LRH-1 coordinates metabolic and epigenetic programs that establish luteal cell identity [ChIP-seq]

Corpus luteum function and consequent progesterone secretion are essential for these processes. Large luteal cells are the primary source of progesterone production, yet the transcriptional programs that define their identity remain unclear.

Here, we identify the nuclear receptor Liver receptor homolog-1 as a key regulator of large luteal cell function. Loss of Liver receptor homolog-1 disrupts lipid droplet accumulation and downregulates key steroidogenic genes. Mechanistically, Liver receptor homolog-1 undergoes chromatin-binding reprogramming during luteinization, establishing regulatory regions that couple lipid metabolism to steroidogenesis.