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- Roles of chromatin structure and epigenetic controls in eucaryotic gene activation
- Roles of mRNA-protein interactions in control of eucarytic mRNA stability and expression
Description of Research
Roles of chromatin structure and epigenetic controls in eucaryotic gene activation
In eukaryotic organisms gene regulation is dependent upon developmentally controlled alterations in chromatin structure. Epigenetic modifications in histones and DNA result in selective activation of gene expression profiles. In many cases these modifications in chromatin structure result in long-range control of gene promoters, reaching over hundreds of kbs. Understanding how these epigenetic modifications are themselves controlled and the mechanisms by which they selectively activate and/or silence cohorts of genes is central to our understanding of development and cellular differentiation. We are approaching these questions using as a model the human Growth Hormone gene cluster. The genes in this cluster are robustly expressed, physiologically and developmentally controlled, and highly specific to either pituitary somatotropes or placental syncytiotrophoblasts. These controls are conserved between mouse and human. Thus our studies are heavily dependent on the use of transgenic mouse models and are complemented where appropriate with in vitro chromatin analyses and cell culture models.
- Roles of chromatin structure and epigenetic controls in eucaryotic gene activation
- Roles of mRNA-protein interactions in control of eucarytic mRNA stability and expression
Description of Research
Roles of chromatin structure and epigenetic controls in eucaryotic gene activation
In eukaryotic organisms gene regulation is dependent upon developmentally controlled alterations in chromatin structure. Epigenetic modifications in histones and DNA result in selective activation of gene expression profiles. In many cases these modifications in chromatin structure result in long-range control of gene promoters, reaching over hundreds of kbs. Understanding how these epigenetic modifications are themselves controlled and the mechanisms by which they selectively activate and/or silence cohorts of genes is central to our understanding of development and cellular differentiation. We are approaching these questions using as a model the human Growth Hormone gene cluster. The genes in this cluster are robustly expressed, physiologically and developmentally controlled, and highly specific to either pituitary somatotropes or placental syncytiotrophoblasts. These controls are conserved between mouse and human. Thus our studies are heavily dependent on the use of transgenic mouse models and are complemented where appropriate with in vitro chromatin analyses and cell culture models.
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