AP Bio Ch.12: The Cell Cycle – Flashcards

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binary fission
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bacterial cell division; asexual reproduction of prokaryotes, and uses no mitosis
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describe the process of binary fission
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circular DNA and organelles replicate, the copies migrate to opposite sides of the elongating cell, and the cell splits in 2, forming two identical cells
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what are the roles of cell division
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reproduction, growth, and repair
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Remember, in all organisms, cell division must distribute
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identical genetic material (an exact copy of the genome) into 2 daughter cells
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genome
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the cell's hereditary endowment of DNA; it is usually packaged into chromosomes for manageability
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chromosomes
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made of DNA and histone protein complex called chromatin; during cell division, the chromatin becomes highly condensed into the chromosomes
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what chromosome structure
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at cell division, each chromosome has been duplicated during interphase; the duplicated chromosome consists of 2 sister chromatids
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centromere
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the point where 2 sister chromatids are connected
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what is the goal of cell division
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to create 2 identical daughter cells by splitting all the sister chromatids and giving one copy of each to each new cell
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what are the 2 parts of the cell cycle
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interphase and mitotic phase (M)
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interphase
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90% of the cell cycle; when the cell grows and duplicates
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mitotic phase (M)
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when the chromosomes split into separate cells; this includes cytokinesis
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what are the 3 parts of interphase
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G1 (first gap--growth) , S (DNA synthesis--copying of the DNA), and G2 (second gap--copy and finish preparation of cell division)
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G1
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cell grows and carries out regular biochemical functions
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S
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when the DNA is replicated/synthesized (chromosomes are replicated)
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G2
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the cell completes preparations for division
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Mitotic phase parts
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mitosis (division of replicated chromosomes) and cytokinesis (division of the cell's cytoplasm)
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mitosis-purpose
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to divide the 2 copies of the DNA equally; to separate the sister chromatids into separate cells
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what are the 5 steps of mitosis
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prophase, prometaphase, metaphase, anaphase, and telophase--*****prophase and telophase are opposites*****
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prophase
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nucleoli disappear, chromatin condenses into the chromosomes, centrioles separate to the opposite ends of the cell, and the mitotic spindle begins to form
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prometaphase
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nuclear envelope dissolves and spindle fibers join with the kinetochore of the centromeres
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kinetochores
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specialized regions of the centromeres where spindle microtubules attach
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metaphase
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centrioles are at opposite ends of the cell, chromosomes line up on the metaphase plate, and spindle apparatus is fully developed
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anaphase
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centromeres break and the duplicate chromosomes are pulled away from each other toward opposite ends of the cell and the cell elongates (stretch out horizontally); poles move slightly further
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telophase
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chromosomes uncoil back to the chromatin, nuclear envelope reforms, nucleoli reappear, spindle fibers disappear, and cytokinesis usually starts
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microtubules do what
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separate cytoplasm
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microfilaments do what
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contract the 2 sides of cytoplasm by wrapping around and squeezing it tight
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cytokinesis-animals
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cleavage furrow forms and the microfilaments contract around the cell membrane and divides the cytoplasm into 2 parts
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cytokinesis-plants
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cell plate develops from golgi vesicles and a new cell wall develps around the cell plate
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the cell cycle is regulated by
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a molecular control mechanism to tell cells when to divide
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this system moves the cell through its stages through
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a series of checkpoints
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at each checkpoint, signals do what
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they tell the cell to either keep dividing or stop
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checkpoints
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a critical control point in the cell cycle
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what are the major checkpoints
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G1, G2, and M phase (after metaphase, before anaphase)
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cells must receive a
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"go-ahead" signal at each checkpoint before proceeding to the next phase
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G1 checkpoint
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the most important checkpoint; if a cell gets the "go-ahead" signal at this checkpoint, it usually completes the whole cell cycle and divides; if it doesn't receive this signal, it enters a non-dividing phase called the G0 phase (most specialized cells are in this state); an example is nerve and cardiac muscle cells; later, if a cell needs to divide, a "go-ahead" signal is given and the cell reactivates into the M-phase
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control of the cell cycle
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kinases are enzymes; they are always in a cell but only active when they are connected to a cyclin protein so they are called cyclin-dependent kinases (CdK)
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when cyclin is connected to a CdK,
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it forms an activated protein complex called MPF (M-phase promoting factor)
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specific kinases give the "go-ahead" signals at
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the G1 and G2 checkpoints
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how is mitosis initiated
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as a specific example, cyclin molecules combine with CdK molecules producing enough molecules of MPF to pass the G2 checkpoint and initiate the events of mitosis
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MPF
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the protein complex required for a cell to progress from G2 to mitosisq
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what is the role of MPF
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to trigger a chain of protein kinase activations
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how does a cell stop mitosis
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during anaphase, MPF switches itself off by starting a process that leads to the destruction of cyclin molecules; it activates a cyclin-degrading enzyme, which lowers the amount of cyclin in the cell; without cyclin molecules, CdK molecules become inactive bringing mitosis to a close
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growth factors
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external signals that affect mitosis
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what are examples of growth factors
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PDGF, density-dependent inhibition, and anchorage dependence
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PDGD
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platelet-derived growth factor what stimulates cell division to heal injuries
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normal cell division has 2 key characteristics
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density-dependent inhibition and anchorage dependency
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density-dependent inhibition
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the process where crowded cells stop dividing; the number of cells in a area force competition for nutrients, space, and growthe factors, so when cells are crowded, they get signals to stop dividing
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in density-dependent inhibition, when density is high
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there is no cell division
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in density-dependent inhibition, when density is low,
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cells divide
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anchorage dependence
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normal cells must be attached to a substratum like the extracellular matrix of a tissue to divide; prevent cells from dividing and floating off in the body
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cancer cells
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don't exhibit either density dependent inhibition or anchorage dependency; the control mechanisms for cell division have failed
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transformation
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the process that changes a normal cell to a cancerous one
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tumor
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a mass of abnormal cells within otherwise normal tissue
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benign tumor
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If the abnormal cells remain at the original site
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malignant tumor
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becomes invasive enough to impair the functions of 1 or more organs; individuals who have malignant tumors have cancer
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metastasis
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a condition where cells from a malignant tumor separate and enter the blood or lymph vessels spreading the cancer to other organs
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regulation of cell divison is a balance between
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mitosis (making new cells) and apoptosis (cell suicide or cell death)
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cancer can result if
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either process doesn't work
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cancer results from genetic changes that affect
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the cell cycle control
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oncogenes
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cancer-causing genes
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proto-oncogenes
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genes that cause cancer and are responsible for stimulating normal cell growth (ex. RAS); they become oncogenes when a mutation occurs that causes them to overstimulate the cell cycle
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cancer
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can also be caused by a mutation in a tumor suppressor gene that normally inhibits cell division
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RAS
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stimulates cells and repairs damage by tagging things on or off; if it never stops, it divides and causes a tumor
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p53 gene
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supresses cancer in three ways; tumor suppressor gene
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1. It halits the cell cycle by
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binding to the cyclin-dependent kinases; this allows time for the DNA to be repaired before the cell division resumes
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2. It turns on what
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genes directly involved in DNA repair
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when DNA damage is too great to repair, it
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activates suicide genes whose products cause cell death, a process called apoptosis
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the multi- step model of cancer development is based on the idea that
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cancer results from the accumulation of mutations that occur throughout life
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the longer we live, the more
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mutations are accumulaed and the more likely that cancer might develop
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