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Unformatted text preview: 204-325 1 Summary of the Last Lecture Development of an organism is controlled by programmed expression of genes. Model organisms are used in developmental genetics to analyze gene regulation. Cell fate determination is followed by differentiation. Drosophila sex determination is the result of three consecutive alternative splicing. Drosophila body plan is progressively defined by morphogen gradients, segmentation genes and Hox genes. Segmentation genes include gap genes, pair-rule genes and segment polarity genes. Hox genes assign segmental identities in both Drosophila and mouse. 2 Today's Topics 1. Control of the Cell Cycle 2. Retrovirus and Oncogenes 3. Tumor Suppressor Genes 4. Multistep Nature of Cancer 3 Topic 1 Control of the Cell Cycle 4 Cell Cycle: G1, S, G2 and M 5 External Regulation of Cell Division (+) 6 External Regulation of Cell Division (-) 7 Signal Transduction Relays Signal from Surface to Genome Signal Response 8 Internal Control of Cell Cycle at Checkpoints 9 Kinase Attaches Phosphate Group to other Molecule Kinase is an enzyme that attaches phosphate group P to molecules, such as proteins. This is called phosphorylation. Inactive Or Active P P 10 Active Inactive CDK: Cyclin-Dependent Kinase (CDK) CDK is regulated by association with cyclin, another protein Active cyclin-CDK phosphorylates other proteins to regulate cell cycle Cyclin and CDK can be regulated by internal checkpoints and external signaling 11 CDK Controls Cell Cycle 12 What are being Checked at Checkpoints ? M 13 Animation 1: Regulation of Cell Cycle 14 Topic 2 Retrovirus and Oncogenes 15 Retrovirus 16 Life Cycle of a Retrovirus 17 Rous Sarcoma Virus (RSV) is a Retrovirus 18 An Integrated Provirus Makes New Virus Transcription mRNA New viruses + 19 New viral genome Translation Viral enzymes and proteins New Retrovirus Initiate a New Round of Integration 20 Chapter 15-2: Retrotransposition Some Similarity Transcription Reverse Transcription New location 21 c-src Proto-oncogene and v-src in Rous Sarcoma Virus 22 Transducing Retrovirus and Oncogenes 23 Functions of Proto-oncogenes 24 Gain-of-function: Turning Proto-oncogene into Oncogene 25 DNA Tumor Virus 26 Viruses and Human Cancer HPV16, 18 27 Topic 3 Tumor Suppressor Gene and Cancer 28 Sporadic and Hereditary Retinoblastoma: Mutation in RB 29 RB is a Substrate of CDK during G1 to S Passage 30 P53 Protein Level is Low in Normal Cells 31 Cell Cycle Arrest: p53 Regulates CDK through p21 (kinase inhibitor) 32 p53 can also Activate Apoptosis (Programmed Cell Death) Kill It if Can't be Fixed DNA Damage death receptor pathway Transcription Activation Translocation to Mitochondria 33 Animation 2: p53 34 Tumor Suppressor Genes in Human 35 Topic 4 Multistep Nature of Cancer 36 Tumor Suppressor Gene and Proto-oncogene Loss-of-function in both alleles (Recessive) Gain-of-function in one allele (Dominant) 37 Many Pathways Leads to Cancer 38 Mutator Genes are Needed for DNA Repair and Genome Integrity 39 Multistep Molecular Events Responsible for Colorectal Cancer 40 Multistep Nature of Prostate Cancer and Glioblastoma 41 Metastasis: From Benign Tumor to Malignant Cancer 42 Summary Most cancers result from mutations of multiple genes, including proto-oncogenes, tumor-suppressor genes and mutator genes. The tumor-suppressor gene products normally inhibit cell proliferation. The products of proto-oncogenes normally stimulate cell proliferation. The mutator genes are required for DNA replication and repair in normal cells. Some cancers are caused by viruses, including DNA virus and RNA retrovirus. 43 ...
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- Spring '08