SNORD116 and SNORD115 change expression of multiple genes and modify each other's activity

Marina Falaleeva; Justin Surface; Manli Shen; Pierre de la Grange; Stefan Stamm

doi:10.1016/j.gene.2015.07.023

SNORD116 and SNORD115 change expression of multiple genes and modify each other's activity

Marina Falaleeva, Justin Surface, Manli Shen, Pierre de la Grange, Stefan Stamm

Research output: Contribution to journal › Article › peer-review

42 Scopus citations

Abstract

The loss of two gene clusters encoding small nucleolar RNAs, SNORD115 and SNORD116 contribute to Prader-Willi syndrome (PWS), the most common syndromic form of obesity in humans. SNORD115 and SNORD116 are considered to be orphan C/D box snoRNAs (SNORDs) as they do not target rRNAs or snRNAs. SNORD115 exhibits sequence complementarity towards the serotonin receptor 2C, but SNORD116 shows no extended complementarities to known RNAs. To identify molecular targets, we performed genome-wide array analysis after overexpressing SNORD115 and SNORD116 in HEK 293T cells, either alone or together. We found that SNORD116 changes the expression of over 200 genes. SNORD116 mainly changed mRNA expression levels. Surprisingly, we found that SNORD115 changes SNORD116's influence on gene expression. In similar experiments, we compared gene expression in post-mortem hypothalamus between individuals with PWS and aged-matched controls. The synopsis of these experiments resulted in 23 genes whose expression levels were influenced by SNORD116. Together our results indicate that SNORD115 and SNORD116 influence expression levels of multiple genes and modify each other activity.

Original language	English
Pages (from-to)	266-273
Number of pages	8
Journal	Gene
Volume	572
Issue number	2
DOIs	https://doi.org/10.1016/j.gene.2015.07.023
State	Published - Nov 10 2015

Bibliographical note

Funding Information:
This work was supported by NIH 01GM083187 (SS), R21 R21HD080035 (SS); NIGMSP30GM110787 , a grant from the Foundation for Prader-Willi Research , and a postdoctoral Fellowship 13POST16820024 from the American Heart Association (M.F.). This work utilized tissue from the NICHD Brain and Tissue Bank for Developmental Disorders (NICHD contract # HHSN275200900011C).

Publisher Copyright:
© 2015 Elsevier B.V..

Keywords

Array analysis
Prader-Willi syndrome
SnoRNA

ASJC Scopus subject areas

Genetics

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.gene.2015.07.023

Cite this

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title = "SNORD116 and SNORD115 change expression of multiple genes and modify each other's activity",

abstract = "The loss of two gene clusters encoding small nucleolar RNAs, SNORD115 and SNORD116 contribute to Prader-Willi syndrome (PWS), the most common syndromic form of obesity in humans. SNORD115 and SNORD116 are considered to be orphan C/D box snoRNAs (SNORDs) as they do not target rRNAs or snRNAs. SNORD115 exhibits sequence complementarity towards the serotonin receptor 2C, but SNORD116 shows no extended complementarities to known RNAs. To identify molecular targets, we performed genome-wide array analysis after overexpressing SNORD115 and SNORD116 in HEK 293T cells, either alone or together. We found that SNORD116 changes the expression of over 200 genes. SNORD116 mainly changed mRNA expression levels. Surprisingly, we found that SNORD115 changes SNORD116's influence on gene expression. In similar experiments, we compared gene expression in post-mortem hypothalamus between individuals with PWS and aged-matched controls. The synopsis of these experiments resulted in 23 genes whose expression levels were influenced by SNORD116. Together our results indicate that SNORD115 and SNORD116 influence expression levels of multiple genes and modify each other activity.",

keywords = "Array analysis, Prader-Willi syndrome, SnoRNA",

author = "Marina Falaleeva and Justin Surface and Manli Shen and {de la Grange}, Pierre and Stefan Stamm",

note = "Funding Information: This work was supported by NIH 01GM083187 (SS), R21 R21HD080035 (SS); NIGMSP30GM110787 , a grant from the Foundation for Prader-Willi Research , and a postdoctoral Fellowship 13POST16820024 from the American Heart Association (M.F.). This work utilized tissue from the NICHD Brain and Tissue Bank for Developmental Disorders (NICHD contract # HHSN275200900011C). Publisher Copyright: {\textcopyright} 2015 Elsevier B.V..",

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AU - Shen, Manli

AU - de la Grange, Pierre

AU - Stamm, Stefan

N1 - Funding Information: This work was supported by NIH 01GM083187 (SS), R21 R21HD080035 (SS); NIGMSP30GM110787 , a grant from the Foundation for Prader-Willi Research , and a postdoctoral Fellowship 13POST16820024 from the American Heart Association (M.F.). This work utilized tissue from the NICHD Brain and Tissue Bank for Developmental Disorders (NICHD contract # HHSN275200900011C). Publisher Copyright: © 2015 Elsevier B.V..

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N2 - The loss of two gene clusters encoding small nucleolar RNAs, SNORD115 and SNORD116 contribute to Prader-Willi syndrome (PWS), the most common syndromic form of obesity in humans. SNORD115 and SNORD116 are considered to be orphan C/D box snoRNAs (SNORDs) as they do not target rRNAs or snRNAs. SNORD115 exhibits sequence complementarity towards the serotonin receptor 2C, but SNORD116 shows no extended complementarities to known RNAs. To identify molecular targets, we performed genome-wide array analysis after overexpressing SNORD115 and SNORD116 in HEK 293T cells, either alone or together. We found that SNORD116 changes the expression of over 200 genes. SNORD116 mainly changed mRNA expression levels. Surprisingly, we found that SNORD115 changes SNORD116's influence on gene expression. In similar experiments, we compared gene expression in post-mortem hypothalamus between individuals with PWS and aged-matched controls. The synopsis of these experiments resulted in 23 genes whose expression levels were influenced by SNORD116. Together our results indicate that SNORD115 and SNORD116 influence expression levels of multiple genes and modify each other activity.

AB - The loss of two gene clusters encoding small nucleolar RNAs, SNORD115 and SNORD116 contribute to Prader-Willi syndrome (PWS), the most common syndromic form of obesity in humans. SNORD115 and SNORD116 are considered to be orphan C/D box snoRNAs (SNORDs) as they do not target rRNAs or snRNAs. SNORD115 exhibits sequence complementarity towards the serotonin receptor 2C, but SNORD116 shows no extended complementarities to known RNAs. To identify molecular targets, we performed genome-wide array analysis after overexpressing SNORD115 and SNORD116 in HEK 293T cells, either alone or together. We found that SNORD116 changes the expression of over 200 genes. SNORD116 mainly changed mRNA expression levels. Surprisingly, we found that SNORD115 changes SNORD116's influence on gene expression. In similar experiments, we compared gene expression in post-mortem hypothalamus between individuals with PWS and aged-matched controls. The synopsis of these experiments resulted in 23 genes whose expression levels were influenced by SNORD116. Together our results indicate that SNORD115 and SNORD116 influence expression levels of multiple genes and modify each other activity.

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KW - SnoRNA

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SNORD116 and SNORD115 change expression of multiple genes and modify each other's activity

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

UN SDGs

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