• Journal of Applied Biological Chemistry
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• v.43 no.1
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• pp.12-17
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• 2000

To understand the signal transduction pathway that leads to the activation of the wound-inducible proteinase inhibitor II (pin2) promoter. $F_2$ progenies of wound (-) mutant crossed with wild-type Arabidopsis plants were biochemically and genetically characterized. Wound (-) mutant was derived from transgenic Arabidopsis plants containing bacterial cytosine deaminase gene under the control of pin2 promoter. The cytosine deaminase assays indicated that wound (-) mutant is a dominant inhibitor of wound-inducibility as only 3 of the $20F_2$ progenies showed cytosine deaminase (CDase) activity, To construct a structural map of the wound (-) mutant chromosomal regions, cleaved, amplified polymorphic sequences (CAPS) markers that cover all Chromosomes were used. Chromosomal regions covered by three different CAPS markers could be candidates for further fine mapping of the location of the wound (-) mutation. g4026, RGA1 and ASA1 located at 84.9 on recombinant inbred (RI) map of chromosome I, at 1.75 on RI map of chromosome II, and 18.35 on RI map of chromosome V, respectively.

• Proceedings of the Korean Society for Bioinformatics Conference
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• 2006.02a
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• pp.125-126
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• 2006

NimbleGen has developed strategies to use its high-density oligonucleotide microarray platform (385,000 probes per array) to map both promoter binding sites and copy number variation at very high-resolution in the human genome. Here we describe a genome-wide map of active promoters determined by experimentally locating the sites of transcription imitation complex binding throughout the human genome using microarrays combined with chromatin immunoprecipitation. This map defines 10,567 active promoters corresponding to 6,763 known genes and at least 1,196 un-annotated transcriptional units. Microarray-based comparative genomic hybridisation (CGH) is animportant research tool for investigating chromosomal aberrations frequently associated with complex diseases such as cancer, neuropsychiatric disorders, and congenital developmental disorders. NimbleGen array CGH is an ultra-high resolution (0.5-50 Kb) oligo array platform that can be used to detect amplifications and deletions and map the associated breakpoints on the whole-genome level or with custom fine-tiling arrays. For whole-genome array CGH, probes are tiled through genic and intergenic regions with a median probe spacing of 6 Kb, which provides a comprehensive, unbiased analysis of the genome.

• Microbiology and Biotechnology Letters
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• v.16 no.6
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• pp.536-539
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• 1988

A mutant of Bacillus subtilis with a defective cdd gene encoding deoxycytidine-cytidine deaminase (EC 3.5.4.5) has been characterized genetically. The genetic lesion, cdd, causing the altered deoxycytidine-cytidine deaminase was mapped at 225 min on the linkage map of B. subtilis by AR9 transduction, Transductional analysis of the cdd region established the gene order in clockwise as trp-lys-cdd-aroD. The cdd gene was linked 72% with the aroD and 20% with the lys.

• Asian-Australasian Journal of Animal Sciences
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• v.12 no.7
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• pp.1129-1134
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• 1999

The rapid development of the sheep genetic linkage map over the last five years has given us the ability to follow the inheritance of chromosomal regions. Initially this powerful resource was used to find markers linked to monogenic traits but there is now increasing interest in using the genetic linkage map to define the complex of genes that control multigenic production traits. Of particular interest are those production traits that are difficult to measure and select for using classical quantitative genetic approaches. These include resistance to disease where a disease challenge (necessary for selection) poses too much risk to valuable stud animals and meat and carcass qualities which can be measured only after the animal has been slaughtered. The goal for the new millennium will be to fully characterise the genetic basis of multigenic production traits. The genetic linkage map is a vital tool required to achieve this.

• Journal of Microbiology and Biotechnology
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• v.11 no.6
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• pp.1115-1119
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• 2001

Eight Escherichia coli cells with aerobic growth deflects were isolated by the insertion of ${\lambda}placMu53$, a hybrid bacteriophage of ${\lambda}$ and Mu, which created transcriptional fusion to lacZY. Two of these mutants, CLIO and CLl2, were irradiated with UV to obtain specialized transducing phages. The phages that took out the neighboring chromosomal DNA of the related gene responsible for deflective aerobic growth were identified. The in vivo cloned chromosomal sequence revealed that the mutated gene of CLIO was located at min 34.5 on the Escherichia coli linkage map and 1,599,515 on the physical map. The physical map indicated that there were 7 cistrons in the operon. We named this operon oxg10. The promoter sequence of oxg10 exhibited a possible binding site far SoxS, a transcriptional regulator that activates the transcription of various SoxRS regulon genes. Transferring the oxg10:: ${\lambda}placMu53$ mutation into the wild-type strain, RZ4500, resulted in the inhibition of normal aerobic growth, while the salute mutation in strain MO inhibited aerobic cell growth completely. The full operon sequences of oxg10 were cloned from the Excherichia coli genomic library. The mutated gene of CLl2 was identified to be a sucA gene encoding the ${\alpha}$-ketoglutarate dehydrogenase El component in the TCA cycle.

• Clinical and Experimental Pediatrics
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• v.59 no.sup1
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• pp.19-24
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• 2016

Constitutional interstitial deletions of the long arm of chromosome 5 (5q) are quite rare, and the corresponding phenotype is not yet clearly delineated. Severe mental retardation has been described in most patients who present 5q deletions. Specifically, the interstitial deletion of chromosome 5q33.3q35.1, an extremely rare chromosomal aberration, is characterized by mental retardation, developmental delay, and facial dysmorphism. Although the severity of mental retardation varies across cases, it is the most common feature described in patients who present the 5q33.3q35.1 deletion. Here, we report a case of a de novo deletion of 5q33.3q35.1, 46,XY,del(5)(q33.3q35.1) in an 11-year-old boy with mental retardation; to the best of our knowledge this is the first case in Korea to be reported. He was diagnosed with severe mental retardation, developmental delay, facial dysmorphisms, dental anomalies, and epilepsy. Chromosomal microarray analysis using the comparative genomic hybridization array method revealed a 16-Mb-long deletion of 5q33. 3q35.1(156,409,412-172,584,708)x1. Understanding this deletion may help draw a rough phenotypic map of 5q and correlate the phenotypes with specific chromosomal regions. The 5q33.3q35.1 deletion is a rare condition; however, accurate diagnosis of the associated mental retardation is important to ensure proper genetic counseling and to guide patients as part of long-term management.

