Single-cell RNA-seq data of ovaries from estrildid finch and non-estrildid bird species under physiological conditions

Extensive research has focused on pathogenic gain-of-function mutations in the human follicle-stimulating hormone receptor (FSHR), such as p.Thr449Ala, which cause spontaneous ovarian hyperstimulation syndrome (sOHSS) during natural pregnancies or after thawed embryo transfer. However, the complete molecular pathophysiology and treatment options for OHSS remain elusive. Intriguingly, a homologous threonine-to-alanine substitution at position 449 (T449A) occurs naturally in the FSHR of estrildid finches. This variant confers increased receptor constitutive activity and sensitivity to hCG, yet estrildid finches do not develop OHSS.To investigate the evolutionary resistance mechanism in estrildid finches, we performed single-cell RNA sequencing on ovaries from adult females under physiological conditions. Our analysis included two estrildid finch species--zebra finch and white-rumped munia--and one non-estrildid control species, the canary. We utilized three biological replicates for the zebra finch and canary, and two for the white-rumped munia. By analyzing this single-cell transcriptomic dataset, we aimed to delineate the cellular and molecular adaptations that protect estrildid finches from OHSS despite harboring the FSHR T449A variant.