• Journal of Animal Science and Technology
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• v.47 no.4
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• pp.547-554
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• 2005

An experiment was conducted to investigate the dietary effects of a transgenic Aspergillus oryzae(AO) culture on the performance, egg quality and intestinal microflora of layers. A total of 840 Hy-line Brown layers of 39wks old were assigned to one of the following 7 dietary treatments: control(C), C+0.2% AO culture, C+0.5% AO culture, C+0.2% transgenic AO culture, C+0.5% transgenic AO culture, C+0.2% transgenic mutant AO culture, and C+0.5% transgenic mutant AO culture. The transgenic AO was made by inserting Salmonella gallinarum gene to AO. And the transgenic mutant AO was made by inserting Salmonella gallinarum gene to mutant AO which was mutated by UV irradiation. Each treatment was replicated six times with 20 birds housed in 2 bird cage. Twenty birds units were arranged according to completely randomized block design. Feeding trial lasted for 8wks under 16 hour lighting regimen. Laying performance and egg quality were significantly(P<0.05) affected by the treatments. Transgenic AO culture supplementation at the level of 0.2% significantly increased egg production, while its egg weight was significantly decreased compared to that of the control. Feed intake and feed conversion ratio(FCR) were not significantly different among the AO treatments and the control. The eggshell strength of the AO treatments was significantly higher than that of the control. Transgenic mutant AO culture supplemented at the level of 0.5% significantly increased egg yolk color. Intestinal microflora were significantly(P<0.05) affected by the treatments. The cfu of Lactobacilli spp. significantly increased and those of Salmonella species and E. coli decreased in the AO treatments. The transgenic AO and transgenic mutant AO culture were more effective than the AO culture in reducing the cfu of Salmonella species and E. coli. It is concluded that supplementation of the transgenic AO culture at the level of 0.2% could be recommended for the improvement of egg production. Supplementation of transgenic AO or transgenic mutant AO culture at 0.2% level effectively controlled intestinal Salmonella species population.

• Journal of Plant Biotechnology
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• v.35 no.3
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• pp.169-176
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• 2008

Salicylic acid(SA) is a phytohormone that is related to plant defense mechanism. The SA accumulation is triggered by abiotic and biotic stresses. SA acts as a signal molecular compound mediating systemic acquired resistance and hypersensitive response in plant. Although the role of SA has been studied extensively, an understanding of the SA regulatory mechanism is still lacking in plants. In order to comprehend SA regulatory mechanism, we have been transformed with a SID2 promoter:GUS::LUC fusion construct into siz1-2 mutant and wild plant(Col-0). SIZ1 encodes SUMO E3 ligase and negatively regulates SA accumulation in plants. SID2(SALICYLIC ACID INDUCTION DEFICIENT2) is a crucial enzyme of SA biosynthesis. The Arabidopsis SID2 gene encodes isochorismate synthase(ICS) that controls SA level by conversion of chorismate to isochorismate. We compared the regulation of SID2 in wild-type and siz1-2 transgenic plants that express SID2 promoter:GUS::LUC constructs respectively. The expressions of $\beta$-GLUCURONIDASE and LUCIFERASE were higher in siz 1-2 transgenic plant without any stress treatment. SID2 promoter:GUS::LUC/siz1-2 transgenic plant will be used as a starting material for isolation of siz1-2 suppressor mutants and genes involved in SA-mediated stress signaling pathway.

• Korean Journal of Poultry Science
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• v.8 no.1
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• pp.1-5
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• 1981

In trying to predict the effect of genetics on the broiler in the year 2000, this is a relatively short period of time as far as broiler genetics in concerned. Modern broiler genetics started around 1945 and tremendous gains when made in past 35 years. Futher improvements on broiler will depend on the evolution and revolution: 1. Evolution: (1) Growth rate has been made 4-5% per year. (2) Feed conversion has improved approximately 1% per year. (3) Abdominal fat is becoming a major complaint in broiler. (4) Because of the changing life-style, broiler meat sales in the future will be more and more in cut-up form. (5) Breeding for stress resistance and selection for docile temperament can be important in order to funker improve fled efficiency. (6) In female parent stock, reproduction characteristics are in many can negatively correlated with the desired broiler traits. (7) Egg production and hatchability in moot commercial parent nod m at a fairly high level. (8) In male parent stock, the heavier and mon super-meat-type male lines are desired to Product better broilers. 2. Revolution: Trying to forecast revolutionary change in broiler genetics is highly speculative, as sudden change are aften unpredictable. (1) Species hybridization, such as a turkey-chicken cross (2) Biochemical tools, such as blood typing. (3) Mutation breeding by radiation or chemical mutagentia. (4) Broiler breeding would be to change the phenotypic appearance by single gene, such as naked, wingless. (5) Changes in production techniques. such as growing in cage or growing in filtered air positive pressure houses.

