Topic 1

Question 1

Give an example of nutrigenomics.

Answer 1

Nutrigenomics: how nutrients influence gene expression

Lac O(peron)

if absence of lactose the result is repression of lactose metabolism genes.

lacI (at promoter) makes a repressor and binds to lacO which represses transcription of lacO so no b-galactosidase.

If lactose is present, the result is induction of lacO which transcribes and then makes b-galactosidase.

Nutrient: lactose- turns on or off the expression of lacO depending its presence or absence.

Question 2

What is the responsive gene if there is no interaction between the gene and the dietary constituent?

Answer 2

If there is no interaction, it is not a responsive gene.

Question 3

What are the three main ways a dietary constituent influences protein translation?

Answer 3

1. responsive gene -> direct regulation
2. physiological modulation -> secondary mediator -> responsive gene -> path 1
3. directely regulated transcription, mRNA or proteins

Question 4

What are the ways nutrients regulate gene expression?

Answer 4

1. signal transduction
2. enter through nutrient transporters -> bind to nuclear receptors -> act as specific transcription factor
3. environmental factors -> epigenetics effects -> affect gene expression
   eg. methylation

All three options funnel to transcription (DNA to RNA),
modifications: polyadenylation & splicing
translation to protein

Question 5

What is an example of signal transduction?

Answer 5

Akt/mTORC1
congregate all nutrients to this pathway

mTORC1 responds to:

1. nutrients
2. cellular energy status -> AMPK
3. growth factors-> Akt

response:
1. stimulates SREBP –> stimulate lipid synthesis

2. stimulates protein synthesis

Overall result: CELL GROWTH

Concept: to increase cell mass (protein), you must increase volume/size (fat)

Question 6

Map out the components of the PI3K/Akt/mTORC1 pathway.

Answer 6

growth factors -> PI3K -> PIP3 -> Akt:

1. stimulates mTORC1:
   - protein synthesis
   - amino acid uptake -> amino acids
   - glucose uptake-> glycolysis -> TCA cycle-> lipid synthesis via citrate/malate pathway
2. SREBP1 -> lipid synthesis

Question 7

How is SREPB activated?

What is its regulation process?

Answer 7

by low sterol concentration

At low sterol concentration:
SREBP: interacts with SCAP and then COPII. It migrates in a vesicle to the Golgi where there is proteolytic cleavage and enzyme modifications. The protein then leaves the Golgi to the nucleus where it can bind to SRE in the nucleus and stimulate transcription of cholesterols synthesis and fatty acid biosynthesis.

At high sterol concentration: SREBP bound to SCAP, binds to INSIG.

INSIG: resident in the ER so it is stuck there and cannot leave.

Since there is no transport (budding) to the Golgi = no stimulation of target gene.

Question 8

What is mTORC1 for in general?

Answer 8

regulates protein and lipid synthesis

Question 9

What does SREBP to?

Answer 9

stimulates genes involved in cholesterol synthesis

Question 10

What are the elemental composition of life that are abundance?

Answer 10

PONCH

Question 11

Name the 9 chemical function group.

Answer 11

ethers: polar
carboxylic acids: protein (hydrogen bonding especially in non-polar solvents)
hydroxyl: carbohydrates, hydrogen bonding, polar
amines: protein, hydrogen bonding
esters: carbonyl group weakly hydrophilic, weakly acidic
carbonyl: lipids, very little H so densely packed with energy
Phosphate: ATP/DNA