test 2

G1 phase corresponds to the interval between cell division and initiation of DNA replication, cell is metabolically active and continuously grows but does not replicate its DNA>S phase (synthesis) during which DNA replication takes place>G2 phase during which proteins are synthesized in preparation for mitosis

separation of daughter chromosomes via mitosis (nuclear division) followed by cell division (cytokinesis)

cellular DNA content can be determined by incubating cells with fluorescent dye that binds to the DNA followed by analysis of fluorescence intensity of individual cells, distinguishing and sorting cells in G1, S, G2/M phases of cell cycle

G1=2n, S=2n to 4n, G2/M=4n until cytokinesis

the beginning phase of mitosis, marked by the appearance of condensed chromosomes and the development of the mitotic spindle, DNA replication has already occurred, centrosomes start to move to opposite ends of the cell

chromosomes align at the equator of the spindle with one chromatid of each pair facing each chromosome

the phase of mitosis during which microtubules begin to shorten and sister chromatids separate and move to opposite poles of the spindle

the final phase of mitosis, during which nuclear envelope reforms, cell starts to pinch between new nuclei in preparation for cytokinesis, contractile ring of actin forms to separate cells

separate and move to opposite sides of the nucleus and serve as two poles of mitotic spindle which begin to form during late prophase and separate sister chromosomes, every cell contains 1 (2 when dividing), consists of two centrioles-defined arrangement of microtubule proteins

DNA replication has already occurred, a second centrosome is added

nuclear envelope breaks down (absorption into the ER), chromosomes attach to spindle microtubules via kinetochores, centrosomes move to opposite ends of the cell, cell cycle checkpoint: monitors tension on kinetichores to ensure that sister chromatids are attached to opposite poles

A regulatory point that prevents entry into the next phase of the cell cycle until the events of the preceding phase have been completed; integrity of the DNA is assessed at G1, proper chromosome duplication is assessed at G2 checkpoint, attachment of each kinetochore to a spindle fiber is assessed at M

function to ensure damaged DNA is not replicated and passed on to daughter cells and coordinate further cell cycle progression with the completion of DNA replication or repair; function in G1, S, and G2

occurs towards the end of mitosis, monitors the alignment of chromosomes in the center of the mitotic spindle (metaphase plate), failure of one or more chromosomes to align properly on the metaphase plate causes mitosis to arrest at metaphase

in frog oocytes purification of the ‘cytoplasmic factor’ yielded this protein, acts as a general regulator of the transition from G2 to M; regulation by phosphorylation and dephosphorylation of Cdk1

in yeast cells random mutations and selection highlighted a protein kinase as essential for passing the START checkpoint, now known as a serine/threonine kinase that is a key regulator of mitosis in eukaryotic cells

in sea urchin embryos these proteins undergo cycles of accumulation and degradation during the cell cycle, now known as member of the family of proteins that regulate the activity of Cdk’s and control the progression through the cell cycle

regulatory subunit required for catalytic activity of the Cdk1 protein kinase, consistent with the notion that MPF activity is controlled by the periodic accumulation and degradation of this

cyclin B is synthesized and forms complexes with Cdk1 during G2, Cdk1 is phosphorylated at two critical regulatory positions (threonine-161 and is required for Cdk1 kinase activity and phosphorylation of tyrosine-15 and threonine-14) Phosphorylation of tyrosine-15, catalyzed by a protein kinase called Wee1, inhibits Cdk1 activity and leads to the accumulation of inactive Cdk1/cyclin B complexes throughout G2, transition from G2 to M is brought about by activation of the Cdk1/cyclin B complex as a result of dephosphorylation of threonine-14 and tyrosine-15 by a protein phosphatase called Cdc25

mitogens: stimulate cell division, growth factors: stimulate cell growth (growth factors>Ras/Raf/MEK/ERK pathway>synthesis of D-type cyclins>Cdk4, 6/CycD, survival factors: promote cell survival

Rb (retinoblastoma) binds to transcription factor E2F and transcription is repressed, Cyclin D-Cd4k,6 dimer phosphorylates Rb releasing E2F, Rb switches E2F from a repressor to an activator of genes which encode proteins required for cell cycle progression

mediated by the activation of Cdk2/cyclin E complexes which results in part from the synthesis of cyclin E, which is stimulated by E2F following phosphorylation of Rb, repression of p27, activated CDK2 phosphorylates p27, degredation of p27, this positive autoregulation further activates Cdk2/cyclin E, which also phosphorylates and inactivates the APC/C ubiquitin ligase, preventing cyclin E degradation

MCM (mini chromosome maintenance protein) and ORC (origin recognition complex) can only form a complex with DNA when MCM is unphosphorylated, cyclin E (and DDK) phosphorylate MCM which allows DNA polymerase association and DNA replication, topoisomerase knicks DNA backbone to relieve supercoiling (allows helicase activity of MCM to proceed down chromosome)

The ATR and ATM protein kinases are activated in complexes of proteins that recognize damaged DNA, ATR is activated by single-stranded or unreplicated DNA, and ATM principally by double-strand breaks, ATR and ATM then phosphorylate and activate the Chk1 and Chk2 protein kinases, respectively, Chk1 and Chk2 phosphorylate and inhibit the Cdc25 protein phosphatases, Cdc25 phosphatases are required to activate both Cdk2 and Cdk1, so their inhibition leads to arrest at the DNA damage checkpoints in G1, S, and G2