A double negative post-transcriptional regulatory circuit mediates the virgin behavioral state
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ABSTRACT:
PROVIDER: PRJNA701272 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13680919_1.fastq.gz | Fastqsanger.gz | |||
| SRR13680919_2.fastq.gz | Fastqsanger.gz | |||
| SRR13680920_1.fastq.gz | Fastqsanger.gz | |||
| SRR13680920_2.fastq.gz | Fastqsanger.gz | |||
| SRR13680921_1.fastq.gz | Fastqsanger.gz |
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Project description:The survival and reproductive success of animals depends on the ability to harmonize their external behaviors with their internal states. For example, females conduct numerous social programs that are distinctive to virgins compared to post-mated and/or pregnant individuals. In Drosophila, the fact that the post-mating switch is initiated by seminal factors implies the default state as virgin. Recently, we uncovered molecular and genetic control of the female virgin state. In particular, repression of the transcription factor Homothorax (Hth) by mir-iab-4/8 within the abdominal ventral nerve cord (VNC) is critical for unmated females to execute virgin behaviors. To elucidate new components of this regulatory circuit, we exploited mir-iab-4/8 deletion and hth-miRNA binding site mutants (hth[BSmut]) to elucidate doublesex (dsx) as a critical downstream factor. While Dsx has mostly been studied during sex-specific differentiation, its activities in neurons are little known. We find that accumulation of Dsx in the CNS is mutually exclusive with Hth, and downregulated in miRNA/hth[BSmut] mutants. Moreover, experimental suppression of Dsx in highly restricted sets of abdominal neurons abrogates female virgin conducts, in favor of mated behavioral programs. Thus, a double negative pathway in the VNC mediates the virgin behavioral state.
2021-06-29 | GSE166562 | GEO
Project description:Virgin females of many species conduct distinctive behaviors, compared with post-mated and/or pregnant individuals. In Drosophila, this post-mating switch is initiated by seminal factors, implying that the default female state is virgin. However, we recently showed that loss of miR-iab-4/8-mediated repression of the transcription factor Homothorax (Hth) within the abdominal ventral nerve cord (VNC) causes virgins to execute mated behaviors. Here, we use genomic analysis of mir-iab-4/8 deletion and hth-microRNA (miRNA) binding site mutants (hth[BSmut]) to elucidate doublesex (dsx) as a critical downstream factor. Dsx and Hth proteins are highly complementary in CNS, and Dsx is downregulated in miRNA/hth[BSmut] mutants. Moreover, virgin behavior is highly dose sensitive to developmental dsx function. Strikingly, depletion of Dsx from very restricted abdominal neurons (SAG-1 cells) abrogates female virgin conducts, in favor of mated behaviors. Thus, a double-negative regulatory pathway in the VNC (miR-iab-4/8 ˧ Hth ˧ Dsx) specifies the virgin behavioral state.
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Project description:We have previously shown that during lactation, osteocytes directly remodel their perilacunar and pericanalicular matrix, thereby mobilizing calcium and contributing to maternal bone loss. To identify genes potentially responsible for perilacunar remodeling, microarray analysis was performed on osteocytes from CD-1 virgin and lactating mice and mice sacrificed on day 7 post weaning. By comparing how gene expression changes in osteocytes among virgin, lactation and post lactation, the goal is to identify the genes osteocytes use to remodel their perilacunar matrix
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Project description:Social behavioral changes are a hallmark of several neurodevelopmental and neuropsychiatric conditions, nevertheless the underlying neural substrates of such dysfunction remain poorly understood. Building evidence points to the prefrontal cortex (PFC) as one of the key brain regions that orchestrates social behavior. We used this concept with the aim to develop a translational rat model of social-circuit dysfunction, the chronic PFC activation model (CPA). Chemogenetic designer receptor hM3Dq was used to induce chronic activation of the PFC over 10 days, and the behavioral and electrophysiological signatures of prolonged PFC hyperactivity were evaluated. To test the sensitivity of this model to pharmacological interventions on longer timescales, and validate its translational potential, the rats were treated with our novel highly selective oxytocin receptor (OXTR) agonist RO6958375, which is not activating the related vasopressin V1a receptor. CPA rats showed reduced sociability in the three-chamber sociability test, and a concomitant decrease in neuronal excitability and synaptic transmission within the PFC as measured by electrophysiological recordings in acute slice preparation. Sub-chronic treatment with a low dose of the novel OXTR agonist following CPA interferes with the emergence of PFC circuit dysfunction, abnormal social behavior and specific transcriptomic changes. These results demonstrate that sustained PFC hyperactivity modifies circuit characteristics and social behaviors in ways that can be modulated by selective OXTR activation and that this model may be used to understand the circuit recruitment of prosocial therapies in drug discovery.
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Project description:We have previously shown that during lactation, osteocytes directly remodel their perilacunar and pericanalicular matrix, thereby mobilizing calcium and contributing to maternal bone loss. To identify genes potentially responsible for perilacunar remodeling, microarray analysis was performed on osteocytes from CD-1 virgin and lactating mice and mice sacrificed on day 7 post weaning. By comparing how gene expression changes in osteocytes among virgin, lactation and post lactation, the goal is to identify the genes osteocytes use to remodel their perilacunar matrix To identify genes responsible for perilacunar remodeling, microarray analysis was performed on tibiae from CD-1 virgin and lactating mice and mice sacrificed on day 7 post weaning. Periosteum and bone marrow were removed from the tibiae and the bone fragments underwent sequential collagenase/trypsin digestion and were examined histologically to ensure removal of all surface cells and confirm osteocyte enrichment prior to RNA extraction. Microarray Affy M430 arrays, n=3 per group were performed and Genepattern and Bioconductor were used to analyse the microdata.
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Project description:P. citri mealybugs cause severe damage in citrus production. We aimed at indentifying genes involved in mealybug sex pheromone biosynthesis. As these should be expressed in virgin females and are presumably downregulated after mating, we looked at genes differentially expressed between mated and virgin females.
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Project description:We demonstrate in mice that perinatal SERT expression in glutamatergic pyramidal neurons in the hippocampus and mPFC modulates sexually dimorphic gene expression during hippocampal circuit assembly and is a source for sex-biased susceptibilities to cognitive and behavioral impairments.
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Project description:In many species, adults care for young offspring that are not their own, a phenomenon called alloparenting. However, most nonparental adults must be sensitized by repeated or extended exposure to pups before robustly displaying of parental-like behaviors. To capture neurogenomic events underlying the transition to active parental caring behaviors, we analyzed brain gene expression and chromatin profiles of virgin female mice co-housed with mothers during pregnancy and after birth. After an initial display of antagonistic behaviors and a surge of defense-related gene expression, we observed a dramatic shift in the chromatin landscape specifically in amygdala of the pup-exposed virgin females, accompanied by a dampening of defense-related gene expression. This epigenetic shift coincided with hypothalamic expression of the oxytocin gene and the emergence of behaviors and gene expression patterns classically associated with maternal care. The results outline a neurogenomic program associated with dramatic behavioral changes and suggest molecular networks relevant to human postpartum mental health.
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