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Gut epithelium modifies enteric behaviors during nutritional adversity via distinct peptidergic signaling axes

ABSTRACT: Gut epithelium modifies enteric behaviors during nutritional adversity via distinct peptidergic signaling axes

PROVIDER: PRJNA1206710 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31896153.fastq.gz	Fastqsanger.gz
	SRR31896154.fastq.gz	Fastqsanger.gz
	SRR31896155.fastq.gz	Fastqsanger.gz
	SRR31896156.fastq.gz	Fastqsanger.gz
	SRR31896157.fastq.gz	Fastqsanger.gz

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Gut epithelium modifies enteric behaviors during nutritional adversity via distinct peptidergic signaling axes

Project description:Interorgan signaling events are emerging as key regulators of behavioral plasticity. The foregut and hindgut circuits of the C. elegans enteric nervous system (ENS) control feeding and defecation behavior, respectively. Here we show that epithelial cells in the midgut integrate feeding state information to control these behavioral outputs via releasing distinct neuropeptidergic signals. In favorable conditions, insulin and non-insulin peptides released from midgut epithelia activate foregut and hindgut enteric neurons, respectively, to sustain normal feeding and defecation behavior. During food scarcity, altered insulin signaling from sensory neurons activates the transcription factor DAF-16/FoxO in midgut epithelia, which blocks both peptidergic signaling axes to the ENS via transcriptionally shutting down the intestinal neuropeptide secretion machinery. Our findings demonstrate that midgut epithelial cells act as integrators to relay internal state information to distinct parts of the enteric nervous system to control animal behavior.

2025-01-06 | GSE285886 | GEO

Human saliva modifies growth, biofilm architecture and competitive behaviors of oral streptococci

Project description:Human saliva modifies growth, biofilm architecture and competitive behaviors of oral streptococci

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Effects of early life adversity on male reproductive behavior and the medial preoptic area

Project description:Early life adversity has been linked to altered reproductive development in humans, including changes in the timing of pubertal onset and sexual activity. One common form of early life adversity is having limited access to resources. This form of early life adversity can be modeled in rodents using the limited bedding and nesting model (LBN), in which rat dams and pups are placed in a low resource environment from postnatal day (PND) 2 through 9. Our laboratory has previously shown that male rats raised in LBN conditions have elevated levels of plasma estradiol compared to control males. Female rats, on the other hand, show no effect of LBN on plasma hormone levels, pubertal timing, or estrous cycle duration in adulthood. Here, we find that LBN males also show changes in adult reproductive behaviors. LBN males acquired the suite of reproductive behaviors more quickly than their control counterparts over the course of 3 weeks of testing, showing shorter latencies to mount, intromit, and ejaculate compared to controls prior to the final week of testing. We also characterized LBN-induced gene transcription changes across sex in the medial preoptic area (mPOA) which underlies reproductive behaviors. Interestingly, there was no effect of LBN on puberty onset (as measured by preputial separation) or masculinization of the sexually dimorphic nucleus of the preoptic area (SDN/POA; as measured by calbindin immunoreactivity) in males, suggesting LBN may not exert effects on hormone-dependent measures until after puberty.

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Prenatal adversity configures the transcriptome of a subpopulation of ventral dentate granule cells for recruitment to drive innate anxiety

Project description:Adverse prenatal environment is a risk factor for the development of psychiatric disorders. Although studies have implicated epigenetic mechanisms, little is known about how epigenomic changes come about and lead to abnormal behaviors in affected individuals. We sought to identify epigenomic and transcriptomic signatures induced by a proinflammatory gestational environment in the ventral dentate gyrus (vDG), a hippocampal region linked to avoidance of threatening contexts, that persist and promote anxiety-like behavior in mice. Here we show that adversity shifted the methylation of enhancers and promoters with intermediate methylation and altered synapse-related gene expression, resulting in epigenetic and transcriptional heterogeneity in the vDG. Exposure to an anxiogenic environment recruited vDG neurons with the most transcriptional impact. Differentially expressed synapse-relevant genes in ensemble neurons tended to be differentially methylated. Finally, this ensemble exhibited higher activity in threatening than safe environment suggesting a prenatal adversity-induced epigenetic and neurobiological sequalae that leads to anxiety.

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Prenatal adversity configures the transcriptome of a subpopulation of ventral dentate granule cells for recruitment to drive innate anxiety

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Project description:Our group recently transcriptomically characterized coculture growth between Streptococcus mutans and several species of commensal streptococci (Rose et al, 2023). However, these experiments were carried out in our lab-based experimental medium, tryptone and yeast extract (TY-). To understand whether culturing these species within a medium that more closely mimics their natural environment alters the interaction, we evaluated both monoculture and coculture growth between the dental caries pathogen Streptococcus mutans and oral commensal species Streptococcus oralis in a half TY- / half human saliva mix that was optimally chosen based on our initial characterization of oral streptococci behaviors in medium mixes containing saliva. Our results surprising show that inclusion of saliva enhances the competition of Streptococcus mutans against commensal streptococci through upregulation of carbohydrate uptake and glycolytic pathways.

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Project description:Exposure to serious or traumatic events early in life can lead to persistent alterations in physiological stress response systems, including enhanced cross-talk between the neuroendocrine and immune system. These programming effects may be mechanistically involved in mediating the effects of adverse childhood experience on disease risk in adulthood. Here, we investigated neuroendocrine as well as genome-wide mRNA expression responses in monocytes to acute stress exposure, in a sample of healthy adults (n=30) with a history of early childhood adversity, and a control group (n=30) without trauma experience. The early adversity group showed altered hypothalamus-pituitary-adrenal (HPA) axis responses to stress, evidenced by lower ACTH and cortisol responses. Analyses of gene expression patterns showed a larger stress-induced increase of cardinal pro-inflammatory transcripts IL6 and FOSB, and an increased activity of pro-inflammatory upstream signaling in the early adversity group. We also identified transcripts that were differentially correlated with stress-induced cortisol increases between the groups. Noteworthy, FKBP5 expression was less responsive to cortisol induction in the early adversity group, with potential effects on the ultra-short feedback loop that balances FKBP5 and glucocorticoid receptor activity. Further exploratory analyses showed differential stress-induced regulation of gene transcription between the groups. Prominent among the differentially regulated transcripts were those coding for genes involved in signal transducer activity, G-protein coupled receptors, and several genes involved in serotonin receptor signaling. We suggest that childhood adversity leads to persistent alterations in transcriptional control of stress responsive pathways, which - when chronically or repeatedly activated - might predispose individuals to stress-related psychopathology.

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Transcriptome analysis in the medial prefrontal cortex of mice exposed to multi-hit early adversity

Project description:We have employed whole genome microarray expression profiling to identify long-term gene expression changes associated with early adversity in male and female C3H/HeN mice

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Molecular Portraits of Social Adversity in Breast Cancer

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Expression profile of Maize (Zea mays L.) Embryonic Axes During Germination: Regulation of Ribosomal Protein mRNAs.

Project description:Seed germination is a critical developmental process in plant propagation. Knowledge of the gene expression patterns in this critical process is important in order to understand the main biochemical reactions involved in successful germination, specially for economically relevant plants such as Maize. The purpose of this study is the gene expression analysis of quiescent and germinated maize embryonic axes to determine the regulatory mechanism for (r)-protein expression during the maize development process. This study analyzed samples of total and polysomal RNA from maize embryonic axes at different time periods during the germination process and under the influence of a specific growth factor. For each condition a biological replicate was included and for the time periods, a technical replicate was also included.

2011-07-31 | E-GEOD-27648 | biostudies-arrayexpress

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