Differentially regulated genes in Esr2-mutant rat granulosa cells
Vincentaben Khristi,
V. Praveen Chakravarthi,
Prabhakar Singh,
Subhra Ghosh,
Archit Pramanik,
Anamika Ratri,
Shaon Borosha,
Katherine F. Roby,
Michael W. Wolfe,
M.A. Karim Rumi
Affiliations
Vincentaben Khristi
Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS 66160, United States
V. Praveen Chakravarthi
Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS 66160, United States
Prabhakar Singh
Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS 66160, United States
Subhra Ghosh
Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS 66160, United States
Archit Pramanik
Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS 66160, United States
Anamika Ratri
Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS 66160, United States
Shaon Borosha
Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, KS 66160, United States
Katherine F. Roby
Department of Anatomy and Cell Biology, University of Kansas Medical Center, Kansas City, KS 66160, United States; Institute for Reproductive Health and Regenerative Medicine, University of Kansas Medical Center, Kansas City, KS 66160, United States
Michael W. Wolfe
Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, KS 66160, United States; Institute for Reproductive Health and Regenerative Medicine, University of Kansas Medical Center, Kansas City, KS 66160, United States
M.A. Karim Rumi
Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS 66160, United States; Corresponding author.
RNA seq analyses were performed in granulosa cells (GCs) collected from gonadotropin treated ESR2 mutant rats. Data obtained from a null mutant with Esr2 exon 3 deletion (∆3) and another DNA binding domain (DBD) mutant with exon 4 deletion (∆4) were compared to that of wildtype (WT) rats. The raw data were analyzed using CLC genomics workbench. High quality RNA-sequencing reads were aligned to the Rattus norvegicus genome. Differentially expressed genes in ∆3 or ∆4 Esr2-mutant GCs were identified based on the following criteria: FDR p-Value ≤0.05 and an absolute fold change of 2. Fewer differentially expressed genes were identified in ∆3 compared to the ∆4 mutant group. As both mutant groups demonstrated a common phenotype of ovulation failure, differentially expressed genes common to both in ∆3 and ∆4 mutant rats were emphasized and further analyzed in the companion article “ESR2 regulates granulosa cell genes essential for follicle maturation and ovulation” [1].