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RISS 인기검색어
- 검색키워드
- 저자 : Jung Hye Roe (검색결과 62 건)
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Roe, Jung Hye,Park, Joo Sang 한국유전학회 1988 Genes & Genomics Vol.10 No.4
We have examined the structures and cellulardistributions of the SV40 late RNAs present in monkey cells at late times after infection. One particular RNA species, spliced at residue 373 (373-RNA), was found to be as abundant as the major late 16S RNAs. This result was unexpected since previous reports showed that the molecular ratio of the 373-spliced 19S RNA to 16S RNA is approximately 0.1 among either cytoplasmic polyadenylated or polysomal viral RNAs. Both sedimentation and electrophoretic analyses indicated that the 373-RNA was approximately 16S to 19S in size. Analysis of the structure of this novel RNA species by S1 mapping and primer extension showed that its 5′ end mapped to the major cap site at nucleotide residue 325 and that nucleotide residue 373 was joined covalently to nucleotide residue 558 as is the case with the majority of the cytoplasmic polyadenylated SV40 late 19S RNAs. However, whereas most SV40 late 16S RNA is polyadenylated and located in the cytoplasm, the majority of 373-RNA was found to lack polyA, exhibit sequence heterogeneity at its 3′ end and be located in the nucleus. The cellular distribution is reversed when the remaining 3′ splice region (around residue 1463) is deleted from this RNA. This implies that the 3' splice region, in the absence of its 5′ splice pair, inhibits the nuclear transport of this 19S spliced RNA, possibly by forming a splicing complex which is an intermediate for the formation of a complete spliceosome.
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Mechanism of E. coli RNA polymerase-promoter interactions
Roe, Jung-Hye,Record.Jr, M.Thomas The Microbiological Society of Korea 1987 微生物과 産業 Vol.13 No.1
The regulation of gene expression in procaryotes is accomplished primarily at the level of transcription. Initiation of transcription is subject to numerous promoter-specific controls which act to ensure coordinate expression of disparate genes. The kinetics of formation of a functional("open") complex at a promoter, prior to the catalytic steps of RNA chain initiation and elongation, is thought to play a major role in controlling the efficiency of transcription of that promotor, since the subsequent processes of nucleotide binding and phosphodiester bond formation are rapid and are not promoter-specific (Mangel and Chamberlin, 1974 Shimamoto et al., 1981)
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The Characterization of an Abundant SV40 Late RNA Species in the Nucleus of the Infected Monkey Cell
Roe, Jung Hye 한국유전학회 1986 Genes & Genomics Vol.8 No.4
Late in the lytic cycle of infection of monkey cells SV40 produces two classes of late RNAs, 16S and 19S in size, which encode the virion proteins VP1 and VP2/3, respectively. These RNAs are made by differential splicing of the primary nuclear transcripts and exhibit heterogeneity in their 5'ends as well as splice sites utilized in processing. The mechanism of selection is not yet known. The relative abundances of the various species of spliced late RNAs present in the cytoplasm of SV40-infected monkey cells has been determined for both polysomal and polyadenylated RNA. The ratio of 16S to 19S cytoplasmic, polyadenylated RNA is approximately four. I have examined the structures and cellular distributions of the SV40 late RNAs present in monkey cells at late times after infection (48 hours after infection). One particular RNA species, spliced at residue 373 (373-RNA), was found to be as abundant as the major late 16S RNAs. This result was unexpected since previous reports showed that the molecular ratio of the 373-spliced 19S RNA to 16S RNA is approximately 0.1 among either cytoplasmic polyadenylated or polysomal viral RNAs. Both sedimentation and electrophoretic analyses indicated that the 373-RNA was approximately 16S to 19S in size. Therefore, it was not a splicing intermediate or the product of premature termination of transcription within the late leader region. Analysis of the structure of this RNA by S1 mapping and primer extension showed that its 5'end mapped to the major cap site (at nt. 325) and that nucleotide residue 373 was joined to residue 558 as is found in the majority of the cytoplasmic, polyadenylated SV40 late 19S RNAs. However, as judged by the oligo (dT)-cellulose chromatography, whereas most SV40 late 16S RNA is polyadenylated and located in the cytoplasm, the majority of 373-RNA was found to lack poly A tail, exhibit heterogeneity at its 3'end and be located in the nucleus. It is probable that the lack of poly A caused the preferential distribution of 373-RNA in the nucleus, thus regulating the amount of the functional mRNA in the cytoplasm. The structure of the 3'end of this RNA is currently under investigation. This will tell whether the 3'end is generated by transcriptional termination or by random degradation. Whether this RNA has ever been polyadenylated will be determined by the pulse-chase type of experiments.
