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Light and sex modify Snord116 genotype effects on metabolism, behavior, and imprinted gene networks following circadian entrainment

ABSTRACT: Light and sex modify Snord116 genotype effects on metabolism, behavior, and imprinted gene networks following circadian entrainment

PROVIDER: PRJNA1265732 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR33651000_1.fastq.gz	Fastqsanger.gz
	SRR33651000_2.fastq.gz	Fastqsanger.gz
	SRR33651100_1.fastq.gz	Fastqsanger.gz
	SRR33651100_2.fastq.gz	Fastqsanger.gz
	SRR33651001_1.fastq.gz	Fastqsanger.gz

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Light and sex modify Snord116 genotype effects on metabolism, behavior, and imprinted gene networks following circadian entrainment

Project description:Mammals utilize imprinted and X-linked epigenetic mechanisms in development, metabolism, and behavior. Imprinted genes, including Prader-Willi syndrome Snord116 noncoding RNAs, are implicated in the regulation of sleep and circadian rhythms through poorly understood mechanisms. Utilizing mouse models of Snord116 deficiency and overexpression, we performed an integrated, sex-stratified analysis of free running behaviors, indirect calorimetry, and cortical transcriptomes following entrainment to a 22 hour light:dark T-cycle. We observed significant interactions of sex, entrainment, and Snord116 genotype in period length at baseline and after-effects of post-entrainment. Snord116 deletion’s effect on respiratory exchange ratio was light sensitive, with sex and entrainment effects dominant under total darkness. Snord116 genotype impacted both rhythmic and non-rhythmic cortical gene networks that integrated sex, light, and entrainment effects with genotype-phenotype correlations. A co-expressed gene network enriched for imprinted, Snord116-target, and Xist-proximal long noncoding RNAs was identified as a light-sensitive regulatory hub of sexual dimorphic responses to a dynamic environment.

2025-05-22 | GSE297702 | GEO

Loss of Snord116 impacts lateral hypothalamus, sleep, and food-related behaviors

Project description:Imprinted genes are highly expressed in the hypothalamus, however whether specific imprinted genes affect hypothalamic neuromodulators and their functions is unknown. It has been suggested that Prader-Willi syndrome (PWS), a neurodevelopmental disorder caused by lack of paternal expression at the chromosome 15q11-q13, characterised with a hypothalamic insufficiency. Here we investigate the role of paternally expressed Snord116 gene within the context of sleep and metabolic abnormalities of PWS, and we report a novel role of this imprinted gene in the function and organisation of the two main neuromodulatory systems of the lateral hypothalamus (LH), namely the orexin (OX) and the melanin concentrating hormone (MCH). We observe that the dynamic between neuronal discharge in the LH and sleep-wake states of mice carrying the paternal deletion of the Snord116 (PWScrm+/p-) is compromised. This abnormal state-dependent neuronal activity is paralleled by a significant reduction of OX neurons in LH of mutants. Therefore, we propose that unbalance between OX- and MCH- expressing neurons in the LH of mutants reflects in a series of deficits manifested in the PWS, such as dysregulation of rapid eye movement (REM) sleep, food intake and temperature control.

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Roles of SNORD115 and SNORD116 ncRNA clusters during neuronal differentiation

Project description:In the snoRNA host gene SNHG14, 29 consecutive introns each generate SNORD116, and 48 tandem introns encode SNORD115. Loss of SNORD116 expression, but not of SNORD115, is linked to the neurodevelopmental disease Prader-Willi syndrome. SNORD116 and SNORD115 resemble box C/D small nucleolar RNAs (snoRNAs) but lack known targets. Both were strongly accumulated during neuronal differentiation, but with distinct mechanisms: Increased host-gene expression for SNORD115 and apparent stabilization for SNORD116. For functional characterization we created cell lines specifically lacking the expressed, paternally inherited, SNORD115 or SNORD116 cluster. Analyses during neuronal development indicated changes in RNA stability and protein synthesis. These data suggested that the loss of SNORD116 enhanced some aspects of developmental timing of neuronal cells. Depleted mRNAs included MAGEL2, causal in the PWS-like disorder Schaaf-Yang syndrome. Comparison of SNORD115 and SNORD116 mutants identified small numbers of altered mRNAs and ncRNAs. These were enriched for functions potentially linked to PWS phenotypes.

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Transcriptomic response to adult hypothalamic deletion of Snord116

Project description:Snord116 deletion mouse models recapitulate aspects of the Prader-Willi Syndrome. In this study, we examine the gene expression changes in the mediobasal hypothalamus for mice which have an adult onset deletion of Snord116 in the mediobasal hypothalamus.

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Roles of SNORD115 and SNORD116 ncRNA clusters in neuronal differentiation

Project description:Prader-Willi syndrome shows features linked to brain development and hypothalamus-related endocrine abnormalities. The smallest clinical deletions fall within the large (∼650Kb) SNHG14 gene, removing 29 consecutive introns that each generate SNORD116. SNHG14 also includes 48 tandem introns encoding SNORD115 and generates multiple, extended snoRNA-related species. SNORD115 and SNORD116 resemble box C/D small nucleolar RNAs (snoRNAs) but lack known targets. Both snoRNAs strongly accumulated during neuronal differentiation. SNORD116 accumulation apparently reflected stabilization, potentially linked to the appearance of FBLL1, a homologue of the ubiquitous snoRNA-associated protein Fibrillarin (FBL). In contrast, SNORD115 was selectively transcribed, apparently due to regulated termination. For functional characterization we created cell lines lacking only the expressed, paternal, SNORD115 or SNORD116 cluster. Analyses during neuronal development indicated changes in RNA stability and protein synthesis. Altered mRNAs included MAGEL2, mutation of which causes the PWS-like disorder Schaaf-Yang syndrome. Comparison of SNORD115 and SNORD116 mutants indicated overlapping or interacting functions. Most changes in mRNA and protein abundance appeared relatively late in development, with roles including cytoskeleton formation, extracellular matrix, neuronal arborization. Comparison with human embryonic midbrain development suggested enhanced progression in neuronal development in the snoRNA mutants. Subtle impairment of relative neuronal maturation during development, might generate the clinical phenotypes.

2025-02-15 | PXD057208 | Pride

Snord116-dependent diurnal rhythm of DNA methylation in mouse cortex

Project description:Rhythmic oscillations of physiological processes depend on integrating the circadian clock and diurnal environment. DNA methylation is epigenetically responsive to daily rhythms, as a subset of CpG dinucleotides in brain exhibit diurnal rhythmic methylation. A major genetic effect on rhythmic methylation was identified in a mouse Snord116 deletion model of the imprinted disorder Prader-Willi syndrome (PWS). > 23,000 diurnally rhythmic CpGs were identified in wild-type cortex, with nearly all lost or phase-shifted in PWS. Circadian dysregulation of a second imprinted Snord cluster at the Temple/Kagami-Ogata syndrome locus was observed at the level of methylation, transcription, and chromatin, providing mechanistic evidence of cross-talk. Genes identified by diurnal epigenetic changes in PWS mice overlapped rhythmic and PWS-specific genes in human brain and were enriched for PWS-relevant phenotypes and pathways. These results support the proposed evolutionary relationship between imprinting and sleep, and suggest possible chronotherapy in the treatment of PWS and related disorders.

2018-02-27 | GSE103249 | GEO

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