• Proceedings of the Korean Society of Embryo Transfer Conference
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• 2003.10a
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• pp.24-25
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• 2003

• Proceedings of the Zoological Society Korea Conference
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• 1994.10a
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• pp.153.1-153
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• 1994

No Abstract, See Full Text

• Proceedings of the Korean Society of Crop Science Conference
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• 2017.06a
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• pp.25-25
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• 2017

Inflorescence architecture mainly contributes to final grain yield in crops. Sorghum inflorescence is basically composed of one fertile sessile spikelet (SS) and two infertile pedicellate spikelets (PS). To identify regulatory factors involved in the inflorescence architecture, we screened an EMS mutagenesis population from the pedigreed sorghum mutant library. We found inflorescent architecture mutants, named as multi-seed mutants, msd, with gained fertile ability in PS and also an increased number of floral branches. In natural sorghum populations, it is not common that are fertile. A detailed dissection of developmental stages of wild type and msd1 mutant described that the PS in wild type do not have floral organs, including ovary, stigma, filament and anther, while the msd1 mutants generate intact floral organ in the sessile spikelet. We found MSD1 encoded a TCP transcription factor using bulk segregant analysis (BSA) of F2 population, and was a strongly enriched expression during inflorescence developmental stages. We proposed that MSD1 functions to suppress floral organ maintenance at PS during inflorescence development in Sorghum. To explore the regulatory network associated with PS fertility, whole genome expression profiling was performed at 4 different developmental stages in 6 various tissue types between wild type and msd1. Taken together, we demonstrated that MSD1 was involved in the plant hormone and maybe influenced program cell death in PS via the activation of plant hormonal pathway.

• Journal of Life Science
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• v.13 no.2
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• pp.184-190
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• 2003

Myxococcus xanthus is a Gram negative, rod-shaped, soil bacterium that displays a social behaviors, and multicellular development upon nutrient deprivation. The csgA gene encoding a cell surface protein is essential for developmental behaviors including rippling, aggregation, fruiting body formation and sporulation. csgA mutants show normal vegetative growth, but lack all these developmental phenotypes. Expression of the CsgA (C-signal) specific genes are eliminated or dramatically reduced in csgA mutants. In order to identify components of C-signal transduction pathway, second site mutations were introduced into csgA mutants and were identified which can fully or partially restore development of csgA mutants (Rhie, H. G. et. al. 1989. J. Bacteriol. 171, 3268-3276). One of such csgA suppressor mutations, socD500 restores only sporulation to csgA mutants at 15$^{\circ}C$. The socD500 mutaion however eliminates the three basic developmental requirements, starvation, high cell density and a solid surface. Only sporulation, not accompanied with fruiting body formation is induced simply by shifting the temperature of vegetatively growing cells from $32^{\circ}C$ to $15^{\circ}C$. Spores induced by socD500 mutation is not as thick as that of wild-type fruiting body. In socD500 genetic background, two of ten C-signal dependent genes, $\Omega$DK4506 and $\Omega$DK4406 are more highly expressed in growing cells at $15^{\circ}C$. These results indicate that the socD500 mutation may be partly involved in the regulation of expression of two C-signal dependent genes and genes for sporulation in this transduction pathway.

• Proceedings of the Korean Society of Developmental Biology Conference
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• 2005.07a
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• pp.34-34
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• 2005

• Development and Reproduction
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• v.25 no.4
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• pp.225-234
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• 2021

The present study aimed to investigate the mechanism of cell surface receptor loss by two constitutively activating mutants (designated L469R, and D590Y) and two inactivating mutants (D417N and Y558F) of the luteinizing hormone receptor (LHR) in the Japanese eel Anguilla japonica, known to naturally occur in human LHR transmembrane domains. We investigated cell surface receptor loss using an enzyme-linked immunosorbent assay in HEK 293 cells. The expression level of wild-type eel LHR was considered to be 100%, and the expression levels of L469R and D417N were 97% and 101%, respectively, whereas the expression levels of D590Y and Y558F slightly increased to approximately 110% and 106%, respectively. The constitutively activating mutants L469R and D590Y exhibited a decrease in cell surface loss in a manner similar to that of wild-type eel LHR. The rates of loss of cell surface agonist-receptor complexes were observed to be very rapid (2.6-6.2 min) in both the wild-type eel LHR and activating mutants. However, cell surface receptor loss in the cells expressing inactivating mutants D417N and Y558F was slightly observed in the cells expressing inactivating mutants D417N and Y558F, despite treatment with a high concentration of agonist. These results provide important information on LHR function in fish and the regulation of mutations of highly conserved amino acids in glycoprotein hormone receptors.

