• Journal of Aquaculture
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• v.8 no.4
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• pp.295-306
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• 1995

The present study was performed to produce supermales and superfemales in Oreochromis niloticus by combination of induced sex reversal and diploid gynogenesis. More than $95\%$ of female was obtained by oral administration of $17\beta-estradiol$ (480 mg/kg diet) to the eutheroembryonic larvae of this species. The result of progeny tests with XY pseudofemales showed that incidences of male progeny were ranged from $71.4\%\;to\;73.7\%$. p.opo.lion of male from XY pseudofemale was not significantly different (P>0.05) from that of $\chi^2$ (1:3), but it was significantly different (P<0.01) from that of $\chi^2$(1:1) Gynogenetic diploids were produced by applying cold shocks 3 min after insemination to the eggs of XY pseudofemale sperms were genetically inactivated by ultraviolet rays of 4,050 $erg/mm^2$. Fertilization rates of gynogenetic diploids were not different from that of their controls, however, hatching rates and early survival rates were silghtly lower than those of controls. In the cytogenetic studies, there was no difference in the size of cell and nucleus between the gynogenetic diploids and the controls. At 80 days after hatching, frequencies of gynogenetic male were higher than those of gynogenetic female (P<0.01) in their population.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.12
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• pp.6311-6318
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• 2012

Background: HER2/neu overexpression due to gene amplification is an important factor in breast cancer, modifying the sensitivity to anti-HER2 monoclonal antibody therapy. The clinical significance of HER2 expression in non small cell lung carcinoma (NSCLC) is currently under evaluation. The tumor suppressor gene PTEN negatively regulates the HER2/PI3K/Akt signalling pathway. The purpose of this study was to evaluate the role of simultaneous alteration in HER2 and PTEN protein expression in relation to biological behaviour of NSCLCs. Materials and Methods: Protein expression was determined by immunohistochemistry in sixty-one (n=61) NSCLC cases along with CISH for HER2 gene analysis and detection of chromosome 17 aneuploidy. Patients were followed-up for a period of 34 to 41 months after surgery. Results: HER2 overexpression (2+/3+score) was detected in 17 (27.9%) patients while loss of PTEN expression was observed in 24 (39.3%) cases, low expression in 29 (47.6%) and overexpression in 8 (13.1%). Simultaneous HER2 overexpression and PTEN low/loss of expression were correlated with metastasis (71.4% vs 36.2% p=0.03). Analysis in the subgroup of 22 patients of pTNM stage III with lymph node status N1 or N2 revealed that there was a relationship between the number of positive regional lymph node groups and simultaneous deregulation of the two genes (p=0.04). Multivariate analysis determined that HER2 overexpression was associated with an increasing risk of developing metastases (OR: 4.3; 95%CI: 1.2-15.9; p: 0.03) while PTEN overexpression was associated with lower risk (OR: 0.1; 95%CI: 0.1, 1.0; p: 0.05). Conclusions: Simultaneous HER2/PTEN deregulation is a significant genetic event that leads to a more aggressive phenotype of NSCLC.

• Development and Reproduction
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• v.2 no.1
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• pp.45-52
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• 1998

An enhncer detector line(EDL) having P[1ArB] insertion in X chromosome with expression of reporter gene (lacZ) in the polar cells and border cell of egg chamber was established and used to monitor the differentiation and migration of border cells during the oogenesis of Drosophila. differentiation of border cell from the anterior polar follicle cells was evident in stage-9 egg chamber of EDL149 which was characterized by migration of columnar follicle cells toward posterior of egg chamber surrounding the oocyte. Migration of border cells was observed in the stage-9 and -10 egg chambers. \beta -galactosidase activities were rapidly increased during the first 4 days after eclosion, and it coincided with the timing of border cell differentiation in the ovary during adult life. Homozygote of EDL149 showed some retardation of border cell migration , resulting absence of migration of some border cells in the anterior part of egg chamber or delayed migration of some border cells in the stage-10 egg chamber. These results suggest that the P[1ArB] of EDL149 is inserted at the locus of the structural gene required for the border cell migration. In addition to the expression in egg chambers, lacZ expression was also detected in the meiotic germ cells of testis and antenna, suggesting the possible requirement of the trapped gene function in these organ. this EDL and enhancer trapped gene might be useful for the study of developmentally regulated cell migration.

