It is believed that both DXS and DXR are rate-determining enzymes, allowing them to regulate carotenoid levels. This was discovered in an experiment where DXS and DXR were genetically overexpressed, leading to increased carotenoid expression in the resulting seedlings. Also, J-protein (J20) and heat shock protein 70 (Hsp70) chaperones are thought to be involved in post-transcriptional regulation of DXS activity, such that mutants with defective J20 activity exhibit reduced DXS enzyme activity while accumulating inactive DXS protein. Regulation may also be caused by external toxins that affect enzymes and proteins required for synthesis. Ketoclomazone is derived from herbicides applied to soil and binds to DXP synthase. This inhibits DXP synthase, preventing synthesis of DXP and halting the MEP pathway. The use of this toxin leads to lower levels of carotenoids in plants grown in the contaminated soil. Fosmidomycin, an antibiotic, is a competitive inhibitor of DXP reductoisomerase due to its similar structure to the enzyme. Application of said antibiotic prevents reduction of DXP, again halting the MEP pathway.