Hebert:Research: Difference between revisions

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Our work seeks to understand nuclear function, with particular emphasis on splicing and transcription efficiency.  
Our work seeks to understand nuclear function, with particular emphasis on splicing and transcription efficiency.  
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[[image: coilin mechanism.jpg]]
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We are also conducting experiments designed to understand the normal cellular dialogue that occurs between some subnuclear domains. For example, it has been known for some time that Cajal bodies and another nuclear structure, known as the PML body, occasionally abut one another. We have found that CBs and PML bodies can simultaneously associate near U2 snRNA gene loci. It is possible that such an arrangement facilitates the transcription of this gene and experiments are underway to confirm this hypothesis. Additionally, since Cajal bodies are especially prevalent in cancer cells, identification and characterization of proteins that induce the formation of this structure may lead to novel cancer therapeutics.  
We are also conducting experiments designed to understand the normal cellular dialogue that occurs between some subnuclear domains. For example, it has been known for some time that Cajal bodies and another nuclear structure, known as the PML body, occasionally abut one another. We have found that CBs and PML bodies can simultaneously associate near U2 snRNA gene loci. It is possible that such an arrangement facilitates the transcription of this gene and experiments are underway to confirm this hypothesis. Additionally, since Cajal bodies are especially prevalent in cancer cells, identification and characterization of proteins that induce the formation of this structure may lead to novel cancer therapeutics.
 


Cajal bodies and PML bodies can associate with the same U2 gene locus. HeLa cells were subjected to antibody staining to mark the location of CBs (red) and PML bodies (blue), followed by DNA FISH using an U2 gene probe (green). The arrow marks an association between CBs, PML bodies and an U2 gene (inset) in four different cells.


In separate studies, we have developed a reporter system to screen small molecules that may benefit patients with Friedreich's ataxia. This disease is caused by a tri-nucleotide repeat expansion in a gene that encodes a vital mitochondrial protein known as frataxin. We have identified several compounds that increase frataxin expression and are currently testing these compounds in patient tissue. We are also conducting a very small pilot study in which patients will be treated with one promising compound our work has identified may be beneficial to those suffering from this insidious disease.
June 2010

Latest revision as of 14:56, 18 April 2011


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