A&P Unit 1 - Membrane and cell signaling

fluid mosaic model

cell membrane is fluid (moves) and has many components (protein, cholesterol, etc)

How does temperature affect membrane fluidity?

\-low temp = crystalline phase. solid. Less kinetic energy, things move less.

\-high temper/body temp = fluid phase. very flexible, lots of mvmt

How does fatty acid tail affect membrane fluidity?

\-shorter chains = more fluid, longer chains = less fluid

\-saturated bond (straight) = more fluid, unsaturated bond (bendy) = less fluid

Common lipid components in plasma membrane

\-phospholipids (bilayer)

\-cholesterol = allow for support/stability

\-glycolipids = only on outside. help form glycocalyx

Glycocalyx

\-on top of cell membrane, formed by glycolipids

\-”sugar antennae”

\-cell marker, recognize cell-to-cell interaction

integral vs peripheral membrane protein

\-integral = embedded thru bilayer. many are glycoproteins. amphipathic

\-peripheral = only on outside, loosely attached. hydrophilic.

What are the types of membrane proteins?

\-Transport proteins

\-cell surface receptors

\-identity markers

\-enzymes

\-anchoring site

\-cell adhesion proteins

transport proteins

\-carry outside things into cell

\-channel, carrier, and pump

cell surface receptors

\-bind molecules called ligands (ex. insulin)

identity markers

\-communicate to immune system whether cell belong or not

\-acts as a marker/flag

enzymes

\-catalyze rxn

\-speed up rxn by lowering activation energy

\-Michaelis-Menten function = even with an enzyme, reaction speed will plateu when the enzyme is all being used (enzyme can't infinitely speed up rxns)

anchoring site protein

secure things into the membrane

cell adhesion proteins (cell adhesion molecules, CAM)

form membrane junctions

\-tight junction, desmosome (CAM), gap junction

tight junction

\-nothing passes

\-__strands protein__ keeps it tight

\-ex. in lumen in stomach

desmosome

\-adhering junction

\-plaque on sides, CAM keeps it together

\-ex. in stretchy tissues

gap junction

\-communication junction

\-connexins make connexon

\-small ions can pass, large can’t

main functions of plasma membranes

1) serve as barrier btwn cell and insterstital fluid

2) regulate movement in and out of cell

3) establish and maintain electrochemical gradient

4) functions in cell communication

simple diffusion

\-molecules move __freely thru plasma membrane__

\-NO energy, goes down gradient

\-__small nonpolar only__

what affects diffusion speed?

temp, surface are, membrane thickness, concentration gradient thickness, type/size of molecule

→ Fick’s Law

hydrostatic pressure vs osmotic pressure

hydrostatic = pressure exerted by fluid on wall of container. “pushing” of water force onto walls

osmotic = “pulling” of water from solutes to places

normal osmolarity of body fluid

300 mOsm

water moves thru membranes called _______

aquaporins

(osmosis is a type of facilitated diffusion)

facilitated diffusion

\-need protein to help, for larger or charged molecules

\-NO energy, use gradient

\-channel and carrier mediated

\-__slower__ than simple diff, because need proteins. when used up diffusion plateus

channel-mediated diffusion

\-small ions move thru water filled protein channel

\-type of passive transport, no energy, down gradient

\-leak channel = always open (ex. sodium potassium)

\-gated channel = usually closed but opens for stuff to pass (ex. glucose or amino acids)

carrier-mediated diffusion

\-polar molecules need carrier protein to pass

\-type of passive transport, no energy, down gradient

\-uniporter = carrier transporting 1 substance

T or F: Some active transport does not require ATP

FALSE.

Active transport always needs energy since it’s going against the gradient

phosphorylation

ATP gives 1 phosphate to protein → changes shape and allows gates to open/close

5 steps for primary active transport

1) ATP phosphorylation increases affinity for binding site (changes shape so smth can bond)

2) ion binds on low concentration side

3) binding causes change in shape, protein opens up to the other side

4) shape change reduces affinity for ion so ion gets released

5) phosphate unbinds, protein goes back to original shape to repeat

Sodium potassium pump

\-type of primary AT

\-3:2:1 ratio = 3 Na+ out, 2 K+ in, require 1 ATP

\-”Too kind” = 2Kin(d)

secondary active transport

\-rely on preestablished gradient (from another pump) to move substances

\-moves against gradient

\-__symport__ = move in same direction ↓↓

\-__antiport__ = move opposite direction ↓↑

Vesicular transport

\-uses vesicle to move large molecules across membrane

\-exocytosis and endocytosis

exocytosis

\-move OUT of cell

\-material packed in vesicle. vesicle fuses w/ membrane to expel material

\-uses V snares and T snares

→ move macromolecules → polysacc and large proteins

V snare and T snare

\-used with exocytosis

\- v-snare = docking marker. on vesicle (v for vesicle)

