Mcb 104 Midterm #2 Cell Biology

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Cell biology

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the study of cell structure and function

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bright field light microscopy

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shine light from below which allows you to see stained structures or other things that absorb light (chloroplasts)

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Dark field light microscopy

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shine light from the side - you see structures that refract light while everything else looks black

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Phase contrast

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detects changes in the phase/speed of light passing through cells due to a changing refractive index

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differential interference contrast (DIC)

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similar to phase contrast, but DIC uses polarized light

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Fluorescence microscopy

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Label individual molecules in a cell using fluorophores, antibodies, or fluorescent proteins in fluorescence microscopy, excite fluorescent molecules with light at one wavelength and then emit light at a longer wavelength

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Stoke's Shift

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Difference between excitation and emission

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Green Fluorescent Protein

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Naturally fluorescent protein originally isolated from jellyfish; can be used to track proteins as they move around in living cells

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Fluorescence activated cell sorting

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allows one to separate cells on the basis of their fluorescence for further analysis

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Deconvolution

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involves computational removal of the point spread function from the image to restore the unblurred object (I = O x PSF)

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Resolution limit

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the distance between two object required for them to be seen as separate objects

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Endocytosis

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bringing something from outside the cell into the cells

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exocytosis

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bringing something from the inside of the cell to the outside

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cell culture

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propagation of cells outside the organism

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Anterograde

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moving vesicles from ER to the Golgi

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Retrograde

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moving vesicles from the Golgi to ER

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COP1

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coat protein associated with retrograde transport

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COP11

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coat protein associated with anterograde transport

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Receptor mediated endocytosis

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the primary way that cells deliberately pull in specific molecules from outside their plasma membrane. To do this, cells express specific receptors on their surfaces which bind to external molecules and concentrate them in special coated vesicles

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Clathrin

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Receptor mediated endocytosis occurs through this; clathrin has a triskelion structure and forms polymers that help to drive budding

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Adaptin

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how receptors interact with clathrin

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Dynamin

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protein that does hydrolyzes GTP in the final stages of vesicle budding during endocytosis

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Transferrin

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protein that carries iron in the blood

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Transferrin receptor

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how iron's endocytosis is mediated

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endocrine signaling

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distant signaling from one cell to target cells, by ligands secreted into the bloodstream

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paracrine signaling

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short-range signaling by a cell to adjacent cells

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autocrine signaling

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signaling by a cell to itself

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contract-dependent signaling

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signaling by plasma-membrane attached proteins

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Rapid extracellular signals

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ones that causes altered protein function

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slow extracellular signals

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ones that deal with altered protein synthesis

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G-protein coupled receptors

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most common type of receptor in eukaryotes; have 7-transmembrane segments (they are sometimes called serpentine receptors). They interact with G-proteins through their cytosolic surface

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GEF

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guanine nucleotide exchanger facto that promotes release of GDP and binding of GTP

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GAPs

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GTPase activating proteins which promote the hydrolysis of GTP to GDP

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Rhodopsin

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A GPCR in the photoreceptor cells of the retina that is activated by light

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CREB

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Transcription factor in the nucleus (cAMP response element binding protein)

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Receptor tyrosine kinase signaling

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Their activation involves dimerization, usually as a consequence of ligand binding. The dimerization leads to intermolecular phosphorylation which further activates their tyrosine kinase activity; have diverse extracellular structures and ligands

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dominant negative mutation

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leads to interference with the normal (wild-type) version of the gene product.

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Ras

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a monomeric GTPase

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Sos

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acts as a GEF for Ras

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Suppressor mutation

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a second mutation that results in a less severe phenotype than the original mutation

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enhancer mutation

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a mutation in another gene results in a more severe phenotype than the original mutation

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bypass suppressors

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in pathways involving positive regulation, gain of function mutations in downstream genes can suppress loss of function mutations in upstream genes

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non-allelic non-complementation

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genetically, it looks like two mutations fail to complement and are thus mutations in the same gene, but they are actually not. happens in parallel pathways or in the same pathway

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Actin filaments are required for:

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1. cell shape and rigidity
2. cell movement
3. cytokinesis
4. cell polarity
5. muscle contraction

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Actin and tubulin have polarity

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= nonequivalence of two ends

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capZ

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limits + end growth

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Tropomodulin

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limits - end shrinkage

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Arp 2/3

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binds to the side of an existing actin filaments to promote branching of actin filaments

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WASP

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(Wiskott-Aldrich syndrome protein) is required for efficient actin polymerization in terms of branching

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ActA

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Listeria protein that behaves like WASP - forms actin comet tails

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myosins

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family of motor proteins that interact with actin filaments; they are ATPases that use energy to generate work (force and motion)

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myosin class I

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Step size: 10-14 nm
Function: membrane association, endocytosis
Moves in an inchworm fashion?

