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TAMU BIOL 213 - Cell Cycle Control and Apoptosis
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BIOL 213 1st Edition Lecture 24 Outline of Last Lecture I. Cyclic AMPa. Produced by adenylyl cyclaseb. Primary target is PKAII. Inositol triphosphate (IP3), diacylglycerol (DAG), and Ca2+ a. IP3 and DAG are generated by phospholipase Cb. IP3 opens Ca2+ channels in the ER and Ca2+ and DAG activate PKCc. Ca2+ can bind to other proteins like calmodulin, which can then bind to CaM-kinaseIII. Enzyme-linked receptorsa. Receptor tyrosine kinases activate signaling proteinsb. PIP3c. RasIV. Some pathways are activated only if multiple signals are presentV. ReviewVI. Plant signalingVII. Receptor downregulationOutline of Current Lecture I. Eukaryotic cell cyclea. Four phasesb. Regulation was discovered by observing mitosis of Xenopus frog eggsII. Cyclin and Cdks control progression through the cell cyclea. M-cyclin binds to Cdk to create an M-Cdk b. The sharp decrease in levels of M-cyclin after M phase is due to degradation of cyclin by proteasomesIII. S Phase – DNA replicationIV. G1 phase arrest due to DNA damage These notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.a. Outline: If DNA damage is detected, p53 will be activated, which will initiate transcription of the p21 gene. The p21 protein (a Cdk) will bind to the active S-Cdk and inactivate it so that S phase cannot be initiatedV. Apoptosis – programmed cell deatha. It’s mediated by an intracellular proteolytic cascade that cuts the cell up into nicelittle piecesb. High stress to the p53 protein causes the p53 to induce apoptosisCurrent LectureI. Eukaryotic cell cyclea. Four phasesi. G1 phase: cell growthii. S phase: DNA replicationiii. G2 phase: cell growthiv. M phase: mitosis and cytokinesisb. Internal and external conditions are monitored during the G1 and G2 phasei. If any of these conditions aren’t met, signals in the cell stop it from going through mitosisii. G1 checkpoint1. Right before the cell goes into the S phase2. It checks external conditions a. such as whether or not the environment is favorableb. If the nutrients necessary and/or signals for replication aren’t there, the cell doesn’t go through replication3. It checks internal conditionsa. Such as whether or not the DNA is intactb. If the DNA isn’t intact, the cell doesn’t want to replicate itiii. G2 checkpoint1. Right before the cell goes through mitosis2. Checks to see if the DNA is intact and fully and properly replicatedc. The cell cycle can be arrested at multiple checkpointsd. Some cells can forever stop dividing and enter the G0 phasei. Cells in the G0 phase never divideii. Cyclin is completely shut ofiii. Ex: neurons, skeletal musclese. Regulation was discovered by observing mitosis of Xenopus frog eggsi. These eggs are really big, so that they can be seen in a microscope, and they go through mitosis quicklyii. Cytoplasm from an egg going through mitosis was injected into an oocyte1. Oocyte: immature precursor of an unfertilized egg2. The oocyte was driven into M phaseiii. Cytoplasm from an egg in interphase (G1, S and G2) was injected into an oocyte1. The oocyte was NOT driven into M phaseiv. They found that something in the cytoplasm of an egg going through M phase somehow initiates M phase. They fractionated the cytoplasm to determine what the specific protein was1. They ran the cytoplasm over one column so that a specific kind of protein remained bonded to the column while the other kinds ran past the column and were collected separatelya. Ex: a negatively charged column would bond and hold to the positively charged proteins while the negatively proteins could be collected2. The diferent solutions were run over other columns with diferentchemistry so that the protein that induced M phase was finally determined - cyclinII. Cyclin and Cdks control progression through the cell cyclea. Cyclin-dependent kinases (Cdks) are proteins that are activated and inactivated by phosphorylation and dephosphorylationb. Their concentration in the cell is constant throughout the entire cell cyclec. They bind to cyclind. The concentration of cyclin varies throughout the cell cyclei. It steadily increases during interphase, is at its highest during M phase, and drastically decreases at the end of M phasee. M-cyclin binds to Cdk to create an M-Cdk i. Initially, the M-Cdk is inactiveii. An inhibitory kinase and an activating kinase each phosphorylate the Cdkiii. The inhibitory phosphate and activating phosphate cancel each other out so that the M-Cdk is still inactiveiv. Activating phosphatase cuts of the inhibitory phosphate so that the M-Cdk is active1. Activating phosphatase is activated by active M-Cdkv. Active M-Cdk initiates M phase1. This activates activating phosphatase2. This is a positive feedback loopvi. Therefore, the level of cyclin determines the progression through the cell cyclevii. Eventually, the amount of active M-Cdk will be just enough more than theinactive M-Cdk so that it will cause a cascade of activation of other M-Cdks and cause mitosis1. This is amplificationf. The sharp decrease in levels of M-cyclin after M phase is due to degradation of cyclin by proteasomesi. Active M-Cdks activate a protein that ubiquitinates the M-cyclin1. Ubiquitin is the protein that tags proteins for degradation by proteasomes2. This is negative feedbackg. Each phase of the cell cycle has its own unique cyclin and Cdki. Ex: S phase has an S-cyclin and S-Cdkii. The mechanism is basically the sameiii. The activated S-Cdk triggers DNA replication machineryIII. S Phase – DNA replicationa. How is the DNA not replicated several times?b. As soon as DNA replication is started, the signal/protein that initiated replication is degradedc. An origin recognition complex (ORC) sits on the origin of replicationd. An inactive Cdc6 is bonded to the ORC e. S-Cdk phosphorylates Cdc6i. This activates it, which activates the ORC to initiate replicationf. Soon after the ORC initiates replication, Cdc6 is degradedi. This prevents re-initiationIV. G1 phase arrest due to DNA damage a. Outline: If DNA damage is detected, p53 will be activated, which will initiate transcription of the p21 gene. The p21 protein (a Cdk) will bind to the active S-Cdk and inactivate it so that S phase cannot be initiatedb. There are always proteins scanning the DNA for damagec. If damage is detected, a protein kinase will be activatedd. This will activate a p53 protein by phosphorylationi. Inactive p53s


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TAMU BIOL 213 - Cell Cycle Control and Apoptosis

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