Practice question

Selenium activation for selenocysteine synthesis relies on selenophosphate synthetase SelD in bacteria and SPS1/SPS2 isozymes in eukaryotes. Using ATP hydrolysis, SelD phosphorylates reduced selenide anion derived from selenite reduction via thiol systems or selenocysteine lyase, producing labile high-energy monoselenophosphate H2SePO3-. Mechanism proceeds through enzyme-bound pyrophosphate intermediate and selenide activation. Free selenocysteine extremely reactive, toxic, so selenophosphate directly delivers selenium within SepSecS or SelA active site onto tRNA-bound intermediate, avoiding cellular release. Deletion of selD eliminates all selenoproteins, causing oxidative stress hypersensitivity, embryonic lethality in mice, illustrating essential link between trace element biochemistry and translation regulation.