Saturday, February 17, 2007

Last Post- Test Review

Dr. Ray was the only one who showed up. Here is my personal study sheet. Pray hard. You'll do fine.
Review sheet for Final in CMB

5 Senogles,1 Skapek, 2 Scott, 2 Zhang, 2 Ray questions on test

Senogles-Review points and sample questions
Senogles Review included
Know pedigrees. Recognize basic forms inheritance. Know about mapping methods and be able to distinguish. Know differences kinds of cloning. Know what’s on this review, and in her objectives. Proband is first individual Identified as having the disorder. Gene is not dominant or recessive. Phenotype is what you can see. Phenotype might be more than one trait. Affected person indicates a disease phenotype or something clinically observable.
I. Human genetics
a. Autosomal and pseudoautosomal
b. X linked
c. Y linked


Sample question:
What kind of inheritance is the following? Justify your answer.





For pedigrees, explain your answers. Use the questions from her lecture 1 for each type of inheritance. EMAIL HER YOUR QUESTIONS.
II. Mapping of the genome by cytogenetic, genetic and physical methods


Sample question:
Explain how one generates a physical vs. a genetic map of a human chromosome?.


III. Positional vs traditional cloning techniques
a. Chromosome walking and jumping
b. exon identification

Sample question: Explain the difference between functional and positional cloning.


IV. Shermans paradox and resolution

V. Genetic anticipation, somatic mosaicism



Skapek
Concepts to cover:
Developmental processes
Determination
Migration
Differentiation

Cell biology of myogenic differentiation

Molecular biology of myogenic differentiation
Key myogenic transcription factors
How myogenic differentiation is controlled
Ray
2 lectures on apoptosis. He put 8 or 9 questions on Blackboard.
Look at how questions can be answered differently under different contexts.
Be able to tell the difference between necrosis and apoptosis. How is apoptosis relevant to development and disease (remember examples to justify- What happens when apoptosis increases and decreases?)
Remember BCl2 protein domains and how they work. Remember caspases and how they work.
Remember CIAPs that inhibit caspase 3 activity. Do not remember the number of amino acids, remember general mechanisms of activation and inhibition of caspases.
Look at the sample questions. Remember that Each question on the test has one compulsory part, one choice part. You will have to use creativity and your understanding to answer questions. They will not be direct.
For example, in a system you induce apoptosis with TNF-CHX (inhibits anti-apoptotic proteins, which have short half lives), one system with caspase inhibitors. Look at beginning and after certain time point. What would happen? Some cell systems, do not need CHX. TNFa induces both pathways (apoptotic and anti-apoptotic) at same time. One overrrides the other. In the papers, proteins may have different names. Gamma irradiation and chemical induction of apoptosis do not go through receptor
Remember slide on p53 and irradiated mice. Classical example of p53 and BCl2 and apoptosis. Remember the slides. Put them in your memory. He will try to find out what we know, not what we do not know.
Q.1 How would you use the understanding of the mechanisms of cell death for the treatment strategies for the diseases involving apoptosis

Q.2 How would you differentiate a cell undergoing apoptosis from necrosis ?

Q.3 Giving suitable examples discuss in brief the significance of apoptosis during development and pathogenesis

Q.4 Discuss in brief the mechanism by which TNF-α and FAS induces apoptosis.

Q.5 Describe the role of Bcl-2 family proteins in the regulation of
Apoptosis.

Q.6 Discuss in brief the mechanisms by which γ-irradiation and chemical agents induce apoptosis.

Q.7 Giving suitable example discuss the role of apoptosis in the development of cancer.

Q.8 Discuss the role of mitochondria in the regulation of apoptosis








Zhang
Review Points

1. For cell-cell adhesion lecture
a. How is cadherin connected to cytoskeleton?
b. What are the structural and functional differences between gap junction and gap junction.
c. Compare the compositions of adherent junction and desmosome
d. List the calcium-independent cell-cell adhesion molecules.
e. What are cadherin-mediated functions?
f. Illustrate the roles of E-cadherin and β-catenin in tumorigenesis and tumor progression.

2. For cell-extracellular matrix adhesion lecture
a. What are the cellular receptors of fibronectin, laminin, and collagen?
b. What are the major components of the stromal environment in connective tissue?
c. Give an example that integrin functions as a cell-cell adhesion molecule.
d. Is the RGD sequence the binding site in collagen for integrin?
e. What are the components of basement membrane?
f. Why is integrin called bi-directional signaling machinery?
Scott
Know the 6-part definition of differentiation.
Know fundamental definitions of other terms: dedifferentiation, transdifferentiation, metaplasia, terms from his cancer lectures. Be able to describe the controversy surrounding transdifferentiation and dedifferentiation. Do stem cells grow in adult tissues into which they are implanted? Do they merely fuse with the cells in the tissue? (There is an article in Science about this from several years back that marked chromosomes in the injected cells with fluorescent dye. They showed cell fusion in heart tissue). Does it depend on the tissue? Be able to state evidence to support arguments either way.
This is what I have, folks. If you need more detail, contact the professors. Have fun studying.

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