• Korean Journal of Poultry Science
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• v.30 no.4
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• pp.245-251
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• 2003

Three experiments were conducted to investigate the effect of feeding yeast accumulated transgenic ferritin(FRT, Saccharomyces cerevisiae) as a probiotic on the performance, iron contents in the liver, spleen, bone and yolk of laying hens and broiler chicks. Effects of feeding FRT were compared with that of feeding wild-type yeast(W0) and yeast grown on 20 mM ferric citrate-added medium (W20). In Expt 1, to investigate the effect of feeding yeast (control, W0 FRT) on performance and iron content of organs of broiler chicks which were fed basal diet supplemented with 75mg/kg iron(Fe75) or not (Fe0), three hundred sixty one-day-old male broiler chicks were fed a corn-sov based diet for five weeks. Weight gain, feed intake and feed conversion were measured weekly. In Expt 2, fifteen 33-week-old ISA Brown laying hens were placed in individual cages and were fed control, W0 and FRT diets for Four weeks. In Expt 3, twenty four 45-week-old ISA Brown laying hens were placed in individual cages and were fed a basal diet for a week. Then, experimental diets (control, W0, W20, FRT) were fed for three weeks. Iron contents in the liver, heart, spleen and tibia were determined at the end of all experiments. Iron content in yolk was measured weekly (expt 2, 3). The level of yeast added and iron concentration of FRT were $1{\times}10^8$cfu/kg diet and 500 mg/kg cell (DM) respectively in Expt 3, yeast was supplemented at $2{\times}10^{10}$cfu/kg diet and the iron content of FRT was 1000mg/kg cell (DM). In Expt 1. birds fed Fe75 showed significantly higher weight gain compared with Fe0 (P<0.05). However, weight gain and feed intake of birds fed FRT was significantly lower than control (P<0.05). In Expt 2, the iron content of the liver was decreased in the FRT treatment (P<0.05). In Expt 3, iron concentration of the liver and spleen tended to be increased by feeding FRt. However, the iron content of the tibia tended to be decreased in the FRT treatment. These results suggest that feeding FRT as a probiotic cannot improve performance and iron content in organs of broiler chicks and laying hens.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.15 no.1
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• pp.29-34
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• 2015

Citrullinemia type1 is an autosomal recessive disorder of the urea cycle characterized by neonatal or late onset of hyperammonemia caused by a deficiency of the enzyme argininosuccinate synthetase (ASS). An ASS1 deficiency demonstrates fatal clinical manifestations that are characterized by the neonatal metabolic coma and early death when untreated. It causes a broad spectrum of effects, ranging from a mild disorder to a severe mental retardation, epilepsy, neurologic deficits. An acute neonatal form is the most common. Infants are normal at birth followed by an acute illness characterized by vomiting, lethargy, seizures and coma. These medical problems are life-threatening in many cases. A later onset form is less frequent and may be milder than the neonatal form. This later-onset form is associated with severe headaches, visual dysfunction, motor dysfunction, and lack of energy. Citrullinemia type1 is caused by mutations in the ASS1 gene located on chromosome 9q34.1 that encodes argininosuccinate synthetase, the third enzyme of the urea cycle catalyzing the formation of argininosuccinic acid from citrulline and aspartic acid. The enzyme is distributed in tissues including liver and fibroblasts. This mutation leads to hyperammonemia, arginine deficiency and elevated citrulline level. In the urea cycle, argininosuccinate synthetase catalyses the conversion of citrulline and aspartate to argininosuccinate.. Here, we describe a female newborn patient with lethargy, rigidity and hyperammonemia who was diagnosed as citrullinemia type1 with a c.[421-2A>G], c.[1128-6_1188dup] mutation.

• Journal of Life Science
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• v.15 no.3 s.70
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• pp.415-422
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• 2005

library of the mutants was prepared by transposon mutagenesis of the Mycobacterium bovis BCG. We screened this library for the resistance to an anti-tuberculosis antibiotic, PA-824. Most of the mutants resistant to the PA-824 were not able to synthesize the coenzyme $F_{420}$ which is normally produced by the wild type M. bovis BCG strains. HPLC analysis of the cellular extract showed that one of those mutants which lost the ability to synthesize $F_{420}$ still produced F0. The insertion site of the transposon in this mutant was determined by an inverse PCR and the transposon was found to be inserted in the Rv2435c open reading frame (ORF). Rv2435c ORF is predicted to encode an 80.3 kDa protein. Rv2435c protein appears to be bound to the cytoplasmic membrane, its N-terminal present in the periplasm and C-terminal in the cytoplasm. The C-terminal portion of this protein is highly homologous with the adenylyl cyclases of both prokaryotes and eukaryotes. There are 15 ORFs which have homology with the class III AC proteins in the genome of the M. tuberculosis and M. bovis. Two of those, Rv1625c and Rv2435c, are highly homologous with the mammalian ACs. We cloned the cytoplasmic domain of the Rv2435c ORF and expressed it with six histidine residues attached on its C-terminal in Escherichia coli to find out if this protein is a genuine AC. Production of that protein in E. coli was proved by purifying the histidine-tagged protein by using the Ni-NTA resin. This protein, however, failed to complement the cya mutation in E. coli, indicating that this protein lacks the AC activity. All of the further attempts to convert this protein to a functional AC by a mutagenesis with UV or hydroxylamine, or construction of several different fusion proteins with Rv1625c failed. It is, therefore, possible that Rv2435c protein might affect the conversion of F0 to $F_{420}$ not by synthesizing cAMP but by some other way.