• Proceedings of the Korean Society of Developmental Biology Conference
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• 2003.10a
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• pp.24-25
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• 2003

The zebrafish (Danio rerio) is now the pre-eminent vertebrate model system for clarification of the roles of specific genes and signaling pathways in development. I will talk about positional cloning of two developmental mutants in zebrafish. The first mutant is headless: The vertebrate organizer can induce a complete body axis when transplanted to the ventral side of a host embryo by virtue of its distinct head and trunk inducing properties. Wingless/Wntantagonists secreted by the organizer have been identified as head inducers. Their ectopic expression can promote head formation, whereas ectopic activation of Wnt signalling during early gastrulation blocks head formation. These observations suggest that the ability of head inducers to inhibit Wntsignalling during formation of anterior structures is what distinguishes them from trunk inducers that permit the operation of posteriorizing Wnt signals. I describe the zebrafish headless (hdl) mutant and show that its severe head defects are due to a mutation in T-cell factor-3 (Tcf3), a member of the Tcf/Lef family. Loss of Tcf3 function in the hdl mutant reveals that hdl represses Wnt target genes. I provide genetic evidence that a component of the Wntsignalling pathway is essential in vertebrate head formation and patterning. Second mutant is mind bomb: Lateral inhibition, mediated by Notch signaling, leads to the selection of cells that are permitted to become neurons within domains defined by proneuralgene expression. Reduced lateral inhibition in zebrafish mib mutant embryos permits too many neural progenitors to differentiate as neurons. Positional cloning of mib revealed that it is a gene in the Notch pathway that encodes a RING ubiquitin ligase. Mib interacts with the intracellular domain of Delta to promote its ubiquitylation and internalization. Cell transplantation studies suggest that mib function is essential in the signaling cell for efficient activation of Notch in neighboring cells. (중략)

• Development and Reproduction
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• v.25 no.3
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• pp.133-143
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• 2021

In contrast to the human lutropin receptor (hLHR) and rat LHR (rLHR), very few naturally occurring mutants in other mammalian species have been identified. The present study aimed to delineate the mechanism of signal transduction by three constitutively activating mutants (designated M410T, L469R, and D590Y) and two inactivating mutants (D383N and Y546F) of the eel LHR, known to be naturally occurring in human LHR transmembrane domains. The mutants were constructed and measured cyclic adenosine monophosphate (cAMP) accumulation via homogeneous time-resolved fluorescence assays in Chinese hamster ovary (CHO)-K1 cells. The activating mutant cells expressing eel LHR-M410T, L469R, and D590Y exhibited a 4.0-, 19.1-, and 7.8-fold increase in basal cAMP response without agonist treatment, respectively. However, inactivating mutant cells expressing D417N and Y558F did not completely impaired signal transduction. Specifically, signal transduction in the cells expressing activating mutant L469R was not occurred with a further ligand stimulation, showing that the maximal response exhibited approximately 53% of those of wild type receptor. Our results suggested that the constitutively activating mutants of the eel LHR consistently occurred without agonist treatment. These results provide important information of LHR function in fish and regulation with regard to mutations of highly conserved amino acids in glycoprotein hormone receptors.

• Development and Reproduction
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• v.7 no.2
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• pp.69-80
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• 2003

The zebrafish(Danio rerio) is a pre-eminent vertebrate model system for clarification of the roles of specific genes and signaling pathways in development. We show examples of positional cloning in two developmental mutants in zebrafish. headless: The severe head defects in headless(hdl) mutants are due to a mutation in T-cell factor-3(Tcf3). Loss of Tcf3 function in the hdl mutant reveals that Hdl represses Wnt target genes. The results provide genetic evidence that a component of the Wnt signaling pathway is essential in vertebrate head formation and patterning. mind bomb: Reduced lateral inhibition in mind bomb(mib) mutants permits too many neural precursors to differentiate as neurons. Positional cloning of mib revealed that it is a gene in the Notch pathway that encodes a ubiquitin E3 ligase. Mib interacts with the intracellular domain of Delta to promote its internalization. The results suggest a model for Notch activation where the Delta-Notch interaction is followed by endocytosis of Delta and transendocytosis of the Notch extracellular domain by the signaling cell.

• BMB Reports
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• v.50 no.1
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• pp.31-36
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• 2017

High-dose caffeine uptake is a developmental stressor and causes food-avoidance behavior (aversion phenotype) in C. elegans, but its mode of action is largely unknown. In this study, we investigated the molecular basis of the caffeine-induced aversion behavior in C. elegans. We found that aversion phenotype induced by 30 mM caffeine was mediated by JNK/MAPK pathway, serotonergic and dopaminergic neuroendocrine signals. In this process, the dopaminergic signaling appears to be the major pathway because the reduced aversion behavior in cat-2 mutants and mutants of JNK/MAPK pathway genes was significantly recovered by pretreatment with dopamine. RNAi depletion of hsp-16.2, a cytosolic chaperone, and cyp-35A family reduced the aversion phenotype, which was further reduced in cat-2 mutants, suggesting that dopaminergic signal is indeed dominantly required for the caffeine-induced food aversion. Our findings suggest that aversion behavior is a defense mechanism for worms to survive under the high-dose caffeine conditions.