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Figure 10.2 The general features of somatic sex determination in D. melanogaster . The ratio of X
chromosomes to autosomes (A) determines whether Sxl + is ON. Sxl + produces a protein, SXL, that
acts as a splicing factor on the RNA produced by the tra + gene, resulting in the production of active
TRA protein. TRA, together with the product of the tra-2 + gene, determine the female-specific splic-
ing of the dsx + and fruitless + RNAs, which results in a cascade of genes functioning to produce a
female. If Sxl + is OFF, the individual becomes a male because male-specific products (DSX M and
FRU M ) of the dsx + and fru + genes are produced.
Sex-lethal + is a key switch gene that, very early in development, affects both
somatic sexual differentiation and dosage compensation in D. melanogaster
( Figure 10.2 ). Sex lethal + codes for an RNA-splicing enzyme. Its action on the next
gene in the cascade, transformer + , is restricted to females in its role in sexual dif-
ferentiation. Sex-lethal + must be ON in females and OFF in males ( Figure 10.2 ).
Once the X:A ratio is read and the Sxl + gene is turned ON or OFF early in embryonic
development, the developmental path chosen is stable ( Cline and Meyer 1996 ).
Sxl + is transcribed in D. melanogaster females in a complex manner. Two dif-
ferent promoters function in somatic cells; one, the establishment promoter,
Sxl Pe , acts very early and only for a brief period during nuclear cell cycle 12 to
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