for you to take? That is, why donât they kill your cells?
â¢ Cancer cells are your own human cells that have become deregulated so that they divide and pile up in an uncontrolled way. Many chemotherapy drugs treat cancer by interfering with cell division and other cell processes.
o Why are there so many more side effects for individuals undergoing chemotherapy than for individuals taking antibiotics?

Tasmanian devils (Sarcophilus harrisii), the worldâs largest carnivorous marsupials, are facing extinction. Not from hunting, or habitat loss, but from within; a transmissible cancerous derivative of Schwann cells, responsible for devil facial tumour disease (DFTD). First seen in 1996, the disease has spread widely though the population, and is now estimated to be present in 80% of the population. With the grim prognosis of ~100% mortality in 12-18 months, animals that once went through multiple breeding cycles are now lucky to reproduce once before death, resulting in a 70% decline in their population over the past decade. The cancer is transmitted by biting (a common ritual used by these animals to establish and maintain social position), with cancer cells from one animal (the biter) being implanted in the wound inflicted on the other animal. Equally common in both sexes, the disease itself is more prevalent in animals higher on the social scale, presumably reflecting higher levels of social interaction (biting). The cancer is usually first evident as facial tumors, from which metastasis to cervical lymph nodes occurs, often followed by dissemination to other organ systems. Cause of death is by organ failure or by malnutrition in those with facial tumors large enough to prevent feeding. Based on what we have covered regarding the Major Histocompatibility Complex, you would expect the passage of a cancer from one individual to another* to be a rare event (to see just how rare, read the accompanying popular press piece from the New York Times). Here are some things that you already know: *Yes, some viruses can cause cancer (example: Hepatitis B virus and liver cancer), and you can transmit a virus from one individual to another; but that is not the same thing as passing the cancer itself. v Almost all nucleated cells express high levels of class I MHC proteins on their surface. v Class I MHC proteins collect peptides produced from endogenous proteins and display them at the cell surface. v Different Class I MHC proteins bind and display different peptides. v Developing cytotoxic T-cells that recognize self-antigens are eliminated. v Mature cytotoxic T-cells conduct surveillance by scanning the peptides displayed by class I MHC proteins. v Mature cytotoxic T-cells that recognize an antigen on a cell will kill that cell (recall that cytotoxic T cell activity is important in rejection of tissue transplants).

Before the questions:
v Tasmanian Devils are not immunosuppressed.
v Tasmanian Devil cytotoxic T-cells are not broken, they can kill cells.
So neither of those should be part of your answers.
This is an ongoing research topic with large gaps in our knowledge; we really donât fully understand how this works
and so there is no âcorrectâ answer. Your job is to provide a logical argument, with some research and details to
support your contention. Note that in questions 1 & 2 class I MHC should be part of your answer, but not in
question 3.

Questions:
1.) Acquiring DFTD is basically like receiving a transplant that is not rejected. How can that be? Suggest a possible
way this could occur. Be sure to explain why you think this would work, and then explain how you would test
that model to determine if it were correct. (10 point question).
2.) Canine Transmissible Venereal Tumor (CTVT) is the other know transmissible cancer in mammals. Unlike
DFTD, CTVT does not usually result in death. Do a little research on this disease and summarize how it is
different from DFTD. Provide an explanation as to why one is lethal and the other is generally not. (10 point
question).
3.) Recently, researchers at Washington State University determined that some Tasmanian devils had developed
resistance to this cancer. By scanning partial genome sequences of resistant and susceptible animals (a
complete devil genome has yet to be assembled) they identified a set of genes where mutations appeared to
enhance resistance. Speculate as to the function of the proteins these genes encode, and explain why that
might provide for resistance (note: they were NOT MHC genes).

Mainly need guidance/ideas for #1's 1 and 3!

1)What experiment was performed that allowed for scientists to finally agree that DNA is the genetic material within living organisms?

a.Understand the materials and scientific techniques used to come to this result.

2)What group of experiments led to the discovery of the mechanism used in DNA replication?

a.Understand the materials and scientific techniques used to come to this result.

i.What is a cesium chloride gradient?

ii.Where do 14N and 15N respectively fall along this gradient?

b.The results revealed that DNA replicates using which of the three proposed models?

i. Describe the mechanism of each model.

3)What is the role of the following proteins in DNA replication?

a.Helicase

b.Single strand binding proteins

c.Topoisomerase

d.DNA polymerase III

e.DNA polymerase I

f.Primase

g.Ligase

4)What extra steps are taken to be sure the lagging strand does not shorten each time DNA is replicated?

a.What is the role of telomerase in these âstepsâ?

5)In DNA repair, which enzyme has âproof-readingâ capabilities?

1)Which type of cells within our bodies use mitosis to reproduce?

2)Does mitosis create a cell that is different or the same as the parent cell undergoing division?

3)Describe the DNA found in sister chromatids.

4)Describe the DNA found in homologous chromosomes.

5)What occurs during the following stages of the cell cycle?

a.G₁ Phase

b.S Phase

c.G₂ Phase

d.M Phase

What are the phases of mitosis? What events occur in each phase?

1)Does mitosis separate homologous chromosomes, sister chromatids, or both?

2)What is cytokinesis?

a.Which fibers of the cytoskeleton contract to pinch parent and daughter cells apart from one another in animals?

b.How do microtubules move chromosomes to the two poles of a dividing cell?

3)How are centrioles involved in this process?

a.How do plants form two complete cells during cytokinesis?

4)How do bacterial cells reproduce?

5)The cell cycle is controlled at âcheckpointsâ. What occurs at each of the following checkpoints?

a.G₁ Checkpoint

b.G₂ Checkpoint

c.M Checkpoint

6)How do cyclin and cdk act to control the G2 checkpoint?

7)If presented with the schematic of the M checkpoint, you should be able to explain perturbations to the system as well as if the cell will divide or stall at metaphase.

8)Cancerous cells form when the cell cycle checkpoints do not function correctly and continues to divide even though it is damaged in some way. How does the protein p53 function to keep these cells from dividing?

9)Normal cells follow certain rules of growth that cancerous cells do not follow. What are these rules (provide a short definition for each as well)?

10)What is the difference between a benign tumor and a malignant tumor?

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BIO 1140 Lecture Notes - Lecture 8: Deoxyribonuclease, Intermediate Filament, Ryanodine

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