A transcriptional control model for doublesex -dependent sex differentiation in Nasonia wasps
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Abstract
The transcription factor Doublesex (DSX) orchestrates insect sex differentiation. DSX affects Drosophila melanogaster male and female transcriptome, yet how DSX regulates gene expression in other species is poorly understood. We investigated sex-biased gene expression during the development of the parasitoid wasp Nasonia vitripennis , finding that more than three-quarters of its genes are sex-biased in at least one developmental point. Next, we transiently knocked down dsx expression to infer its role in sex-specific transcriptome regulation, revealing thousands of affected genes in males and a more subtle effect in females. Finally, we performed an in vitro DNA-protein interaction assay to identify DSX binding sites on the genome and primary DSX target genes. By integrating these three datasets, we defined DSX’s regulatory function for all genes in N. vitripennis , revealing that DSX acts mainly in males as both an activator and a repressor. This male-centric model for DSX-mediated regulation is likely to apply to many other insect species.
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The data from every time point were then merged to obtain a global table explaining the sex-bias expression for every gene and the DSX mode of action
What is the phenotype of a DSX knockdown in males and in females? I'm just curious if the larva/animals used to examine gene expression changes in DSX knockdowns are sick.
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To this end, we compared transcriptomes of dsx knockdown individuals with those of control individuals per time point and sex
This is a very interesting study helping to elucidate the role of DSX in N. vitripennis development! Since there are male- and female-specific isoforms of DSX and DSX can act as both a transcriptional activator and repressor in both females and males, is it possible that a gene knockdown (not isoform specific) could obscure the sex-specific roles of DSX? Can you generate DSX knock ins that can only produce female specific isoforms and then examine the outcome on gene expression? (Presumably, a male-specific isoform can not be propagated.)
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