• Applied Biological Chemistry
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• v.38 no.2
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• pp.111-117
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• 1995

In Escherichia coli, CRP forms a complex with cAMP and acts as a transcriptional regulator of many genes, including sugar metabolism operons. The E. coli MK2001, which is introduced the altered crp, is functional in the expression of lac, ara and man, in the absence of cAMP. However, the expression of mal gene is fully activated by the addition of cAMP or cGMP. The object of the study is cloning of the sfs (sugar fermentation stimulation) genes, which was involved in regulation of mal gene expression with the altered crp gene, and structural analysis and characterization of the genes at the molecular level. We have cloned 5 different E. coli genes which stimulate the maltose metabolism in a crp, cya::km (MK2001) background. Newly identified genes were designated as sfs. One of the sfs genes (pPC1), located at the 53.2 min map position on the E. coli chromosome, was further analyzed. Expression of the genes, which is involved in maltose metabolism, malQ (amylomaltase), was increased to 5.8-fold in the presence of a plasmid, pAP5, containing the subcloned sfs4 gene. The nucleotide seguence of a common 2,126 bp segment of the pPCM1 was determined and two open reading frames (ORF1 and ORF2) were detected. The ORF1 encodes the sfs4 gene and ORF2 encodes a truncated protein. Potential CRP binding site is located in the upstream of the putative promoter in the regulatory region. Expression of the cloned sfs4 gene was positively regulated by the cAMP-CRP complex.

• KOREAN JOURNAL OF CROP SCIENCE
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• v.56 no.2
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• pp.124-133
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• 2011

Bacterial blight (BB), cuased by the vascular pathogen Xanthomonas oryzae pv. oryzae, is one of the major threats in rice fields worldwide. In Korea, two resistance genes against BB, Xa1 and Xa3 had been intensively used for developing high quality japonica rice cultivars. Those traditional resistance sources have being rapidly ified by the adopting of BB pathogen through mutations of the corresponding avr-genes, such as K3a exhibiting high compatibility to both Xa1 and Xa3. To expanding genetic resource against BB in Korea, the Suweon506, an introgression line between a Korean japonica cultivar, Hwaseong and a wild relative, Oryza minuta, was be subjected for genetic analysis owing to the BB resistance. Through association analyses between the pathotyping and genotyping results for each $F_2$ progenies, derived from a cross between Suweon506 and a Tongil type cultivar, Milyang23, a major resistant dominant gene is localized on the subterminal region of rice chromosome 4, where at least three BB resistancde genes, Xa1, Xa2, and Xa22, were reported previously.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.15 no.1
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• pp.35-39
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• 2015

Medium-chain acyl-CoA dehydrogenase (MCAD) deficiency is the most common mitochondrial fatty acid oxidation disorder which is inherited as an autosomal recessive pattern. MCAD deficiency is caused by mutations in the ACADM gene; medium-chain acyl-CoA dehydrogenase gene (ACADM; OMIM 607008) on chromosome 1p31 which encodes MCAD, the mitochondrial enzyme which catalyzes the first reaction in beta-oxidation of fatty acids with medium-chain length. Here, we describe one Korean pediatric case of MCAD deficiency, which was diagnosed during newborn screening by tandem mass spectrometry and confirmed by molecular analysis. The level of hexanoyl (C6), octanoyl (C8), decenoyl (C10:1) carnitine, and C8/C2 ratio was elevated. Homogenous c.1189T>A (p.Tyr397Asn) mutation of ACADM gene was identified by direct sequencing. He has been asymptomatic and has shown normal growth and development by 25 months of age without any intervention. There was no episode of metabolic acidosis during follow-up period.

• Korean Journal of Biological Psychiatry
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• v.13 no.4
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• pp.260-266
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• 2006

Objectives : Synapsin III near VCFS region on chromosome 22q affects. It could be an interesting candidate gene for schizophrenia. D22S280 is a highly polymorphic genetic marker residing in synapsin III. We examined association of D22S280 marker on synapsin III with Korean patients with schizophrenia. Methods : The subjects were 46 male Korean patients with schizophrenia and 60 male normal controls. Using polymerase chain reaction, gel electrophoresis, ABI 310 genetic analyzer, and GeneScan Collection 3.1 software, we confirmed genotypes of D22S280 marker. We examined Hardy-Weinberg equilibrium and case-control association using SAS/Genetic 9.1.3. Results : Genotypes of both schizophrenia and control groups were in Hardy-Weinberg equilibrium. We could not find any significant statistical differences in allele-wise(${\chi}^2$=10.4, df=6, p=0.098) and genotype-wise (${\chi}^2$=22.1 df=19, p=0.258) analyses of D22S280 marker between schizophrenia and normal controls. Individual allele analyses with df=1 showed significant differences in A1(p=0.025) and A7(p=0.034) allele, which were not significant following Bonferroni corrections(A1:p=0.177, A7:p=0.235). Conclusion : We couldn't find any association between schizophrenia and the synapsin III gene. Given the small number of subjects studied, further investigations are needed.

