• The Korean Journal of Zoology
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• v.33 no.1
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• pp.6-11
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• 1990

Analysis of genetic structure in Kimpo natural population of Drosophila was carried out by utilizing the deleterious gene on the second chromosome of Drosophila melanogaster. Male flies tested were continuously collected for eight years; in late September 1974 and 1981-1987. The frequency of deleterious gene (lethal plus semilethal) ranged from 27.02% in 1983 to 41.48% in 1987, and the values estimated from the eight years samples are highly signihcent from each other with a homogenety test (X$^2$=52.0157, d.f.=28, P<0.005). Allelic rates ranged from 1.30% in 1981 to 5.03% in 1974. And the effective population size by using the rate of allelism was estimated average at 3, 300 pairs. Elimination rate by homozygous of lethal gene ranged from 0.0004 in 1984 to 0.0019 in 1974, and that is for smaller than mutation rate(0.005) at second chromosome. We suppose that stable frequency (about 20%) lethal genes of D. melanogaster in Kimpo natual population are maintained by invade of P-type mutator factor (P element) versus eliminated in heterozygous and homozygous condition of lethal gene.

• International Journal of Industrial Entomology and Biomaterials
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• v.18 no.2
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• pp.113-120
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• 2009

Embryonic lethal abnormal visual (elav) is a lethal gene in Drosophila inducing the abnormal development and function of nervous system. We cloned a Bm-elav gene by bioinformatics and biological experiment, based on sequence of ELAV protein and dbEST of Bombyx mori. The full-length of Bm-elav cDNA is 1498 bp, contains a 906 bp open read frame (ORF) encoding a precursor of 301 amino acid residues with a calculated molecular weight of 34 kDa and pI of 8.99. Bm-ELAV protein precursor contains three RNA recognition motifs (RRM) in $24{\sim}91$, $110{\sim}177$ and $222{\sim}295$ bit amino acid residues respectively, and belongs to RNA-binding protein family. Bm-ELAV shared varying positives, ranging from 56% to 60% (Identities from 41% to 45%), with RRM from other species of Xenopus tropicalis, Apis mellifera, Tribolium castaneum, Branchiostoma belcheri and Drosophila. Gene localization indicated that Bm-elav is a single-copy gene, gene mapping within 12-chromosome from 7916.68 knt to 7918.16 knt region of nscaf2993. Spatiotemporal expressions pattern analysis revealed that Bm-elav expressed higher in most tested tissues and developmental stages in whole generation, such as silk gland, fat body, midgut, hemopoietic organ and ovary, but almost no expression in terminated diapause eggs. This suggested that the expression of Bm-elav in early developmental embryonic stages might induce abnormal development like in Drosophila. Cloning of the Bm-elav gene enables us to test its potential role in controlling pests by transferring the gene into field lepidopteran insects in the future.

• Animal cells and systems
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• v.2 no.1
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• pp.123-131
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• 1998

The unc-29 region on the chromosome I of Caenorhabditis elegans has been mutagenized in order to obtain lethal mutations. In this screen, the uncoordinated phenotype of unc-29 (e193) mutant was used to identify any lethal mutations closely linked to the unc-29 gene, which encodes a subunit of nicotinic acetylcholine receptors. We have isolated six independent mutations (jh1 to jh6) out of approximately 5,200 ethyl methanesulfonate(EMS) treated haploids. Four of the six mutations demonstrated embryonic lethal phenotypes, while the other two showed embryonic and larval lethal phenotypes. Terminal phenotypes observed in two mutations (jh1 and jh2) indicated developmental defects specific to posterior part of embryos which appeared similar to the phenotypes observed in nob (no back end) mutants. Another mutation (jh4) resulted in an interesting phenotype of body-wall muscle degeneration at larval stage. These mutations were mapped by using three-factor crosses and deficiency mutants in this region. Here we report genetic analysis and characterization of these lethal mutations.

• Journal of Sericultural and Entomological Science
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• v.33 no.2
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• pp.72-74
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• 1991

The recessive lethal mutation 'non-molting of Nho' (symbol, ㎚n) was founded on one preservation stocks. All dwarf larvae continued to eat a few mulberry leaves and very slightly increasing body-size over a 7 days, and then died without entering into molt. Linkage experiments showed that ㎚n was linked with Knob(K) on the 11th linkage group. Precise localization of the gene was performed by mating with ㎚ gene. This mutant was confirmed to be allelic with the ㎚ gene located on the same chromosome.

• Journal of Microbiology
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• v.35 no.3
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• pp.234-238
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• 1997

Conditional lethal mutation nup49-1 of a nuclear pore complex component gene was constructed in Saccharomyces cerevisiae. This mutation deleted one third of the essential NUP49 gene at the carboxy-terminal, but retained 13 repeats of the highly conserved GLFG domain. The nup49-1 mutant strain was viable with a slow-growth phenotype, indicating that the C-terminal is dispensable at normal growth temperature. This strain exhibited both temperature-sensitivity at 37.deg.C and cold-sensitivity at 16.deg.C. Temperature shift experiments revealed that the arrest phenotype at 37.deg.C was random in the cell division cycle. The nup49-1 mutation was tested to be recessive and is expected to be useful for the functional analysis of nuclear pore complex proteins as well as for studies of nuclear transport systems.

