BIOL 3510 1st Edition Lecture 23 Outline of Last Lecture I. Roles of Actin NetworksII. Microfilament Growth and DisassemblyIII. Actin in ActionIV. Resting and Contracting Muscle CellsOutline of Current Lecture I. Intro to Cell CycleII. G1 PhaseIII. Control of S PhaseIV. ProphaseV. Prometaphase Current LectureCell cycle: duplication and division of a cell and its contents.The cell cycle has four phases:1. G1 phase (Gap) = Cell growth2. S phase (synthesis) = DNA replication3. G2 phase (Gap) = Cell growth4. M phase = mitosis and cytokinesisProgress through the cell cycle controlled by the cell-cycle control system.Cyclin-dependant kinases (Cdks) are major components of the cell cycle control systemCdk = kinase that activates cell machinery – constant amount, cyclical activationCyclin = activates a Cdk – cyclical amountsCyclin concentrations are regulated by transcription and proteolysis.Transcription: gradual increase in cyclinsProteolysis: quick decrease in cyclinsAPC = anaphase promoting complexThese 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.In addition to cyclins, Cdks are regulated by phosphorylation, dephosphorylation, and inhibitory proteins.Different Cdk-cyclin combos trigger different cell cycle events.G1 Phase- At the end of M, all S-Cdks and M-Cdks are inactivated by cyclin degradation and inhibitor protein activation- In mammalian cells, mitogens promote cyclin transcription needed for entry into S phaseMitogens promote cell division by activating G1-Cdk and G1/S-Cdks which inactivate Retinoblastoma (Rb) proteins.Cell cycle progression is paused if the DNA is damaged (or incompletely replicated)1. Inactivation of G1/S and S-Cdks during G1 and S by p53 activation pauses the cell cycleo DNA repair or cell deatho No p53 leads to the replication of damaged DNA promoting cancerCentrosome cycle: centrosome duplication initiated in G1 is triggered by G1/S Cdk and S-CdkControl of S phase – initiation of replication1. DNA synthesis is initiated at origins of replication2. Pre-existing origin of recognition complexes (OCRs) recruit Cdc6 to origins of replication during G1.3. Helicase binding generates the prereplicative complex (pre-RC)4. Activation of S-Cdk:a. Activates helicases causing the assembly of the remainder of the replication forkb. Phosphorylates Cdc6 targeting it for degradation preventing re-replicationSister chromatids are held together by cohesion ring complexes until anaphase.Activation of M-Cdk by Cdc25 leads to entry into M phase. M-Cdk is activated at the end of G2.6 Stages of MitosisProphase: phosphorylation by M-Cdk triggers formation of condensing complexes that condensechromosomes. Increased MT dynamic instability and spindle formation is triggered by phosphorylation of MAPs by M-Cdk. Motor proteins and MAPs crosslink interpolar microtubules forming the mitotic spindle.Prometaphase: breakdown of the nuclear envelope begins with the M-Cdk dependent phosphorylation of nuclear pore proteins and lamins. Microtubules connect to the centromeres of sister chromatids via kinetochore protein complexes.There are three types of microtubules in a spindle. Bi-orientation of kinetochore microtubules generates tensionChromosomes line up on the metaphase plate via the action of dynamic instability and motor proteins-Prometaphase: alignment period-Metaphase: begins when the chromosomes are aligned on the metaphase
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