Final answer:
Δ-aminolevulinic acid synthase is regulated by negative feedback from heme and glucose. Heme acts as an aporepressor inhibiting its own production via ALA synthase, while glucose inhibits the transcription factor PPAR-y, affecting ALA synthase synthesis. This is a mechanism of maintaining homeostasis within the heme synthesis pathway.
Step-by-step explanation:
Δ-aminolevulinic acid synthase (ALA synthase) plays a critical role in the regulation of heme synthesis, acting as the key regulatory enzyme in this biological pathway. It is subject to negative feedback by heme, the end product of its own synthesis pathway, which acts as an aporepressor, inhibiting the gene responsible for the production of ALA synthase-I. This regulatory mechanism is an example of how end products can control enzymatic activity to maintain homeostasis.
Similarly, glucose also regulates ALA synthase through inhibitory action on PPAR-y, a transcription factor that normally induces the synthesis of ALA synthase. As an example of broader metabolic regulation, enzymes involved in various pathways, including glycolysis and the TCA cycle, like glucose-6-phosphate dehydrogenase and G-3-P dehydrogenase, are also regulated by end products and other metabolites through feedback inhibition and allosteric effects.