cells and organelles: 2

Question 1

lumen of a membrane bound organelle

Answer 1

= congruent/ in harmony with exterior of cell

Question 2

constitutive pathway

Answer 2

direct transport
=> exit from trans-golgi network straight to cell membrane

Question 3

regulatory secretary pathway

Answer 3

particular proteins are synthetised
They are left in a matured secretory granules and when they are needed there is an external signal that is sent to release the molecules

Question 4

lysosomal pathway

Answer 4

which is responsible for the degradation of materials that are not necessary for that particular process at that time.
vesicles diffuse to late endosomes and this fusion makes them form lysosomes

Question 5

mobility of transport vesicles

Answer 5

Proteins are packed into transport vesicles.
The transport vesicles are pulled by various motor proteins (e.g., Kinesin or Dynein).
The motor protein pulls the vesicles along the microtubules.

Question 6

kinesin

Answer 6

a molecular motor protein that transport vesicles away from an organelle along the microtubule

Question 7

dynein

Answer 7

pull vesicles back to the organelle

Question 8

microtubles spread out from the cell centre as tracks

Answer 8

Most microtubules emanate from the centrosome.
The Golgi is usually located close to the centrosome in the cell centre.
Other organelles may move or are positioned on microtubules.

Question 9

centrosome

Answer 9

Centre for organising microtubules.
Centrosomes contain two centrioles (9 array of microtubule triplets).
The role of centrosome is to initiate microtubule growth.

Question 10

lysosomes

Answer 10

ph = 5 =>
high level activity that allows the activation of the acidic hydrolysis, which are enzymes that are responsible for the degradation of materials
=> materials are dissolved bcs of acidity
fusion of vesicle transported out of golgi and late endosome

high concentration of hydrogen ion to maintain pH
And because of that constant process, it means that it requires energy.
That’s why you have the presence of ATP present here.

Question 11

cytosol

Answer 11

ph = 7

Question 12

degradation of mitchondria

Answer 12

fusion between a lysosome and this particular organelle.
This non-functional organelle in this case turns to form autophagosomes.

Question 13

lysosomal storage disease

Answer 13

lysosomal storage disease means that the lysosome lacks the capability to degrade these materials, which is a disease.

Question 14

recycling endosome pathway vs lysosome

Answer 14

external molecules surrounded by external vesicle which is fused to early endosomes

either go to late endosomes and then lysosomes (like a bacteria that needs to be degraded) or recycling endosomes

recycle path => once molecules are used by early endosome => receptor is recycled back into the plasma membrane to trap more molecules into the cell.

Membrane/cargo internalised delivered to endosomes and then passed to lysosomes for degradation. Some membrane is recycled back to the cell surface.

Question 15

how is uptake done? + 3 types

Answer 15

Uptake is by endocytosis

=> large particles by phagocytosis
=> small molecules by pinocytosis
=> receptor-mediated endocytosis.

Question 16

autophagy

Answer 16

Portions of the cell itself can be walled off and digested in lysosomes

Question 17

endocytocis

Answer 17

inside cell injection

Question 18

exocytosis

Answer 18

outside cell ejection

Question 19

receptor-mediated endocytosis

Answer 19

surface of cell => receptor ligand interaction in a region called clathrin coated pit

receptor binds to ligand

membrane carved + invaginate towards cytiplasmic side

recruitement of clathrin => clathrin coated vesicle
=> vesicle hangs and dynamin chops it off so its internalised

fusion with endosome => low ph => ligands dissasociate
LDL receptor + cholestrol is taken down to late endosome, lysosome and cholesterol is released

Question 20

Familial Hypercholesterolemia

Answer 20

mutation in low-density lipoprotein (LDL) receptor causes poor uptake of cholesterol bound to LDL in the blood.

