Zoology 101: Animal Biology Last Lecture Outline Lecture 14 1. Cell division in Eukaryotes vs prokaryotes 2. Mitosis3. Cell Cycle 4. Prokaryote IntroCurrent Lecture 1. Normal Cells • Cell cycle • Cell division • Properties of normal cells • how external signal regulates cell division2. Cancer cells• Properties • Cell division3. How proto-oncogens become oncogens4. Proteins that inhibit cell division Normal Cells• Checkpoint- critical point in the cell cycle that is regulated • Regulated molecules at each checkpoint decide if division should proceed ◦ G1 checkpoint: cell gets signal to divide only if the cell a growth factor is present, the cell is big enough, and when all is okay, if the DNA is undamaged. The gate will go down, allowing the cell to continue. ◦ G2 checkpoint: is DNA replication complete? ◦ Metaphase checkpoint: are chromosomes attached to the kinetochore• Normal Cell division◦ Problem gets fixed; continues division◦ Problem can't be fixed: apotosis; cell suicide pathway▪ cell DNA degraded ▪ cell blebs apart and dies▪ remnants engulfed by other cells• Properties of normal cells:◦ need growth factors present to stimulate cells to divide (start and stop reproducing at the right time ◦ Cell exhibit anchorage dependance▪ must be touching some kind of surface in order to divide. i.e. extracellular matrix ◦ Cell exhibits density dependent inhibition: cell stops dividing at critical density• How external signal regulates cell division◦ Signal transduction: getting your message across the membrane ◦ Reception: signal binds to receptor. Receptor is activated and shape changes◦ Transduction: converting external signal to internal message (phosphorylation- adding P from ATP, changes shape). Relays molecules in signal transduction pathway◦ Response: activate cell cycle control proteins or turn on cell cycle control genes → regulation of cell division◦ genes encode signals, receptors, signaling molecules, control proteins ▪ proto-oncogens. Can be mutated into into oncogens → cancer causing genes Cancer Cells • Properties of Cancer cells◦ Problem doesn't get fixed and cell goes past checkpoint ▪ get proliferating cancer cells forming a tumor ▪ cells are immortal (HeLa cells)◦ Tumor grows from a single cancer cell ▪ Benign- not cancerous but still growing uncontrollably ◦ Cancer cells invade neighboring tissues▪ Malignent tumor: cells ignore cell density dependent inhibition ◦ Cancer cells may survive and establish a new tumor in another part of the body How proto becomes onco• Point mutations: protein folds abnormally → activated all the time. Hyperactive or degradation (resistant protein)• Gene amplification: normal growth- stimulating protein in excess • Her2 proto-oncogen: a membrane receptor. Signal binds → ends in cell division or anti-apotosis • Amplification/overexpression◦ increased gene copy number ◦ increased mRNA transcription◦ increased number of surface receptors ◦ increased rate of cell division ◦ Herceptin: smart bomb type drug, mimics binding recptor, cell won't divide Proteins that inhibit Cell division • Tumor suppressor proteins (these are good, normal cells)◦ shut down cell division if conditions are not favorable (at checkpoints)◦ detect positive or repair DNA damage ◦ Promote apotosis and density-dependent inhibition ◦ If mutated, cell cycle checkpoints ignored, damage cells proliferate◦ BRAC 1 or BRCA 2; helps repair damaged DNA in 62, recognizes double stranded breaks in chromosome, recruits repair enzymes◦ p53: master watchmen▪ mutated-> damaged cells go through mitosis ◦ tumor suppressors can be silenced by aberrant methylation▪ epigenetic phenomenon▪ methyl groups on gene increase, gene gets turned off. Tumor suppressor not made • Telomerase activity is detected in almost all human tumors → cell
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