Transcript cell plate
Jill before teaching go to this hyperlink (on these words) THE CELL CYCLE Chapter 9 Continuous balance between cell division and cell death Mitosis – A process that forms two genetically identical cells from one Product of mitosis: daughter cells Apoptosis – natural cell death – precise – geneticallly programmed(?) The Cell Cycle (hyperlink) Checkpoints – 1. when certain proteins interact in a way that ensures the proper sequence of events is unfolding 2. allows a pause so newly formed DNA can be checked and repaired before dictating orders Cell cycle, con’t Events that occur in the life of a cell. Includes 3 major stages: • Interphase • Karyokinesis (mitosis) • Cytokinesis Interphase • Cell is not dividing, but there is GREAT activity G1 Phase - carries out basic functions & performs specialized activities. • duration is extremely variable • Synthesizes proteins, lipids and carb in case of cell division G1 Phase, con’t contains restriction checkpoint ~ cell “decides” to: - Divide - Stops to repair DNA damage - enter a quiescent phase (G0) - die Interphase, con’t G0 Phase – a cell can exit the cycle at G1 to enter this phase • The cell maintains specialized characteristics, but does not divide. • No replication of DNA • Must be at this stage in an egg for cloning to work Ex. neurons & muscle cells Interphase, con’t Phase – •Great Synthetic activity – replicating DNA • cell replicates chromosomes & synthesizes associated proteins. (also those that coordinate events of nucleus and cytoplasm (animal cells replicate centrioles as well) •S G2 Phase – • Makes more proteins – especially tubulin for microtubules • Membrane materials stored in vesicles under the cell membrane • DNA winds tightly around proteins to start mitosis • Interphase ends Karyokinesis ( aka mitosis hyperlink); M phase) Equal distribution of replicated genetic material (chromosomes). Nucleus actively dividing (hyperlink) See mitotic spindle (diagram pg 141) Participants in Mitosis Centromere chromatids – link sister Participants, cont 2 identical copies of chromosomes (sister chromatids) Participants, cont Spindle grows from the centrosome/centrioles Proteins around the centriole initiate spindle growth Mitosis Phases - hyperlink Prophase (hyperlink) • DNA coils tightly around proteins • replicated chromosomes condense • centrosomes separate & migrate toward opposite sides of cell • mitotic spindle forms (microtubules grow out from centrosomes) • nucleolus disappears Prometaphase • • nuclear membrane breaks down- into small pieces and lay parallel to the cell membrane spindle fibers attach to centromeres of chromosomes Metaphase • chromosomes are lined up single-file along equator of mitotic spindle. • Chromosomes seem motionless because they are pulled equally by both sides of the cell • Anaphase • • Centromeres, one per chromatid, move apart separating the chromatids to opposite Microtubules in the spindle shorten and some lengthen in a way that moves the poles farther apart • Telophase • • • • • • Cell begins to look like a dumbell (cytokinesis has begun) mitotic spindle breaks down chromosomes decondense nuclear membranes reform around two nuclei nucleoli reappear End of Mitosis 3. Cytokinesis Distribution of cytoplasm and all other contents to daughter cells. • begins during anaphase or telophase depending on the cell type • differs in animal & plant cells Cytokinesis in animal cells: • cleavage furrow (hyperlink)(slight indentation) forms around equator of cell. • Contractile ring of actin & myosin microfilaments act like a drawstring to pinch the cell in two. • Asters determine the number of cleavage furrows • usually an equal division. Cytokinesis in animal cells Cytokinesis in plant cells hyperlink: New cell wall must be built • phragmoplast (microtubule structure) forms in cytoplasm & traps vesicles containing cell wall material. (between daughter cells) • vesicles fuse, forming a cell plate across midline of cell. • cell plate gives rise to two primary cell walls. Does cytokinesis always accompany karyokinesis? Karyokinesis in the absence of cytokinesis results in a syncytium (mass of multinucleated cells). Control of the Cell Cycle hyperlink( what turns mitosis on or off) Checkpoints - groups of interacting proteins that ensure cell cycle events occur in the correct sequence. Survivins override signals that tell the cell to die, keeping it in mitosis, not apoptosis Telomeres At tip of chromosomes 100’s-1000’s of repeating sequences on end of chromosome Each time mitosis occurs, DNA looses 50-100 sequences After 50+ divisions DNA signals cell division to cease Telomere, con’t A few cells, DNA does NOT shrink (bone marrow, small intestine, blood cells, germ cells for sperm) If DNA shrinks, no telomerase made Telomerase add DNA to tips of chromosome Plant cells produce telomerase and divide more than 50 times Shortening of telomeres - loss of telomere DNA signals cell to stop dividing. Some cells produce telomerase (enzyme that continually adds telomere DNA). Signals to Divide: Signals from outside the cell effect cell cycles Contact Inhibition - healthy cells stop dividing when they come in contact with other cells. Signals to Divide, con’t Hormones - stimulate cell division. Ex. Estrogen stimulates uterine cell division Growth factors - proteins that stimulate local cell division. Ex. Epidermal growth factor (EGF) stimulates epithelial cell division filling in new skin underneath a scab Ex. Produced in salivary glands of animals – aids in wound healing Interaction of kinases & cyclins - activate genes that stimulate cell division. Control at the Tissue level – stem cells and cell populations Stem Cells (hyperlink) • Cells used to replenish tissues Stem cell’s con’t When a stem cell divides, one daughter cell will specialize and the other daughter cell will remain a stem cell Ex: basal layer of skin, bone marrow, & small intestine, heart and ventricles of brain Cell populations – up to 3% are dividing. (expanding population) or if all are dividing it is called a renewel population Static populations- cells are no longer dividing in the tissue- nerves and muscles (these enlarge-not divide) • Cell death is part of life B. Apoptosis (hyperlink) Programmed cell death; part of normal development. Eliminates excess cells and cells that could grow uncontrollably. Tadpole tail, webbing between fingers) Steps of Apoptosis: Apoptosis rapidly and neatly dismantle cell into membrane bound pieces that phagocyte will mop up (as opposed to necrosis due to injury death receoptor receives signal caspases (enzymes that snip cell components) are activated within caspases destroy proteins and other components. caspases destroy adhesion molecules so cell can’t cling to another cell cell undulates, forming bulges called blebs nucleus bursts releasing chromatin cell shatters loose membrane surrounds pieces phagocytes mop up Similar in plant cells, but parts are digested by enzymes Why cells die Brain cell example pg. 158 To distinguish self from non-self protective function-to detect and weed out cells that could grow uncontrollably C. Cancer (loss of cell cycle control) Condition resulting from excess cell division or deficient apoptosis. Characteristics of Cancer Cells: • • • • • • • • can divide uncontrollably & eternally dedifferentiation are invasive are heritable & transplantable lack contact inhibition readily metastasize exhibit angiogenesis exhibit genetic mutability Cancer (hyperlink)- con’t given nutrients and space, cancer cells reproduce uncontrollably growth rate depends on the type of cell fast growing must be 1 centimeter in diameter- may produce 1 million new cells/hour loss of cell cycle control is inherited by descendents injectable lack contact adhesion often undergo mutations stimulate angiogenesis (blood vessel growth) Causes of Cancer: mistimed or misplaced mitosis Absence of normal apotosis (hyperlink) Over-expression of oncogenes Oncogenes are genes that trigger limited cell division. Inactivation of tumor suppressor gene Tumor suppressor genes prevent a cell from dividing or promote apoptosis. Normal functioning of oncogenes & tumor suppressor genes may be affected by environmental factors: • carcinogens • radiation • viruses • diet • exercise habits