A Sexual Shift Induced by an Androgenic Gland Insulin-Like Gene Silencing in Intersex Crayfish


Meeting Abstract

56.3  Tuesday, Jan. 5  A Sexual Shift Induced by an Androgenic Gland Insulin-Like Gene Silencing in Intersex Crayfish ROSEN, O.*; MANOR, R.; WEIL, S.; LINIAL, A.; AFLALO, E.D.; SAGI, A.; Ben-Gurion University of the Negev; Ben-Gurion University of the Negev; Ben-Gurion University of the Negev; Ben-Gurion University of the Negev; Ben-Gurion University of the Negev; Ben-Gurion University of the Negev ohadrosen1@gmail.com

Male sexual differentiation in crustaceans is controlled by a unique male specific androgenic gland (AG). In the Australian red claw crayfish Cherax quadricarinatus, a phenomenon of sexual plasticity is exhibited in form of intersex individuals bearing both a fully active male reproductive system and masculine secondary sex characters along with a constantly arrested ovary. In the present study, the intersex model was used for the examination of changes caused by silencing of Cq-IAG, an insulin-like gene specifically expressed in the AG, through dsRNA injection. Upon the silencing of this single gene, intersex crayfish went through a wide array of sex-related alterations. The pleopods of injected individuals were transformed and exhibited characteristics associated with egg bearing and maternal care. The formerly spermatophore-filled sperm duct had emptied and the spermatogenic testis went through extensive apoptosis. Simultaneously, expression of the female specific vitellogenin gene was induced and a significant increase in the ovary size was highly evident. This observation is attributed to the accumulation of the yolk protein vitellin in the developing oocytes. In addition to the functional determination of Cq-IAG as the pivotal androgenic hormone encoding gene in the crayfish, the necessity of its product as an anti-apoptotic maintenance agent of the male gonad had been unequivocally elucidated. This study provides the first evidence that silencing of a single insulin-like gene can manipulate and transform a wide array of male-related phenotypes into female-unique characteristics.

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