TCA's reg & connection to PDHC reg

Question 1

ETC-OCPHOS

Answer 1

req tight coupling of the use of O2, because it is the terminal e- acceptor. If last e- acceptor, must have enough O to be able to do this. (to exit ETC)

NADH must be re-ox, because it will inject e- into ETC (enter ETC)

ATP synthesis: this is the ox-phos part, made ATP and sends it to the ETC

Question 2

TCA makes…

Answer 2

NADH, so TCA coordinates amount of NADH with amount of ATP needed bc TCA, ETC. Ox-PHOS which are all coupled.

Question 3

CS

Answer 3

citrate synthase originally thought to be controlled by concentration of OA affecting amount of citrate produced.
How does this link to previous info?
Lagre delta G, but this enzyme operates close to equilibrium (cellular conditions diff from standard).
Means: OA is still going to control by substrate availability… delta G is not as big as we thought…

Big E drop cannot be paid by CS

Question 4

control points

Answer 4

IDH (isocitrate DH) and a-KGDH, are the control points, which are inhibited with isocitrate being the major point (like with PFK1)

Question 5

Succinyl-CoA and NADH

Answer 5

CoA is a larger part of the molecule, succ is small (only 4 C).

These two are CI of a-KGDH…
NADH is CI of E2 and inhibits a-KG binding to E1.

Question 6

a-KGDH affinity

Answer 6

ADP, Pi, and Ca2+ increase E1’s a-KG affinity, kind of similar to PDHC… but a-KGDH doesnt have cov modifier.
; ATP inhibits by opposing ADP’s activity… two diff but related allosteric effectors, one opposing the other.

Question 7

How/where/why for IDH and a-KGDH

Answer 7

How: CI or something
where:
why : either have a lot of E or not a lot of E.

Question 8

PFK1 and 2 are both inhibited by cit

Answer 8

means:
if glyc inhibited and the flux controller, dont want to ber unning glycolysis. Getting E from somewhere else or have enough E