• Korean Journal of Microbiology
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• v.35 no.1
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• pp.13-17
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• 1999

Shigella sonnez is important causes of human enleric infcctions. S. sonnei KNIH104S was isolated from patient of shigellosis in Korea and previously reported. We cloned 1.7 kb BamHI fragment containing the asd gene encoding an aspartate $\beta$-semialdehyde dehydrogenase from chromosomal DNA of S. sonnei KNIH104S. This recombinant plasmid was named as pSAB17. E. coli $\chi$6097, an a d mutant, cannol grow on the LB medium without DL-$\alpha$, $\varepsilon$-diaminopimclic acid (50 pgiml) but E. coli x 6097(pSAB17) can grow on the same medium. We sequenccd the asd gene ol Shigella for the first time. The asd gcne was composed of 1,104 base pairs with ATG initiation codon and TAA termination codon. Sequence comparison of the asd gene exhibited 99.9% nucleolide sequence hornology with that of E. coli. Also, We constructed the balanced-lethal vector using pBluescrip SK(+) and asd gene of S. sonnei KNIH104S.

• BMB Reports
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• v.41 no.5
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• pp.363-368
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• 2008

Two genes of temperate mycobacteriophage L5, namely, gp63 and gp64, were hypothesized to be toxic to M. smegmatis. An identical L5 gp64 ortholog (designated hlg1) was cloned from homoimmune mycobacteriophage L1 and characterized at length here. As expected, hlg1 affected the growth of M. smegmatis when overexpressed from a resident plasmid. HLG1 (the protein encoded by hlg1) in fact caused growth retardation of M. smegmatis and the region encompassing its 57-114 C-terminal amino acid residues was found indispensable for its growthretardation activity. Both nucleic acid and protein biosynthesis were severely impaired in M. smegmatis expressing HLG1. Interestingly, HLG1 also affected E. coli almost similarly. This putative delayed early lipoprotein did not participate in the lytic growth of L1.

• BMB Reports
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• v.38 no.1
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• pp.89-96
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• 2005

Earlier, we reported that the bacteriophage $\lambda$ P gene product is lethal to Escherichia coli, and the E. coli rpl mutants are resistant to this $\lambda$ P gene-mediated lethality. In this paper, we show that under the $\lambda$ P gene-mediated lethal condition, the host DNA synthesis is inhibited at the initiation step. The rpl8 mutation maps around the 83 min position in the E. coli chromosome and is 94% linked with the dnaA gene. The rpl8 mutant gene has been cloned in a plasmid. This plasmid clone can protect the wild-type E. coli from $\lambda$ P gene-mediated killing and complements E. coli dnaAts46 at $42^{\circ}C$. Also, starting with the wild-type dnaA gene in a plasmid, the rpl-like mutations have been isolated by in vitro mutagenesis. DNA sequencing data show that each of the rpl8, rpl12 and rpl14 mutations has changed a single base in the dnaA gene, which translates into the amino acid changes N313T, Y200N, and S246T respectively within the DnaA protein. These results have led us to conclude that the rpl mutations, which make E. coli resistant to $\lambda$ P gene-mediated host lethality, are located within the DNA initiator gene dnaA of the host.

• Korean Journal of Microbiology
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• v.41 no.4
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• pp.275-280
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• 2005

Anthrax is an infectious disease caused by the gram-positive bacterium, Bacillus anthracis. Anthrax toxin is a tripartite toxin comprising of protective antigen (PA), lethal factor (LF) and edema factor (EF). PA is the receptor-binding component, which facilitates the entry of LF or EF onto the cytosol. LF is a zinc-dependent metalloprotease, which is a critical virulence factor in cytotoxicity of infected animals. Therefore, it is of interest to develop its potent inhibitors for the neutralization of anthrax toxin. The first step to identify the inhibitors is the development of a rapid, sensitive, and simple assay method with a high-throughput ability. Much efforts have been concentrated on the preparation of powerful assays and on the screening of inhibitors using these system. In the present study, we have tried to construct anthrax lethal factor in yeast expression system to prepare cell-based high-throughput assay system. Here, we have shown the results covering the construction of a new vector system, subcloning of LF gene, and the expression of target gene. Our results are first trial to express LF gene in eukaryote and provide the basic steps in design of cell-based assay system.

• Journal of Microbiology
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• v.42 no.1
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• pp.32-36
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• 2004

We have previously isolated three synthetic lethal mutants from Schizosaccharomyces pombe in order to identify mutations in the genes that are functionally linked to spmex67 with respect to mRNA export. A novel rsm1 gene was isolated by complementation of the growth defect in one of the synthetic lethal mutants, SLMex1. The rsml gene contains no introns and encodes a 296 amino-add-long protein with the RING finger domain, a C3HC4 in the N-terminal half. The Δrsm1 null mutant is viable, but it showed a slight poly(A)$\^$＋/ RNA accumulation in the nucleus. Also, the combination of Δrsm1 and Δspmex67 mutations confers synthetic lethality that is accompanied by the severe poly(A)$\^$＋/ RNA export defect. These results suggest that rsm1 is involved in mRNA export from the nucleus.