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Feminization of the Blood Brain Barrier changes the brain transcriptome of Drosophila melanogaster males

ABSTRACT: Beyond its crucial role as a tight barrier to protect the nervous system, the Blood Brain Barrier (BBB) is increasingly being recognized for its physiological processes that affect brain function and behavior. In Drosophila melanogaster, the BBB expresses sex-specific transcripts, and a change in the sexual identity of adult BBB cells results in a significant reduction of male courtship behavior. The molecular nature of this BBB/brain interaction is unknown. Here we feminize BBB cells by targeted expression of the Drosophila female specific master regulator TraF in otherwise normal males. We examined the effect on RNA expression in dissected brains by RNA sequencing. We find that 284 transcripts change in comparison to normal males. Transcripts representing cell signaling processes and synaptic communication are enriched, as are hormonal mediators. These transcripts are candidates for the sex-specific interaction between the BBB and the brain circuits that regulate behavior.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE302328 | GEO | 2025/08/01

REPOSITORIES: GEO

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Project description:The blood-brain barrier (BBB) is an evolutionary conserved tissue interface that possesses potent chemical protection properties functioning to strictly modulate the central nervous system (CNS) microenvironment. These same properties, including tight cellular junctions and efflux transporters, also limit access of CNS-active pharmaceuticals. For this reason, understanding the molecular mechanisms that regulate BBB chemical protection is of great biomedical interest. The BBB of Drosophila consists of two surface glia layers that completely surround the brain. This tissue interface contains both “tight” cellular junctions (termed septate junctions) and drug efflux transporters; thus, the Drosophila BBB can potentially serve as a model for understanding complex regulation of BBB physiology. In this study, we show reciprocal compensatory responses following disruption of critical BBB genes: deletion of the septate junction regulator Moody causes increased drug efflux and up-regulation of the P-glycoprotein ortholog Mdr65; conversely, disruption of Mdr65 expression causes increased septate junction tightness and up-regulation of Moody. We reveal these homeostatic interactions with physiologic observations, gene expression data, and anatomical images of the BBB surface. Whole brain microarray data point to responses that are consistent with our physiologic observations and these responses are likely localized to the BBB. To our knowledge, this is the first observation of a reciprocal compensatory interaction at a tissue barrier. Furthermore, this study paves the way for future studies elucidating the direct pathways that link GPCR signaling and drug transporter regulation at the BBB. The main comparisons are between WT_new, C17 (Moody null), and PMdr65 (Mdr65 null). Since WT_new were processed on a different day than C17 and PMdr65, we also included another WT sample (WT_old) to control for genes that change depending on batch effects. Since the mutants are also in a different genetic background than WT, we also included a control that is in a similar background (UAS_control).

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Feminization of the Blood Brain Barrier changes the brain transcriptome of Drosophila melanogaster males

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