Ovarian RNAseq of Female Estrildid and Non-Estrildid Birds

Extensive research has focused on pathogenic mutations in the human follicle-stimulating hormone receptor (FSHR), which lead to spontaneous ovarian hyperstimulation syndrome (sOHSS) during natural pregnancy or following thawed embryo transfer. However, the underlying molecular mechanisms and therapeutic strategies for OHSS remain incompletely understood. Notably, a threonine (T) to alanine (A) substitution at amino acid position 449, corresponding to the human p.Thr449Ala mutation found in OHSS patients, occurs naturally in estrildid finch FSHR orthologs. This variant enhances the receptor's constitutive activity and sensitivity to hCG. To investigate why estrildid finches carrying the natural FSHR T449A variant do not develop OHSS, we performed bulk RNA-sequencing transcriptomic analysis on ovaries from four avian species under normal physiological conditions. This included two estrildid finch species (zebra finch and white-rumped munia) and two non-estrildid species (canary and chicken), with three biological replicates per group. The analysis of this transcriptomic data aims to elucidate the evolutionary resistance mechanisms in estrildid finches.