• Journal of Life Science
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• v.32 no.2
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• pp.161-166
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• 2022

Mitosis is a process in which a replicated genome is distributed to two daughter cells, and it is necessary for cell survival and organismal development. During mitosis, the spindle assembly checkpoint (SAC) ensures faithful chromosome segregation by monitoring the kinetochore attachment to the mitotic spindle. Although the SAC mechanism has been extensively studied over the last 30 years, the mechanism by which a single unattached kinetochore activates the SAC remains unclear. The key components of the SAC are Mad1, Mad2, Mad3 (BubR1 in higher eukaryotes), Bub1, Bub3, and Cdc20, which are all required for SAC activation. An essential step for SAC activation is the formation of the Mad2 - Cdc20 complex in the unattached kinetochore, which is kinetically disfavored. Although the mechanism by which Mad2 and Cdc20 are recruited to unattached kinetochores is well-known, it is not clear how they form a complex. Recently, a key mechanism for the formation of the Mad2 - Cdc20 complex has been identified, which is catalyzed by an unattached kinetochore. This supports the evidence that a single unattached kinetochore can activate the SAC signaling. Herein, we discuss the known key mechanism for SAC activation, review the recent studies on SAC, and conclude how their discoveries improved the understanding of mitosis.

• Proceedings of the Korean Society of Developmental Biology Conference
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• 2003.10a
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• pp.84-84
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• 2003

DNA methylation is involved in epigenetic processes such as X-chromosome inactivation, imprinting and silencing of transposons. DNA methylation is a highly plastic and critical component of mammalian development The DNA methyltransferases (Dnmts) are responsible for the generation of genomic methylation patterns, which lead to transcriptional silencing. The maintenance DNA methyltransferase enzyme, Dnmt 1, and the de novo methyltransferase, Dnmt3a and Dnmt3b, are indispensable for development because mice homozygous for the targeted disruption of any of these genes are not viable. The occurrence of DNA methylation is not random, and it can result in gene silencing The mechanisms underlying these processes are poorly understood. It is well established that DNA methylation and histone deacetylation operate along a common mechanistic pathway to repress transcription through the action of methyl-binding domain proteins (MBDs), which are components of, or recruit, histone deacetylase (HDAC) complexes to methylated DNA. As a basis for future studies on the role of the DNA-methyl-transferase in porcine development, we have isolated and characterized a partial cDNA coding for the porcine Dnmt1. Total RNA of testis, lung and ovary was isolated with TRlzol according to the manufacture's specifications. 5 ug of total RNA was reverse transcribed with Super Script II in the presence of porcine Dnmt 1 specific primers. Standard PCRs were performed in a total volume of 50 ul with cDNA as template. Two DNA fragmenets in different position were produced about 700bp, 1500bp and were cloned into pCR II-TOPO according to the manufacture's specification. Assembly of all sequences resulted in a cDNA from 158bp of 5'to 4861bp of 3'compare with the known human maintenance methyltransferase. Now, we are cloning the unknown Dnmt 1 region by 5'-RACE method and expression of Dnmt 1 in tissues from adult porcine animals.

• Journal of Ginseng Research
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• v.15 no.3
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• pp.171-178
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• 1991

The results ok feeding experiments to the mice with ginseng extract, ginseng Powder, and ADAPTAGEN, for 30 days before X-ray irradiation and for 40 days after the X-ray irradiation at 750 rads were as follow: 1. The 50% lethals days (LD50, ) by the X-ray irradiation were 9 days at 1, 000 rads. 10 days at 900 rads, 11 days at 800 rads, 14 days at 760 rads, and 19 darts at 750 rads. Therefore, the standard radiation dose was set at 750 radb/8 min. 2. The 80% of the control group mice exposed to the X-ray radiation without ginseng feeding died in periods ranging from 14 to 24 days and the 20~30% of the ginseng extract and ginseng powder feeding groups died. But the 100% of the mice fed with ADAPTAGEN survived. 3. Testicles of the control group became smaller in weight than the nomad group by 26.5 to 29.0% and those of the ginseng extract and ginseng powder feeding group reduced by 44.6 to 60.4%. However, testicles of the ADAPTiIGEN feeding group increased in size by 77.4% to 87.1% and in weight by 61%, showing a recovery phenomenon approarhing to those of the ordinary mice. The ADAPTAGEN feeding group mice were also as active in color as the ordinary ones. 4. An electron micrograph(X8, 000X2.2) of the liver cells of the mice which had been 40 days after X-ray irradiation showed as follows; The control group appeared that is physiological action stopped due to the frequent occurrence of morphological change of the nucleus and diffusion of chromosome, reduction in microspores and expansion of microsomts, and endoplasmic change of mitochondria. The liver cells or the ADAPTAGEN feeding group were in a state similar to those of the ordinary mice restoring to normalcy In contrast, the liver cells of the ginseng extract and ginseng powder feeding groups were still far from being normal. 5. A serological analysis showed that the control group sharply decreased in albumin, Y-g1obu1in, and IgG so far as to cause dystrophy and to weaken antibody resistance but that ginseng extract and ginseng powder feeding groups, though in a little more restoring state than the control group, were still far from the normal group. The ADAPTAGEN feeding group restored to a state as comparable to the normal group in the contents of albumin ${\gamma}$-globulin, IgG and serum protein. In order words, it is noteworthy that ADAPTAGEN feeding was effective in revitalizing the destroyed cells of a living body and that it has the function of normalizing antibody components.