\- t-snare = docking acceptor. on membrane

endocytosis

\-move INTO cell

\-via vesicle

\-3 parts - phagocytosis, pinocytosis, receptor mediated endocytosis

phagocytosis

\-cellular eating

\-pseudopods reach out, sac internalized

\-then vesicle binds with lysosome and gets digested

\-ex. WBC to bacteria

pinocytosis

\-cellular drinking

\-intake droplets of extracellular fluid with solutes

receptor-mediated endocytosis

\-needs ligand to bind

\-ligand bind causes __clathrin coated pit__

\-pit turns to clathrin coated vesicle, and then intake

\-ex. neurotransmitter intake

direct vs indirect cell signaling

\-direct = cell to cell contact (ex. linkup of surface markers, or gap junctions)

\-indirect = release ligand into IF where it will go to other cells

signal reception, signal transduction

\-reception = how cell detects signals. receptor can be inside or outside cell

\-transduction = convert signal into response

→ fast = AP, modify existing protein. slow = make new proteins

extracellular chemical messengers

\-act on target cells, bind to specific receptors

\-4 types

\-paracrines, neurotransmitters, hormones, neurohormones

paracrines

\-type of extracellular chemical messenger

\-very local, immediate cells nearby only

\-diffuse thru membrane

\-ex. histamine during inflammatory response

neurotransmitters

\-type of extracellular chemical messenger

\-respond to electric signals

\-released by nervous system

\-very short range (between neuron synapses)

hormones

\-type of extracellular chemical messenger

\-released by endocrine system

\-long range, long acting, go thru blood

kinase

enzyme that phosphorylates a protein

signal amplification

signaling happens in small concentrations because response will be amplified every step

what are the types of receptor proteins?

\-ligand gated channel

\-enzyme receptors

\-intracellular receptors

\-g-protein couples receptor/GPCR

Ligand-gated channel

\-type of receptor protein

\-outside cell, on membrane

\-ligand binds, opens ion channel to let things in

a-conotoxin

\-targets ligand-gated channel → nicotinic ligand

\-block acetylcholine → prevent signal transmission for muscle contraction → organism can’t breathe & is paralyzed

enzyme receptors

\-type of receptor protein

\-outside cell on plasma membrane

\-after binding to ligand, receptor acts as an enzyme and increases \[ \] of an __intracellular 2nd messenger__

intracellular receptors

\-type of receptor protein

\-inside cell, hydrophobic

\-ligand goes thru membrane, bind to receptor inside cell → alter gene expression

\-ex. go in nucleus and tell to make new proteins

G-protein coupled receptor (GPCR)

\-type of receptor protein

\-on membrane outside cell

1) receptor is associated with G-protein

2) ligand binds, activate G protein

3) G-protein moves to activate another effector protein in the membrane

4) effector protein increases \[ \] of intercellular 2nd messenger

→ cAMP and DAG/IP3

cAMP pathway

\-GPCR pathway

\- __adenylyl cyclase__ = effector protein (activated by GTP)

\-cAMP phosphorylated via __PKA__

\-__PKA__ = protein kinase A. activates glycogen synthesis

DAG & IP3 pathway

\-GPCR

\-__phospholipase C__ = effector protein (activated by GTP)

\-PIP2 split into DAG & IP3

\-IP3 moves to endoplasmic reticulum to activate calcium channel

\-calcium activate protein kinase C

what are the functions of the endocrine system?

\-regulate development, growth, metabolism

\-maintain homeostasis of blood composition and vol

\-control digestive processes

\-control reproductive processes

Steroids

\-circulatory hormone

\-lipophilic (bind INSIDE cell)

\-made from cholesterol

→ gonadal steroids (testosterone), and adenyl cortex

Biogenic amines

\-circulatory hormone

\-hydrophilic

\-modified amino acids

→ catecholamines (epinephrine), thyroid hormone, melatonin

proteins \[in relation to endocrine system\]

\-circulatory hormone

\-hydrophilic

→ most hormones

local hormones

\-local

\-don’t circulate in blood, instead bind to self or to neighboring cells

→ paracrine & autocrine

endocrine dysfunction

result from abnormal concentration of hormone in blood

\-hyposecretion = too little hormone made

\-hypersecretion = too much hormone made

compare up-regluation vs down-regulation

up = increase # of receptors and sensitivity to hormone

→ happens when hormone levels are __low__

down = decrease # of receptors and sensitivity to hormone

→ happens when hormone levels are __high__

(think negative feedback → inversely corelated)