Membranes 2: Transport

Question 1

Transport functions

Answer 1

• regulation of cell volume and the maintenance of pH and ion concentration
• uptake of nutrients and extrusion of waste
• develop ionic gradients for excitability
• uptake and degradation of pathogenic organism

Question 2

passive transport

Answer 2

does not require energy and occurs spontaneously

Question 3

uniport
description
metabolism

Answer 3

the movement of one molecule or ion down its concentration graditent, passive

Question 4

cotransport

Answer 4

• the movement of two molecules, one down its concentration gradient, the other up its concentration grad
• the physical direction of the movement could be any combination as long as the first rule is followed

Question 5

symport
description
example

Answer 5

• type of co-transporter where both molecules move in the same physical direction
• one up, the other down the concentration gradient
• Na glucose exchanger

Question 6

anti-port
description
example

Answer 6

• type of co-transporter where the molecule move in opposite physical direction with regard to the cell
• the molecule moving down its gradient goes first, creating the energy to move the other up its gradient
• Band 3 ion exchanger

Question 7

Active transport

Answer 7

transport that requires energy to move iones or solutes up their concentration or chemical gradients
-ATP or GTP hydrolysis is required
-NA/K ATPase which achieves a high internal conc of K and high external con of Na
CFTR regulates the anion transport in epithelial cells, is a member of the ABC class of ATPases

Question 8

Cystic Fibrosis and its relevance to trnasport

• cause
• chemical effect

Answer 8

• caused by a mutation in the CFTR protein, an ABC ATPase

- without this protein, chloride concnetrations cannot be reulated across the membrane

Question 9

Tangier Disease

Answer 9

-cause by a defect in a ABC ATPase, ATP Binding Cassette 1
-cannot shuttle cholesterol out of the cells due to defective transporter causing an HDL deficiency and a build up of cholesterol in the blood vessel wall
-results in premature CHD
usually die in 40s or 50s
-studying this disease has revealed the pathway of reverse chol transport and insight into the roles of HDL and LDL
-reduced HDL is the most common lipoprotein defect in patients with CHD

Question 10

P-glycoprotein/MDR complex

Answer 10

-ABC ATPase that is capable of pumping out toxins
-to treat cancer we use toxic drugs
some cancer cells over-express this protein, allowing the to pump out the drug before it can destroy the cancer cell.
-this leads to an advantage and replication and therefore therapeutic failure

Question 11

endocytosis
what
function

Answer 11

• the cell receives protions of the membrane in vesicle form
• function sin normal recylcing of the mem, uptake of solute from EC space, uptake of foreing object, and selective uptake of nutrients/ligands

Question 12

steps of endocytosis

Answer 12

• mem invag/evagination tp engulf particles/fluid/molecules
• membrane fission (pinching off)
• acidification of vesicles
• fusion of endocytic vesicle target

Question 13

pinocytosis
another name and metabolic req
process
clinical correlate

Answer 13

• fluid pahse endocytosis that requires ATP
• avesice is formed after uptake of EC and can form with primary lysosome to form the secondary lysosome
• disruption of pinocytosis is the resp for the diruption of the blood brain barrier after a stroke

Question 14

receptor mediated endocytosis
what it does
how it does it
clathrin

Answer 14

• selective uptake, concentration, and processing of nutrients and cell-modulating molecules (hormones) and the degradation of viruses
• proteins or viral particles bind to specific receptors on the mem (typically areas with clathrin) which helps concentrate ligand-receptor complexes (extrinsic peripheral protein)

Question 15

dynamin

endosome

Answer 15

-functions in endocytosis by pinching off the small vesicle (endosome) from the membrane

Question 16

endosome process in endocytosis

after being pinched off

Answer 16

• quickly become acidified by an H+ATPase in the membrane
• are coated with clathrin
• loase their clathrin coat and then fuse with another vesicle called CURL (compartment for uncoupling receptor and ligand). ligan and receptor are seperated into different parts of this vesicle. Most often the receptor buds off and goes back to mem and ligand is sent to the lysosome for degradation

Question 17

adaptins in endocytosis

Answer 17

-help link the clathrin on the cell mem

Question 18

familial hypercholesterolemia and endocytosis
inheritance
3 things that can go wrong
results of the disorder

Answer 18

• due to defective RME
• rare autosomal dominant disease, homozygotes have extremely high chol and dies before their second decade of life
• failure of LDL to bind to receptor properly
• normal binding of LDL but failure for the receptor to cluster into coated pits
• mutant LDL receptor that is missing the mem spanning segment. LDL binds normally but since the receptor isnt anchored properly, it is secreted from the cell
• all of these result in the failure to uptake chol into the cel and therefore leave it in the blood (high chol) and lead to ateriosclorosis

Question 19

rabies, influenza, and other viruses with regards to RME

Answer 19

-all use RME to enter the cell to cause infection

Question 20

phagocytosis

Answer 20

• receptor mediated process that internalizes and degrades large objects such as bacteria and cell debris
• after binding, the cell surface evaginates to engulf the particle, forming a phagosome
• phagosome rapidly acidified by H+ATPase in vesicle mem
• phagosome fuses with the primary lysosome to become a phagolysosome
• lysosomal enzymes degrade biological material but not innert material

Question 21

asbestos and phagocytosis
causes
black lung

Answer 21

• asbestos is recognized by the cell and is attempted to be phagocytosed by can not be degraded by the phagolysosome
• this can cause asbestosis and mesothelioma
• this is the same as black lung and silica fibers

Question 22

streptococcus and phagocytosis

Answer 22

• second most comon bacterial pathogen in humans after staph

- evolved a carbohydrate coat that renders it unrecognizable by macrophages and other immune cells

Question 23

Legionnaires disease and phagocytosis

Answer 23

• caused by L. pneumophila which is phagocytosed by epithelial cels of the resp tract
• once in the phagosome, this bact neutralizes the enviroment, prevents fusion with the lysosome
• then proliferates causing a deadly infection

Question 24

Leishmania and Leprosy and phagocytosis

Answer 24

leishmania is a protozoan and leprosy is a mycobacterium

-these both survive very well in the acidic environment of the phagolysosome

Question 25

Mechanism of phagocytosis

Answer 25

Fc receptors on the plasma membrane recognize IgG molecules attached to the particle to be ingested via phagocytosis. This particle might be a bacterium, yeast, protozoa, damaged erythrocyte, or even an asbestos particle or iron filing!