Abstract
ABSTRACTSome mAL neurons in the male brain form the ipsilateral neurite (ILN[+]) in a manner dependent on FruBM, a male-specific transcription factor. FruBM represses robo1 transcription, allowing the ILN to form. We found that the proportion of ILN[+]-mALs in all observed single cell clones dropped from ∼90% to ∼30% by changing the heat-shock timing for clone induction from 4-5 days after egg laying (AEL) to 6-7 days AEL, suggesting that the ILN[+]-mALs are produced predominantly by young neuroblasts. Upon EcR-A knockdown, ILN[+]-mALs were produced at a high rate (∼60%), even when heat shocked at 6-7 days AEL, yet EcR-B1 knockdown reduced the proportion of ILN[+]-mALs to ∼30%. Immunoprecipitation assays in S2 cells demonstrated that EcR-A and EcR-B1 form a complex with FruBM. robo1 reporter transcription was repressed by FruBM and ecdysone counteracted FruBM. We suggest that ecdysone signaling modulates the FruBM action to produce an appropriate number of male-type neurons.
Highlights
It is widely thought that the sex-determination mechanism is distinctly different between vertebrates and insects; in vertebrates, systemic androgens and estrogens primarily determine the sex of an entire body (Sekido and Lovell-Badge, 2009), whereas in insects, every cell adopts a sexual fate according to its own chromosomal composition, without any involvement of androgens and estrogens (Salz, 2011)
EcR is a genetic modifier of fru In searches for genes that interact with fru, we took advantage of a visible phenotype induced by overexpression of the normal form of FruB in the compound eye (Goto et al, 2011)
The EcR mutant heterozygosity induced only a moderate roughness of the compound eye (Fig. 1B,C), which cannot explain the observed suppression of FruB-induced eye phenotypes by a mutant copy of EcR, suggesting that EcR genetically interacts with fru, at least when FruB is ectopically expressed in the eye
Summary
It is widely thought that the sex-determination mechanism is distinctly different between vertebrates and insects; in vertebrates, systemic androgens and estrogens primarily determine the sex of an entire body (Sekido and Lovell-Badge, 2009), whereas in insects, every cell adopts a sexual fate according to its own chromosomal composition, without any involvement of androgens and estrogens (Salz, 2011). The major components of steroids that induce molting are systemic α-ecdysone, synthesized in the prothoracic gland (Karlson, 1996), and its derivative, 20-hydroxyecdysone Division of Neurogenetics, Tohoku University Graduate School of Life Sciences, Sendai, 980-8577, Japan. Ecdysones bind to a heterodimeric nuclear receptor composed of EcR and Ultraspiracle (Usp) proteins, thereby regulating the transcription of downstream genes that are hierarchically ordered to orchestrate a complex series of biological events, leading to molting (Hill et al, 2013). The EcR subunit has three isoforms, EcR-A, EcR-B1 and EcR-B2, each with distinct roles and expression patterns (Hara et al, 2013; Hill et al, 2013; Yamanaka et al, 2013)
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