Abstract
DNA sequence information alone cannot account for the immense variability between chromosomal alleles within diverse cell types in the brain, whether these differences are observed across time, cell type, or parental origin. The complex control and maintenance of gene expression and modulation are regulated by a multitude of molecular and cellular mechanisms that layer on top of the genetic code. The integration of genetic and environmental signals required for regulating brain development and function is achieved in part by a dynamic epigenetic landscape that includes DNA methylation, histone modifications, and noncoding RNAs. These epigenetic mechanisms establish and maintain core biological processes, including genomic imprinting and entrainment of circadian rhythms. This chapter will focus on how the epigenetic layers of DNA methylation and long, noncoding RNAs interact with circadian rhythms at specific imprinted chromosomal loci associated with the human neurodevelopmental disorders Prader–Willi, Angelman, Kagami–Ogata, and Temple syndromes.
| Original language | English (US) |
|---|---|
| Journal | Progress in Molecular Biology and Translational Science |
| DOIs | |
| State | Accepted/In press - Jan 1 2018 |
| Externally published | Yes |
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Keywords
- circadian rhythm
- DNA methylation
- epigenetic
- imprinting
- neurodevelopmental disorder
ASJC Scopus subject areas
- Molecular Medicine
- Molecular Biology
Cite this
Epigenetics of Circadian Rhythms in Imprinted Neurodevelopmental Disorders. / Coulson, Rochelle L.; LaSalle, Janine M.
In: Progress in Molecular Biology and Translational Science, 01.01.2018.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Epigenetics of Circadian Rhythms in Imprinted Neurodevelopmental Disorders
AU - Coulson, Rochelle L.
AU - LaSalle, Janine M
PY - 2018/1/1
Y1 - 2018/1/1
N2 - DNA sequence information alone cannot account for the immense variability between chromosomal alleles within diverse cell types in the brain, whether these differences are observed across time, cell type, or parental origin. The complex control and maintenance of gene expression and modulation are regulated by a multitude of molecular and cellular mechanisms that layer on top of the genetic code. The integration of genetic and environmental signals required for regulating brain development and function is achieved in part by a dynamic epigenetic landscape that includes DNA methylation, histone modifications, and noncoding RNAs. These epigenetic mechanisms establish and maintain core biological processes, including genomic imprinting and entrainment of circadian rhythms. This chapter will focus on how the epigenetic layers of DNA methylation and long, noncoding RNAs interact with circadian rhythms at specific imprinted chromosomal loci associated with the human neurodevelopmental disorders Prader–Willi, Angelman, Kagami–Ogata, and Temple syndromes.
AB - DNA sequence information alone cannot account for the immense variability between chromosomal alleles within diverse cell types in the brain, whether these differences are observed across time, cell type, or parental origin. The complex control and maintenance of gene expression and modulation are regulated by a multitude of molecular and cellular mechanisms that layer on top of the genetic code. The integration of genetic and environmental signals required for regulating brain development and function is achieved in part by a dynamic epigenetic landscape that includes DNA methylation, histone modifications, and noncoding RNAs. These epigenetic mechanisms establish and maintain core biological processes, including genomic imprinting and entrainment of circadian rhythms. This chapter will focus on how the epigenetic layers of DNA methylation and long, noncoding RNAs interact with circadian rhythms at specific imprinted chromosomal loci associated with the human neurodevelopmental disorders Prader–Willi, Angelman, Kagami–Ogata, and Temple syndromes.
KW - circadian rhythm
KW - DNA methylation
KW - epigenetic
KW - imprinting
KW - neurodevelopmental disorder
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UR - http://www.scopus.com/inward/citedby.url?scp=85045252109&partnerID=8YFLogxK
U2 - 10.1016/bs.pmbts.2017.11.023
DO - 10.1016/bs.pmbts.2017.11.023
M3 - Article
C2 - 29933957
AN - SCOPUS:85045252109
JO - Progress in Molecular Biology and Translational Science
JF - Progress in Molecular Biology and Translational Science
SN - 1877-1173
ER -