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Rous sarcoma virus RNA: Splicing sup...

Giles, Keith E.

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Rous sarcoma virus RNA: Splicing suppression and pseudogene formation.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Rous sarcoma virus RNA: Splicing suppression and pseudogene formation./
作者:	Giles, Keith E.
面頁冊數:	129 p.
附註:	Source: Dissertation Abstracts International, Volume: 65-12, Section: B, page: 6192.
Contained By:	Dissertation Abstracts International65-12B.
標題:	Biology, Molecular. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3155618
ISBN:	049616340X

Rous sarcoma virus RNA: Splicing suppression and pseudogene formation.
Giles, Keith E.

Rous sarcoma virus RNA: Splicing suppression and pseudogene formation. - 129 p.

Source: Dissertation Abstracts International, Volume: 65-12, Section: B, page: 6192.

Thesis (Ph.D.)--The Johns Hopkins University, 2005.

Rous sarcoma virus generates three RNA species. A fraction of the unspliced primary transcripts are singly spliced. The maintenance of unspliced RNA is critical to retroviral replication because it serves as both genomic RNA and mRNA for gag and pol. In an effort to understand the molecular mechanism of splicing suppression, I characterized a small cis-acting RNA element, known as the negative regulator of splicing (NRS). I originally hypothesized that the NRS functioned via an abnormal, extended interaction with U6 snRNA. To this end, I demonstrated that approximately one molecule of U6 is packaged into each RSV virion on average via an RNA-RNA interaction with the RSV genome. However, this packaged U6 snRNA did not base pair with the NRS region of RSV RNA. Interestingly, the packaged U6 snRNA was reverse transcribed and was capable of recombining with the RSV genome. A bioinformatic analysis identified similar recombinations between small RNAs and the LTRs of endogenous retroviruses. This process is likely conserved from chickens to humans and may shape genome evolution via the formation of pseudogenes.

ISBN: 049616340XSubjects--Topical Terms:

1017719
Biology, Molecular.

Rous sarcoma virus RNA: Splicing suppression and pseudogene formation.
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502 $a Thesis (Ph.D.)--The Johns Hopkins University, 2005.
520 $a Rous sarcoma virus generates three RNA species. A fraction of the unspliced primary transcripts are singly spliced. The maintenance of unspliced RNA is critical to retroviral replication because it serves as both genomic RNA and mRNA for gag and pol. In an effort to understand the molecular mechanism of splicing suppression, I characterized a small cis-acting RNA element, known as the negative regulator of splicing (NRS). I originally hypothesized that the NRS functioned via an abnormal, extended interaction with U6 snRNA. To this end, I demonstrated that approximately one molecule of U6 is packaged into each RSV virion on average via an RNA-RNA interaction with the RSV genome. However, this packaged U6 snRNA did not base pair with the NRS region of RSV RNA. Interestingly, the packaged U6 snRNA was reverse transcribed and was capable of recombining with the RSV genome. A bioinformatic analysis identified similar recombinations between small RNAs and the LTRs of endogenous retroviruses. This process is likely conserved from chickens to humans and may shape genome evolution via the formation of pseudogenes.
520 $a To address the mechanism of NRS-mediated splicing suppression, I utilized a chimeric RNA molecule that places an adenoviral 3' splice site and exon downstream from the NRS (NRS-Ad3'). Assembly of RNP complexes onto NRS-Ad3' was compared to that of a functional splicing substrate in vitro. In the absence of heparin these two RNAs assembled complexes that sedimented at similar rates in a sucrose gradient. However, after the addition of heparin to destabilize unstable protein:RNA interactions, the WT NRS-Ad3' RNA complex was unable to assemble a normal B complex. This defect is likely due to the lack of an interaction between the tri-snRNP protein, hPrp8, and the WT NRS. I propose that it is this inability of hPrp8 to bind directly to the WT NRS pseudo 5' splice site that prevents it from functioning as a splice site. However, the presence of U1 snRNP allows the WT NRS to sequester the downstream 3' splice site and prevent its interaction with the upstream 5' splice site.
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