Figure 2: Testicular deformity in ERR deficiency is consistent with the reduced levels of, sox100B in the adult testes as well as larval gonads of ERR knockdown males.

(A) The male reproductive tract of control male, with elongated testes (T) and normal accessory glands (AG). (B) Underdeveloped testes in ERR knockdown males produced from ERR-miRNA. (C) Extremely deformed and globular testes in ERR knockdown males produced from ERR-TRiP line. (D) The levels of Sox100B transcripts were reduced to 2 folds in testes of ERR-miRNA knockdown males (*p < 0.05, represented as ERR-miRNA) while 4 folds reduction was evident in ERR-TRiP knockdown males (**p < 0.01, represented as ERR-TRiP). The ∆ct values were determined through normalization against Act-5c, which was used as an internal control for the quality of the template. (E) The adult testes of ERR knocked down males, probed with Sox100B antibody reflected marked decrease in the levels of Sox100B protein when compared to their respective control (Panel Sox100B); α-tubulin served as loading control (Panel α-tubulin). (F) Immunofluorescence based detection of Sox100B in larval male gonad revealed higher Sox100B positive signals (green dots marked by white arrows) in the central transparent region of control male gonad and (G) Very few Sox100B positive cells with relatively weaker signal intensity (faint green dots, marked by white arrows) in ERR knockdown (ERR-TRiP) male gonads. The panels represent the overlay of nuclear (DAPI in blue) and Sox100B (green) staining.