The Ty elements of yeast are a dispersed repetitive gene family of 30 transposable elements. Ty elements are of interest to molecular biologists from several perspectives. The elements transpose to new genetic locations by a mechanism shared with both bacterial transposons and retroviruses. This process involves illegitimate recombination and results in the production of terminal duplications surrounding the newly inserted element. The DNA sequence of Ty elements contains sites which are similar to the retroviral primer binding sites required for reverse transcription of retroviral RNA. For retroviruses reverse transcription immediately precedes the illegitimate process of integration. It is not clear whether Ty elements also transpose via an RNA intermediate. One of the goals of this project is to determine if this is the case. Ty elements encode 10% of the cell's mRNA; this transcript is repressed in the a/Yield cell type presumably in response to the action of the matal and matYield2 genes which are known to turn off genes expressed in haploid cells. Ty elements are thus a paradigm for developmentally regulated genes. The mechanism by which matal and matYield 2 control the family of haploid-specific genes is unknown; analysis of the mode of control of Ty elements, one of the few well characterized haploid-specific genes, should help illuminate this problem. The expression of the Ty elements includes two unusual situations. The Ty promoter lies within the 5' delta long-terminal-repeat (LTR); the identical lTR at the 3' end of the element does not have promoter activity. Our hypothesis is that elongation of the 5' transcript into the 3' LTR disrupts initiation at that site. The effect is similar to ones seen in prokaryotes and retroviruses but is much more drastic. It would be interesting to obtain mutations which eliminte this effect, either site mutations or suppressors. A second aspect of Ty expression is the facct that the two Ty-encoded proteins are translated from a single messenger, which unlike the usual case is not processed by splicing. This might occur by specific translational frameshifting within a region of overlap between the two genes. Such a mechanism may be used in expressing a class of low-abundance retroviral proteins (e.g. Rous sarcoma virus po1), and may be a rarely-used mechanism in eukaryotes in general.

Agency
National Institute of Health (NIH)
Institute
National Institute of General Medical Sciences (NIGMS)
Type
Research Project (R01)
Project #
5R01GM029480-06
Application #
3277092
Study Section
Genetics Study Section (GEN)
Project Start
1981-09-01
Project End
1989-03-31
Budget Start
1987-04-01
Budget End
1989-03-31
Support Year
6
Fiscal Year
1987
Total Cost
Indirect Cost
Name
University of Connecticut
Department
Type
School of Medicine & Dentistry
DUNS #
City
Farmington
State
CT
Country
United States
Zip Code
06030
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Nord, Stefan; Bhatt, Monika J; Tükenmez, Hasan et al. (2015) Mutations of ribosomal protein S5 suppress a defect in late-30S ribosomal subunit biogenesis caused by lack of the RbfA biogenesis factor. RNA 21:1454-68
Manickam, Nandini; Nag, Nabanita; Abbasi, Aleeza et al. (2014) Studies of translational misreading in vivo show that the ribosome very efficiently discriminates against most potential errors. RNA 20:9-15
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Kramer, Emily B; Farabaugh, Philip J (2007) The frequency of translational misreading errors in E. coli is largely determined by tRNA competition. RNA 13:87-96
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Taliaferro, Dwayne L; Farabaugh, Philip J (2007) Testing constraints on rRNA bases that make nonsequence-specific contacts with the codon-anticodon complex in the ribosomal A site. RNA 13:1279-86

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