• Proceedings of the Korean Society for Applied Microbiology Conference
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• 1986.12a
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• pp.512.2-512
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• 1986

A mutant of bacillus subtilis with a defective cdd gene encoding deoxycytidine-cytidine deaminase(EC 3.5.4.5.) has been characterized genetically. The genetic lesion causing the altered deoxycytidine-cytidine deaminase, cdd, was mapped at 225 min on the linkage map of B.subtilis by AR9 transduction Transductional analysis of the cdd region established the gene order as trp-lys-dnaE-cdd-aroD. The cdd gene was linked 72% with the aroD and 20% with the lys.

• Journal of Microbiology and Biotechnology
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• v.6 no.6
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• pp.386-390
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• 1996

The ${\beta}$-galactosidase gene from Lactococcus lactis subsp. lactis ATCC 7962 was cloned and its enzymatic properties were characterized, with a view to assessing its potential use as a selection marker in the food-grade cloning vector. Chromosomal DNA from L. lactis subsp. lactis 7962 was cleaved with PstI and ligated into pBR322 for transformation into Escherichia coli TGl. Transformants showing ${\beta}$-galactosidase activity possessed the pBR322 plasmid containing a 10 kilobase (kb) PstI fragment and this plasmid was named pCKL11. The cloned ${\beta}$-galactosidase gene came from the chromosomal DNA of L. lactis subsp. lactis 7962 was confirmed by Southern hybridization. A restriction map of pCKL11 was constructed from the cleavage of both pCKL11 and the purified 10kb insert fraqment. The. optimum pH of the ${\beta}$-galactosidase determined with the E. coli harboring the pCKL11 was 7.0. The optimum temperature was $50^{\circ}C$, while the pI of the enzyme was 7.4. These values were the same as those of the enzyme from the parent strain.

• Molecules and Cells
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• v.21 no.3
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• pp.360-366
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• 2006

Up to 35% of the rice genome consists of various kinds of transposons, and CACTA and MITE are two of the major class 2 DNA transposons in the genome. We have employed the consensus sequences of Rim2/Hipa CACTA, Stowaway MITE Pangrangja, and Tourist MITE Ditto for transposon display (TD) analysis to locate them on a genetic map, with 58 SSR markers used to anchor them. The TD analysis produced a high profile of the polymorphisms between the parental lines, Oryza sativa var. Gihobyeo/O. sativa var. Milyang, in intraspecific $F_{15}$ RIL lines, locating 368 markers of Rim2/Hipa CACTA, 78 markers of Tourist MITE Ditto, and 22 markers of Stowaway MITE Pangrangja. In the segregation analysis, non-parental segregating bands and segregation distortion bands were observed. The recombinant genetic map spans 3023.9 cM, with 5.7 cM the average distance between markers. The TD markers were distributed unequally on the chromosomes because many TD markers were located in pericentric chromosomal regions except in the cases of chromosomes 2, 3, 6 and 9. Although the number of transposon markers was not sufficient to include all rice class 2 transposons, the current map of CACTA and MITE transposons should provide new insight into the genome organization of rice since no previous DNA transposon map is available.

• The Journal of the Korean Society for Microbiology
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• v.34 no.6
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• pp.519-532
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• 1999

Helicobacter pylori is a causative agent of type B gastritis and plays a central role in the pathogenesis of gastroduodenal ulcer and gastric cancer. To elucidate the host-parasite relationship of the H. pylori infection on the basis of molecular biology, we tried to evaluate the genomic diversity of H. pylori. An ordered overlapping bacterial artificial chromosome (BAC) library of a Korean isolate, H. pylori 51 was constructed to set up a genomic map. A circular physical map was constructed by aligning ApaI, NotI and SfiI-digested chromosomal DNA. When the physical map of H. pylori 51 was compared to that of unrelated strain, H. pylori 26695, completely different restriction patterns were shown. Fifteen known genes were mapped on the chromosome of H. pylori 51 and the genetic map was compared with those of strain 26695 and J99, of which the entire genomic sequences were reported. There were some variability in the gene location as well as gene order among three strains. For further analysis on the genomic diversity of H. pylori, when comparing the genomic structure of 150 H. pylori Korean isolates with one another, genomic macrodiversity of H. pylori was characterized by several features: whether or not susceptible to restriction digestion of the chromsome, variation in chromosomal restriction fingerprint and/or high frequency of gene rearrangement. We also examined the extent of allelic variation in nucleotide or deduced amino acid sequences at the individual gene level. fucT, cagA and vacA were confirmed to carry regions of high variation in nucleotide sequence among strains. The plasticity zone and strain-specific genes of H. pylori 51 were analyzed and compared with the former two genomic sequences. It should be noted that the H. pylori 51-specific sequences were dispersed on the chromosome, not congregated in the plasticity zone unlike J99- or 26695-specific genes, suggesting the high frequency of gene rearrangement in H. pylori genome. The genome of H. pylori 51 shows differences in the overall genomic organization, gene order, and even in the nucleotide sequences among the H. pylori strains, which are far greater than the differences reported on the genomic diversity of H. pylori.