Question 21

Protein Degradation by Proteasome

Answer 21

‘junk proteins’ = tagged with ubiquitin
Proteasome consists of a central barrel complex with a narrow hollow core line with proteolytic enzymes

No membrane involved

Micromolecular complex

In the cytoplasm not in lysosomes

bad protein goes through central pore into central burrow => polypeptide molecule turns into peptide

Question 22

ubiquitin proteasome pathway = ubiquitination

Answer 22

ubiquitin is tied to the junk protein => forms a poly ubiquitin chain

ubiquitin binding to the carboxy terminal of the ubiquitin activating enzyme = E1=> process is driven by ATP.
E1 = activated

E3 ubiquitin ligase and E2 ubiquitin conjugated enzymes forms a complex.

Once the complex is formed, the E1 moves the ubiquitin molecules and transfer them onto the E2 and E3 complex.
And as a result, those ubiquitin molecules are then fused into the junk proteins.

So now this particular protein is tagged ready for degradation.

The polyubiquitinated protein is recognised and degraded by a proteasome

Once the protein is degraded into small peptides, ubiquitin is released in the process for re-use in another cycle.

Question 23

mitochondria

Answer 23

produces ATP = chemical energy
2 billion yrs ago archaea engulfs bacteria
has its own DNA
2 membranes => During further evolution cell membrane invaginates to form internal membranes + bcs of power generated
Two membranes – inner membrane folded into interior
108 ATP
Enable cells to grow bigger
Present in all eukaryotic cells

Contain their own DNA – reproduce by dividing in two
All your mitochondria come from your mother’s egg

Question 24

what does the matrix contain

Answer 24

contains mitochondrial genome and enzymes responsible for reactions of the citric acid cycle and fatty acid oxidation.

Question 25

what does the inner mitochondrial membrane contain

Answer 25

enzymes required for oxidative phosphorylation thus a critical site for ATP generation.

Question 26

what does cytoskeleton allow for

Answer 26

moving
positioning
supporting
protecting

Question 27

microtubules

Answer 27

consist of two polymerised globular proteins subunits called alpha – and beta-tubulin.
negative end of tubulin must be fused into centrosome
Involved in intracellular movement of cell organelles and vesicles.
Form mitotic spindle in centrosomes

Question 28

microfilaments

Answer 28

They are made of double strands of actin and are able 7nm thick.
Microfilaments are linked with membrane proteins which provides structural shape to cells in respect to their environment.
Provides contractile forces enabling cells to move around if necessary.
Two subunits – actin + myosin (motility

Question 29

intermediate filaments

Answer 29

(10 – 12nm): they are formed from a variety of proteins.
form alpha- helix dimers around each other.
There are over 70 intermediate filaments
They are the most stable cytoskeletons.
Support nuclear envelope (lamins)
Provide support for cytoplasm (keratins)
Other known intermediate filaments with cytoskeletal functions include – vimentin and desmin.
Neurofilament proteins –major parts of neurones within the brain
They are not dynamic

Question 30

microvilli

Answer 30

actin is present inside
and gives it they have the capability to sort of protrude into the particular molecule.
They tend to engulf and form an invagination around a particular molecule.
provide us skeletal support or assist in the movement of cell for the core process of phagocytosis.

plays a role when it comes to the
epithelial cells within the stomach when it comes to absorption of nutrients.

Question 31

disease caused by defects at celullar level

Answer 31

Hypercholesterolaemia (defective uptake of lipoproteins)
Cystic fibrosis (misfolding of key protein resulting in defective Cl- ion transport)
Hypertension (defective cell-cell adhesion in the kidney)
Congenital heart defects (errors in cell migration during development)
Muscular dystrophy (defective attachment of the plasma membrane to the cytoskeleton)
Lysosomal storage disease (defective intracellular transport of enzymes)
Food-borne illness (Salmonella, E. coli)
Cancer (errors in cell division, migration, cell polarity, growth, etc)
Ageing

Question 32

familial hypercholesterolemia => origines possibles

Answer 32

LDLR is not properly transported from RER to Golgi for expression on cell surface (X)
LDLR bound to LDL does not cluster in endocytic vesicles on plasma membrane (X)
LDLR is not recycled back to the cell surface (X)