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Positive and negative regulation of ...

Miller, Myrna.

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Positive and negative regulation of transcription from the chicken infectious anemia virus promoter-enhancer and implications for latency and activation.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Positive and negative regulation of transcription from the chicken infectious anemia virus promoter-enhancer and implications for latency and activation./
作者:	Miller, Myrna.
出版者:	Ann Arbor : ProQuest Dissertations & Theses, : 2005,
面頁冊數:	152 p.
附註:	Source: Dissertations Abstracts International, Volume: 66-12, Section: B.
Contained By:	Dissertations Abstracts International66-12B.
標題:	Molecular biology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3163168
ISBN:	9780496971954

Positive and negative regulation of transcription from the chicken infectious anemia virus promoter-enhancer and implications for latency and activation.
Miller, Myrna.

Positive and negative regulation of transcription from the chicken infectious anemia virus promoter-enhancer and implications for latency and activation. - Ann Arbor : ProQuest Dissertations & Theses, 2005 - 152 p.

Source: Dissertations Abstracts International, Volume: 66-12, Section: B.

Thesis (Ph.D.)--Cornell University, 2005.

This item must not be sold to any third party vendors.

Chicken infectious anemia virus (CIAV) is a ubiquitous and highly resistant virus of chickens belonging to the family Circoviridae. The long term presence of CIAV DNA in antibody positive and negative chickens suggested the possibility of a latent or chronic infection. In addition, detection of viral mRNA in embryos indicated that transcription from the viral promoter could be tightly controlled and limited to specific days of incubation. The focus of this research became to further characterize the cellular mechanisms and proteins that interact with the CIAV promoter to control transcription and allow for a latent or chronic infection. The initial hypothesis was that elements in the previously identified promoter-enhancer region that resembled hormone response elements were binding sites for members of the hormone/nuclear receptor superfamily. Unexpectedly, CIAV promoter was found to have a high level of basal expression that could express well in LMH, LMH/2A, and DF1 cells lines, and in primary theca and granulosa cells. The expression could be modulated by estrogen and COUP-TFI in cells expressing large amount of these transcription factors. A long CIAV promoter-expression vector construct that included 80 nt downstream of the transcription start site (TSP) induced less expression of enhanced green fluorescent protein (EGFP) then a shorter construct that ended at the TSP. Examination of the extra sequences found several possible regulating elements, including an E box-like element located at the TSP. Transfection assays and DNA-protein binding assays found that the E box site was functionally able to repress transcription, and the transcription regulator dEF1 was identified as one of the proteins binding to this site. Mutation of 3 nt in the potential E box restored EGFP expression to that of the short construct and altered the pattern of protein binding in DNA-protein binding assays. A promoter with high basal level activity ensures that the virus can function in all susceptible cells, but does not allow for a chronic or latent infection. Negatively regulating element(s) provides the possibility for the virus to become dormant, avoid immune detection, and with a presence in the reproductive tract, to be passed to the next generation.

ISBN: 9780496971954Subjects--Topical Terms:

517296
Molecular biology.
Subjects--Index Terms:

Chicken infectious anemia virus

Positive and negative regulation of transcription from the chicken infectious anemia virus promoter-enhancer and implications for latency and activation.
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520 $a Chicken infectious anemia virus (CIAV) is a ubiquitous and highly resistant virus of chickens belonging to the family Circoviridae. The long term presence of CIAV DNA in antibody positive and negative chickens suggested the possibility of a latent or chronic infection. In addition, detection of viral mRNA in embryos indicated that transcription from the viral promoter could be tightly controlled and limited to specific days of incubation. The focus of this research became to further characterize the cellular mechanisms and proteins that interact with the CIAV promoter to control transcription and allow for a latent or chronic infection. The initial hypothesis was that elements in the previously identified promoter-enhancer region that resembled hormone response elements were binding sites for members of the hormone/nuclear receptor superfamily. Unexpectedly, CIAV promoter was found to have a high level of basal expression that could express well in LMH, LMH/2A, and DF1 cells lines, and in primary theca and granulosa cells. The expression could be modulated by estrogen and COUP-TFI in cells expressing large amount of these transcription factors. A long CIAV promoter-expression vector construct that included 80 nt downstream of the transcription start site (TSP) induced less expression of enhanced green fluorescent protein (EGFP) then a shorter construct that ended at the TSP. Examination of the extra sequences found several possible regulating elements, including an E box-like element located at the TSP. Transfection assays and DNA-protein binding assays found that the E box site was functionally able to repress transcription, and the transcription regulator dEF1 was identified as one of the proteins binding to this site. Mutation of 3 nt in the potential E box restored EGFP expression to that of the short construct and altered the pattern of protein binding in DNA-protein binding assays. A promoter with high basal level activity ensures that the virus can function in all susceptible cells, but does not allow for a chronic or latent infection. Negatively regulating element(s) provides the possibility for the virus to become dormant, avoid immune detection, and with a presence in the reproductive tract, to be passed to the next generation.
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