BIOL 2013 1st Edition Lecture 20Outline of Last LectureI. Carbohydrate CatabolismII. FermentationOutline of Current LectureI. ReviewCurrent Lectureviruses obligate intracellular parasite non living purpose is replication know why they aren’t living 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.components nucleic acid: either DNA or RNA (single or double stranded) capsid: protein coat that surround nucleic acid made of capsomeres protection and shape envelope: surrounds capsid some have them and some don’t (naked) through the budding process the virus will acquire the envelope viral shapes helical: rod polyhedral: many side complex: bacteriophage will inject their nucleic acidvirus enters the cell by fusion and leaves by budding lytic: kills the cell (lyse the cell) lysogeny: the viral genome integrates with the host cell’s genome could revert to lytic phage: a virus that infects prokaryotes oncogenic virus: virus that causes cancer how to control viral infections vaccination: passive (antibodies) and active (viral particles) sanitation interferon: best antiviral product viroids smallest infectious pathogensmostly plant pathogens(potato spindle tuber disease single stranded RNA prions infectious particles they are proteins metabolism: sum of all chemical reactions in the cell catabolic: breaking down (release energy) anabolic: building up (takes energy) metabolic pathways are controlled by enzymes and enzyme are controlled by genes enzymes catalyze spontaneous reactionsapoenzyme: protein portion (inactive) cofactor: nonprotein portion (active) holoenzyme: whole enzymecoenzymes are organic (B vitamins) Collision Theory: chemical reactions happen when atomic particles collide enzymes lower activation energy (faster) substrate will attach to the active site on enzyme 4 things about enzyme catalyst specific proteins some require cofactors enzymes end in -ASE factors that effect influence enzymes temp: heat denatures and cold slows them downpH: can denature enzyme substrate concentration: if you increase substrate then all active sites will be occupied (saturation) inhibitors competitive: compete for active site noncompetitive: attach to the allosteric site which alters the active site ATP is main energy source PEP had twice the energy but takes too much energy to make 3 ways of phosphorylation (ADP to ATP) substrate level: ADP + phosphate = ATPoxidative: coupled with electron transport photophosphorylation: couple with electron transport in photosynthetic cells growth curvelag: preparation log: population growth stationary: equilibrium decline: decease in population requirements for growth physical temp(min,max, and optimum) pH 6.5-7.5 acidophiles: grow in acid osmotic pressure isotonic obligate halophiles: want high osmotic pressurechemical measurement of growth direct microscope count: counting the cells no incubation time but you can’t tell between dead and living cells dilution and plating requires incubation time but you can tell between dead and living cells optical density (turbidity): gets measurements quickly with out disturbing the culture but cannot differentiate between dead and living cells oxidation: lossreduction: gain phototrophs (light) heter: organic compounds auto: CO2chemotrophs (cemicals) heter: organic compounds auto: CO2 carb catabolism glycolosis: glucose to pyruvate then to acetyl CoA lipids are connected by Krebs cycle krebs cycle electron transport
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