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myosin class II

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Step size: 5-10 nm
Function: contraction
Non-processive, erratic, ratchet mechanism

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myosin V

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Step-size: 36 nm
Function: organelle transport
Highly processive, stepwise motion
hand-over-hand mechanism

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Tropomyosin

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at low concentrations of calcium, tropomyosin blocks the myosin binding site on actin filaments

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Troponin

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binding of calcium to troponin shifts the tropomyosin complex out of the way of myosin

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chemotaxis

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oriented movement in a chemical gradient

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dynamic instability

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they switch between growth and shrinkage unpredictability

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colchine

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drug that stimulates the GTPase activity of B-tubulin and promotes depolarization

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taxol

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drug that stabilizes the GTP cap and inhibits depolymerization

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MAPs

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stabilizing proteins

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Stathmin/Op18

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enhances catastrophe by "bending" the + ends of the microtubules and accelerating removal of subunits

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Kinesin-13

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sequesters (2) tubulin dimers (lowers free dimer concentration) promotes GTP hydrolysis at + ends (reduces GTP cap stability)

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Katanin, Spastin

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Sever microtubules: remove internal subunits

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kinesins

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mostly + end-directed motors

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Kinesin 1 and 2

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walk in a hand-over-hand mechanism

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Kinesin 5

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Sliding mechanism

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Kinesin 13

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end disassembly

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dynein

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- end directed motors

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interphase

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chromosome duplication and cohesion; centromere duplication

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prophase

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breakdown of interphase microtubule display and its replacement by mitotic asters
mitotic aster separation
chromosome condensation

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metaphase

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chromosomes align at the metaphase plate

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anaphase

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APC/C activated and cohesins degraded

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anaphase A

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chromosomes move toward poles

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anaphase B

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spindle pole separation

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telophase

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nuclear envelope reassembly
assembly of contractile ring

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cytokinesis

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reformation of microtubule array
contractile ring forms cleavage furrow

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XMAP215

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stabilizes microtubules; loss of XMAP215 activity in mitosis leads to increases in microtubule instability/shrinkage

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kinetochores

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large protein complexes that ssemble on chromosomes and bind to spindle microtubules

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cell cycle

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sequence of events that occur during each round of cell duplication and division

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G1 (gap)

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cell growth

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S (synthesis)

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DNA replication

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G2 (gap)

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cell growth

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CDK1

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cyclin dependent kinase 1, induces mitosis by phosphorylating specific downstream targets on serine and threonine

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cyclin B

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regulatory subunit that activates CDK1, abundance oscillates during the cell cycle

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APC/C activation

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leads to the destruction of mitotic cyclins and leads to the metaphase-anaphase transition

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securin

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an inhibitor of a protease called Separase which cuts one of the subunits of cohesin

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START

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main regulatory or restriction point in the budding yeast cell cycle is at start

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high copy suppressor screen

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high expression of a protein by introduction of many copies of the gene can behave as a gain of function mutation that can sometimes suppress loss of function mutations in upstream or associated components

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SCF

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major ubiquitin ligase that regulates entry into S-phase

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Sic1

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inhibits the S-phase cyclin CDK complex; phosphorylated by G1 cyclin-CDKs leading to its polyubiquitination by SCF and degradation by the proteasome

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Reverse Genetic Screens

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major technological advance that enables identification of genes and molecules that regulate any cell behavior

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carcinomas

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malignant growth of epithelial tissue

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sarcomas

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malignant growths of mesoderm

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Leukemias

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derived from blood cell precursors and do not form solid tumors

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lymphomas

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derived from lymphocytes and do form solid tumors

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Glioblastomas

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derived from glial cells in the brain

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bengin

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unregulated growth of cells in a solid mass, noninvasive

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malignant

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invasive cells that can spread into adjacent/distant tissues

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oncogenes

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gain of function, dominant mutations

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tumor suppressors

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genes whose normal function protects a cell from genomic instability; loss of function, recessive mutations (ex DNA replication, DNA repair, chromosome segregation, cell cycle checkpoint, and apoptosis-promoting genes

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p53

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transcription factor that induces expression of DNA repair genes and CDK inhibitor p21; potent tumor suppressor

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Hematopoietic cells

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in the bone marrow undergot extensive gene rearrangements to generate antibodies. Errors in this process can give rise to oncogenes; leukemias and lymphomas often caused by oncogenes resulting from chromosome translocations

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Bcr-Abl

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chimeric kinase that results from a fusion between human chromosomes 9 and 22

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Gleevac

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drug that binds to an inhibits bcr-abl

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mutagens

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chemical or physical agents that increase the rate of mutation above the "spontaneous baseline"

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Ames Test

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provides a way to quantify the mutagenic activity of chemical compounds

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apoptosis

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programmed cell death

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synthetic lethality

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hypomorphic mutations in two genes in the same essential pathway and together they fatally cripple the pathway