The waterborne parasite, Giardia lamblia, is a major cause of intestinal illness (giardiasis) worldwide. Giardia is classified as a model organism to study evolution because of its compact genome, reduced metabolic pathways, and lack of emblematic eukaryotic organelles. The infection by Giardia is transmitted by osmotically‐resistant cysts in contaminated food, water, and feces. It has been shown that giardial glucosylceramidesynthase (gGlcT1), an important enzyme of the sphingolipid metabolic pathway, plays a critical role in inducing encystation and cyst production. Modulation of gGlcT1 expression by overexpression interferes with cyst production and cyst viability in culture. In addition, our laboratory has reported that gGlcT1 is a dual‐substrate enzyme, with separate catalytic domains that facilitate the synthesis of both glucosylceramide and galactosylceramide, and its overexpression increases the uptake of membrane lipids and cholesterol significantly. Interestingly, although this parasite has a limited lipid synthesis ability, it expresses a long chain fatty acid elongase (gFAELO) gene, which is mostly expressed in cysts. Because FAELO enzymes are involved in remodeling of fatty acyl chain of membrane lipids and gGlcT1 overexpression increases lipid uptake by Giardia, we investigated whether the interplay between gGlcT1 and gFAELO is important for maintaining the lipid homeostasis in this parasite and whether that drives the process of cyst production. Five clones were developed to track gGlcT1 and/or gFAELO expression. Under different promoters, it was found that the enzyme expression of both enzymes and the enzymatic activity of gGlcT1 was modulated depending on life stage and co‐expression with gFAELO. The production and morphology of cysts was also affected as evaluated by encystation and confocal microscopy. These results suggest that the coordinated temporal expression of gGlcT1 and gFAELO alters lipid homeostasis in Giardia, which could be critical for infective cyst production.Support or Funding InformationThis work was supported by grant R01AI095667 from the NIH (NIAID). Vanessa was supported by the NIH RISE Grant 5R25GM069621 from NIGMS. The biochemical, molecular, and confocal microscopy experiments were carried out at the Genomic Analysis, Cytometry, Screening, and Imaging Core Facilities at the Border Biomedical Research Center (UTEP), supported by grant G12MD007592 from NIMHD (NIH).