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The Late Transcripts of SV40 Accumulated in The Nucleus of Infected Monkey Cells
( Jung Hye Roe,Joo Sang Park ) 한국유전학회 1988 Genes & Genomics Vol.10 No.4
We have examined the structures and cellular distributions of the SV40 late RNAs present in monkey cells at late times after infection. One particular RNA species, spliced at residue 373 (373-RNA), was found to be as abundant as the major late 16S RNAs. This result was unexpected since previous reports showed that the molecular ratio of the 373-spliced 19S RNA to 16S RNA is approximately 0.1 among either cytoplasmic polyadenylated or polysomal viral RNAs. Both sedimentation and electrophoretic analyses indicated that the 373-RNA was approximately 16S to 19S in size. Analysis of the structure of this novel RNA species by S1 mapping and primer extension showed that its 5` end mapped to the major cap site at nucleotide residue 325 and that nucleotide residue 373 was joined covalently to nucleotide residue 558 as is the case with the majority of the cytoplasmic polyadenylated SV40 late 19S RNAs. However, whereas most SV40 late 16S RNA is polyadenylated and located in the cytoplasm, the majority of 373-RNA was found to lack polyA, exhibit sequence heterogeneity at its 3` end and be located in the nucleus. The cellular distribution is reversed when the remaining 3` splice region (around residue 1463) is deleted from this RNA. This implies that the 3` splice region, in the absence of its 5` splice pair, inhibits the nuclear transport of this 19S spliced RNA, possibly by forming a splicing complex which is an intermediate for the formation of a complete spliceosome.
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Effect of Sequence of Variations within λPR Promoter on Its Strength in Vivo and In Vitro
Roe, Jung Hye,Cho, Eun Jung,Ko, Young Sang,Chung, Hyun Chae 한국유전학회 1990 Genes & Genomics Vol.12 No.4
The effect of changing GC content within DNA melting region as well as deletion of promoter upstream AT-rich sequences on the strength of promoter was measured in vitro and in vivo. The in vitro promoter strength was estimated by measuring the rate of formation and dissociation of promoter open complexes. At 37℃, the rate of formation of open complexes were similar for wild type, high GC, low GC, and AT-deletion mutant. At 18℃, the rate was faster in the order low GC> wild type= AT-deletion> low GC mutant. The in vivo promoter strength was estimated by measuring the activity of galactokinase (GalK) directed by promoters cloned into pK0100 plasmid in E. coli HB101. Since this plasmid contains transcriptional terminator downstream of GalK gene, we expected that the cloning of strong promoters would not affect plasmid stability significantly. At 37℃, however, all the recombinant plasmids, especially the one with low GC mutant promoter, was very unstable, and the reproducible measurement of GalK activity was not possible. At 30℃ the plasmids were relatively stable and the promoter strength was estimated to be in the order low GC> AT-deletion≥wild type> high GC mutant. Plasmid copy number was similar for each recombinant plasmids as determined by DNA hybridization and assay for β-lactamase. These results suggest that the upstream AT-rich sequences in P_R promoter does not facilitate the rate of transcriptional initiation and the GC content in the promoter melting region is another important factor in determining promoter strength.
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Isolation and Genetic Mapping of Paraquat Resistant Sporulating Mutants of Streptomyces Coelicolor
Chung, Hye-Jung,Kim, Eun-Ja,Park, Uhn-Mee,Roe, Jung-Hye The Microbiological Society of Korea 1995 The journal of microbiology Vol.33 No.3
S. coelicolor A3(2) cells were treated with various redox-cycling agents on nutrient agar plates and examined for their effect on the growth and differentiation. When treated with plumbagin, severe effect on cell viability was observed at concentrations above 250 $\mu$M. However, the surviving colonies differentiated normally. When treated with 100 $\mu$M paraquat, growth rate was decreased and morphological differentiation was inhibited, while the survival rate was maintained at about 100% even at 5 mM paraquat. Menadione or lawsone did not cause any visible changes at concentrations up to 1 mM. The effect of paraquat was also observed when it was added to nutrient agar plate before spore inoculation. Paraquat had also observed when it was added to nutrient agar plate before spore inoculation. Paraquat had no effect on colonies growing on R2YE agar plates. Among the components of R2YE medium selectively added to nutrient agar medium, CaCl$_2$ was found to have some protective function from the inhibitory effect of paraquat. As a first step to study the mechanism of the inhibitory effect of paraquat on differentiation, resistant mutants which sporulate well in the presence of paraquat were screened following UV mutagenesis. Three paraquat-resistant mutants were isolated with a frequency of 3 $\times$10${-5}$. Their mutation sites were determined by genetic crossings. All three mutations were mapped to a single locus near arg4 at about 1 o'clock on the genetic map of S. coelicolor A3(2).
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