The intricate balance between fertility and immune function is a well-documented phenomenon across various organisms. However, the mechanisms connecting these two crucial and energy-intensive processes remain poorly understood, particularly in complex, slow-reproducing animals. Our lab previously discovered that TCER-1, the homologue to the human Transcription Elongation & Splicing Factor 1 (TCERG1), links reproductive fitness to innate immunity in the nematode Caenorhabditis elegans. TCER-1 mutants show reduced fertility but enhanced innate immunity against the human opportunistic pathogen Pseudomonas aeruginosa strain PA14 (PA14). This study aims to investigate the epigenetic modifications of TCER-1 and how its downstream lysosomal lipolysis pathway influences reproductive health, specifically egg integrity. Our preliminary studies suggest that TCER-1 modulates lipid metabolism to repress immunity and enhance reproductive health. Gas chromatography-mass spectrometry revealed that the absence of TCER-1, especially during maternal infection, leads to a deficiency in essential fatty acids in the embryos. These fatty acids are crucial for developing the permeability barrier of the eggshell. Using BODIPY dye exposure, we observed that eggshell defects predominantly occur in TCER-1-deficient mothers. This indicates that TCER-1 is vital for ensuring that essential fatty acids are available for eggshell development, particularly under stress conditions.