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51 Cards in this Set

  • Front
  • Back

gap junction

cell signaling: b.t cells next to one another

local signaling (3)

cells in a multicellular organism communicate by chemical messengers




animal cells communicate by direct contact or cell-cell recognition




e.g. synaptic signaling

local regulators

messenger molecules that travel only short distances

paracrine signaling

short distance communication




cell secretes material in close proximity to other cells

synaptic signaling

short distance communication




neurotransmitter travels across a synapse

hormone signaling

long distance communication




travels into blood stream and binds to receptors




*ability of a cell to respond to a signal depends on whether or not it has a receptor specific to that signal

three stages of cell signaling

1) reception: signaling molecule binds to the receptor


2) transduction: signal is converted into an intracellular response


3) response: the action that happens

ligand

molecules that bind to a specific molecule

conformational change

shape change that leads to signal transduction

ligand-gated ion channel

when a signal molecule binds as a ligand to the receptor, conformational change, channel opens, gate allows certain ions to pass through. once ligand disconnects, gate closes.

fight or flight response

lungs: relaxes muscle cells, more oxygen to blood




heart: beats faster -> everything moves faster throughout bloodstream




liver: releases glucose into blood

G protein-coupled receptor

adrenaline/epinephrine binds to receptor, signals molecules




release of glucose is the response (glycogen broken down)

insulin and glucose

insulin binds to insulin receptor, triggers cascade of phosphorylations




one outcome is that vesicles containing glucose transporters are moved to cell surface; glucose enters the cell




glucose is converted to glycogen

intracellular receptors

*not all signaling molecules are hydrophilic (some are hydrophobic and can go directly through membrane)



receptors that are inside the cell can then bind to the hydrophobic molecules



e.g. testosterone (steroid)

endergonic rxns

require energy, yield products rich in potential energy




e.g. photosynthesis

exergonic rxns

release energy, incr kinetic energy (break chem bonds)

hydrolysis of ATP

ATP + H2O -> ADP + Pi




exergonic, spontaneous




energy coupling to drive chem rxns

sucrose + H2O -> glucose + fructose

exergonic, but not spontaneous at a high enough rate




need enzymes to catalyze rxn (e.g. sucrase)

enzymes

dG unaffected, rate affected, activation energy decr




highly specific; active site where enzyme interacts with its substrate

induced fit (5)

a change in protein structure that the substrate causes




1) enzyme is available with empty active site


2) substrate binds to enzyme with induced fit


3) substrate is converted to products


4) products are released

competitive vs noncompetitive inhibition

competitive: blocks substrate binding




noncompetitive: changes shape elsewhere so that substrate cannot bind

allosteric enzyme regulation

molecule binds on another active site and causes a shape change (can be either activators or inhibitors)

feedback inhibition

enzyme #2 (product) can feedback info into enzyme #1 (reactant) and stop process when no more porduct is needed

mitochondria, its parts (6)

responsible for carrying out cellular respiration




outer & inner membrane, intermembranous space




matrix: inside cavity of mitochindrion




cristae: folds that incr surface area of matrix

cellular respiration (4)

glucose + O2 -> CO2 + H2O + ATP




occurs in both plants and animals




occurs in two places: cytoplasm & mitochondria (starts in cytoplasm & continues in mitochondria)




occurs in 3 stages: glycolysis, citric acid/krebs cycle, oxidative phosphorylation (electron transport chain and chemiosmosis)

Glycolysis

Glucose -> pyruvate



Pyruvate enters mitochondria and is oxidized to CoA



Final products: 2 pyruvate, 2H2O, 2ATP, 2NADH + 2H+

Citric acid cycle

Occurs in mitochondrial matrix



Organic molecules -> CO2, NADH, FADH2, ATP

Oxidative phosphorylation

Occurs in mitochondrial matrix



Chemiosmosis: makes ATP; energy storee in the form of H+ ion gradient across membrane is used to drive cellular work



electron transport chain: located in inner membrane of mitochondria; final electron acceptor O2 -> H2O



ATP synthase

ATP synthase

Protein complex; molecular motor



Protons enter, causes motor to spin, creates ATP



Composed of many alpha helices

Review of cellular respiration steps

Chem (potential) energy stored in molecules



Relocation of electrons released energy stored in organic molecules



Electrons transferred from one molecule to another



After each transfer, electrons at a lower energy state



Energy released at each step, used to make ATP



Last electron transfer is to oxygen, forming water

Chloroplasts, structure

Outer membrane, inner membrane, membranous space (like mitochondria)



Thylakoids: membrane stacks, where the light rxns of photosynthesis occur

Thylakoid membrane

Sunlight comes in, H2O comes in, O2 is made



Generates ATP & NADPH, whi h feeds into calvin cycle

Calvin cycle (P)

Input is CO2, output is glucose & other organic compounds



Takes place in stroma

Chlorophyll

Main pigment molecule



Absorbs physical light

Photosystem II

First step in the two photosystems



1) photon of light excites electron in pigment molecule. when electron falls back into ground state, energy gets transferred from one pigment molecule to the next.



2) energy eventually gets transferred to a special pair of chlorophyll molecules in the middle. electrons are bumped to a specialized primary electron acceptor molecule



3) electrons are passed on to the electron transport chain



4) electron hole left behind is replenished by pulling electrons from H2O, leaving behind O2 (chlorophyll molecules are strong electron acceptors)

Photosystem I

Second step in the two photosystems



Same as photosystem II, but electron hole is refilled by electrons from the electron transport chain

Chromosomes

DNA wrapped protein, made up of chromatin

cell cycle: G0

"rested phase", no change happening



Cell waits in g0 until they get the go-ahead

cell cycle: G1

gap phase #1; wait, grow



Cell checks the Stop and Go signals

cell cycle: S

synthesis of DNA

cell cycle: G2

gap phase #2; checks to see if DNA was duplicated properly; prepares cytoskeleton for cytokinesis (a pair of centrioles move to opposite ends of cell and form spindles)



Cell checks the Stop and Go signals

cell cycle: M

mitosis; divides DNA and cytokinesis



without full chromosome attachment, stop signal is received

Mitosis spindle

a bunch of microtubules that set up a structure that allows chromosomes to align on them and be pulled apart evenly. chromosomes become condensed, gather toward center




mitosis spindles attach to sister chromatids

Kinetochore
the actual protein complex that microtubules are attaching to

Metaphase

Imaginary metaphase plate at middle of the cell where sister chromatids align exactly in a row

Mitosis cont.

Sister chromatids get pulled apart, daughter chromosomes go to either side




Cytoplasm gets indentation (result of microfilaments and other cytoskeletal filaments)




Two nuclei reform with exactly the same complement in both of them

Evidence for a control system (experiment)

A factor present in the cytoplasm of the S phase or the M phase controls the progression of the cell cycle

Growth factor

chemical factors that will promote cell growth (e.g. platelet-derived growth factor PDGF gives cell the go signal so cells divide)

Physical factors

Anchorage-dependence: need to be attached to a surface to grow




Density-dependent inhibition: when a cell come into contact with other cells, it stops division, forming a monolayer of cells

Cancer

Cancer cells escape cell cycle controls




Cancer cells divide rapidly, often in absence of growth factors (RAS protein: activating "go" signals)




Growth uninhibited by other cells, tumors form (benign tumors remain at original site, malignant tumors spread to other locations by metastasis)



p53 gene
most frequently altered gene in cancers



tumor suppressor; when mutated, doesn't read stop signals