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Fig. 1 | BMC Genetics

Fig. 1

From: Targeting the autosomal Ceratitis capitata transformer gene using Cas9 or dCas9 to masculinize XX individuals without inducing mutations

Fig. 1

Genetic pathway of sex determination in Ceratitis capitata. Cctra and Ccdoublesex (Ccdsx) pre-mRNAs exon-intron structures and sex-specific transcripts are shown. Female-specific and male-specific Cctra exons are indicated as pink and dark blue boxes, respectively. Cctra female-specific transcript on the left contains a 429 aa long ORF. Cctra male-specific exons introduce premature stop codons in male-specific longer transcripts (orange vertical bars). CcTRA M1 and M2 male-specific isoforms contain truncated CcTRA ORFs represented by azul regions. In XX embryos, maternal CcTRA (orange circle) and CcTRA-2 (green circle) proteins promote female-specific splicing of newly transcribed Cctra pre-mRNA, suppressing male-specific splicing by binding to TRA/TRA-2 cis regulatory elements (red spots). Female-specific Cctra mRNA encodes zygotic CcTRA (violet circle) that maintains (together with zygotic CcTRA-2; dark green circle) the Cctra autoregulation induced by the maternal contributions by a feedback loop. Both CcTRA and CcTRA-2 proteins promote also female-specific splicing of the downstream Ccdsx pre-mRNA, producing mRNAs that include a female-specific exon (pink) and encode CcDSXF isoform inducing female sexual differentiation [6]. In XY embryos the Y-linked Maleness-on-the-Y gene (MoY) induces male-specific Cctra splicing and, hence, the collapse of the positive feedback loop [7]. By default, male-specific splicing of Ccdsx leads to male-specific splicing and CcDSM isoform inducing male sexual differentiation [6, 8]

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