Schematic summary of the results from the present experiment for the response of expression of various genes in goat mammary epithelial cells to unsaturated fatty acids t10,c12-CLA, DHA, and EPA. Genes are clustered in functional groups related to milk fat synthesis. As reported, it is also the possible interaction of LCFA with PPARγ or other unidentified transcription factors (TF) to elicit the observed responses. Grey shade denotes no significant change, red shade denotes upregulation, and blue shade denotes downregulation relative to control. In connecting lines, arrow head denotes induction while flat head denotes inhibition. Lightning symbol denotes induction of TF by the LCFA. t10,c12-CLA decreased the transcription of 9 genes via a TF (in blue) which activity was induced by activation of PPARγ. The increase in transcription of 6 genes (i.e., LPL, CD36, FABP3, AGPAT6, MID1IP1, and NCOR1) by t10,c12-CLA was via a TF (in orange) which activity was inhibited by PPARγ. The transcription of only two of the measured genes (FABP4 and PLIN2) was increased by t10,c12-CLA acting upon an unknown TF (in black) that was independent from PPARγ. DHA decreased the transcription of 16 genes and increased the transcription of 2 genes (LPL and CD36) via a TF (in orange) which activity was inhibited by the activation of PPARγ. Transcription of 3 genes (AGPAT6, MID1IP1, and PLIN2) was upregulated and transcription of BDH was downregulated by DHA via a TF that was independent from PPARγ (in black). EPA decreased the transcription of 12 genes but none directly via PPARγ. However, the transcription of AGPAT6 and PPARG was upregulated and transcription of ACACA, RXRA, MID1IP1, and PLIN2 was downregulated by EPA via a TF which activity was inhibited by PPARγ (in orange). The transcription of ACSL1, SCD1, and INSIG1 was downregulated and the transcription of LPL was upregulated by EPA through one or more TF that were dependent from an activation of PPARγ (in blue). Transcription of 9 genes was decreased or increased by EPA via one of more TF (in black) that were independent from PPARγ.