11:10-12:00, Rm 103

Development and regenerationE-17-13GTP binding protein Nog1 regulate fat storage, development andlifespanHo-Hyun Lee, Jeong-Hoon ChoDepartment of Biology Education, Chosun University, KoreaGTP binding protein, nog1, is identified as one of downstream of TOR(target ofrapamycin) pathway and play an important role in 60S ribosome biogenesis. According torecent study, Target Of Rapamycin(TOR) regualate fat storage, metabolic geneexpression, development, reproduction and especially lifespan. And an inhibition of TORincrease lifespan of various organisms including yeast, Caenorhabditis elegans, mice.Here we shows that nog1 homologue in C. elegans regulate lifespan, fat metabolism,development. GFP promoter assay revealed ubiquitous expression of the C.elegansnog1 from early embryo through adult. GFP tagged Nog1 protein localized in nucleus andespecially concentrated in nucleolus. In fuctional study of Nog1, knock down result showsslow growth, small broodsize, more fat storage, and increased life span. On the contraryto this Nog1 overexpression decrease life span. Taken together nog1 homologue inC.elegans may be one of downstream of TOR and has important roles in fat storage,development and lifespan.E-17-16Phosphatidylserine receptor stabilin-2 acts a receptor for myoblastfusion and muscle regenerationSeung-Yoon Park², Youngeun Yun¹and In-San Kim¹¹Department of Biochemistry and Cell Biology, Cell and Matrix Research Institute, School ofMedicine, Kyungpook National University, Daegu 700-422, Korea, ²Department of Biochemistry,School of Medicine, Dongguk University, Gyeongju 780-714, KoreaMyoblast fusion to form multinucleated myotubes is required for myogenesis as well asmuscle regeneration, but few molecules are known to be involved in myoblast fusion inmammals. We demonstrate here that phosphatidylserine (PS) receptor stabilin-2 act as afunctional receptor for myoblast fusion. Anti-PS antibody significantly inhibits muscle cellfusion. Among recently identified PS-receptors, stabilin-2 expression was markedly upregulatedduring myoblast differentiation and muscle regeneration. Knockdown ofendogenous stabilin-2 expression significantly decreased the formation of myotubes inC2C12 cells. Conversely, overexpression of stabilin-2 caused an increase in cell fusion.Down-regulation of stabilin-2 significantly inhibits muscle regeneration in an in vivo animalmodel. Furthermore, stabilin-2 expression in muscle cells is regulated by NFATc1 andNFATc3 that contribute to skeletal muscle growth, including muscle cell fusion. Theseresults support a role of stabilin-2 in myotube formation and muscle regeneration.E-17-14Nkx3.2-Barx1 Crosstalk and Its Implication in OsteoarthritisHye-Jeong Choi¹, Da-Un Jeong¹, Byung-Joo Kim², Jeong-Ah Kim¹, Byung HyuneChoi³, Byung Hyun Min²and Dae-Won Kim¹¹Yonsei University Department of Biochemistry, ²Ajou University School of Medicine Departmentof Orthopedics, ³Inha University School of Medicine Department of Medical SciencesBarx1 is a homeoproteins playing a role in craniofacial development, odontogenesis andstomach organogenesis. We have previously shown that Nkx3.2-mediated NF-kBactivation supports chondrocyte viability in cartilage. Interestingly, it has beendemonstrated that Nkx3.2 and Barx1 exhibit complementary expression patterns in thedeveloping cartilage. However, the role of Barx1 in chondrocyte has not been fullycharacterized. Here we show that Barx1 is expressed in mouse embryonic tissues andregulates chondrogenesis. Furthermore, Barx1 triggers chondrocyte apoptosis and itspro-apoptotic function is selective for chondrogenic lineage cells. Intriguingly, Barx1effectively disrupts the interaction between Nkx3.2 and IkB and attenuates NF-kBactivation mediated by Nkx3.2. In addition, we have found that Nkx3.2-Barx1 expressionbalance is shifted in favor of Barx1 in STR/ORT OA model mice, wildtype aging mice, andDMM-induced OA model mice. Furthermore, DMM-induced OA progression can bemodulated by altering expression of Barx1 and Nkx3.2. These results suggest thatNkx3.2-Barx1 plays a role in chondrocyte viability control and osteoarthritis progression.E-17-17Novel cell cource for elastic cartilage regenerationEunAh Lee, SeungWoo Nam, Wheemoon Cho, Youngsook SonDepartment of Genetic Engineering, College of Life Science, Kyung Hee University, Seochon-dong,Kiheung-gu, Yong-in, Gyeonggi-do 446-701, KoreaCartilages can be classified to three different types based on ECM composition andhistological morphology-hyaline cartilage, elastic cartilage, and fibrocartilage. Elasticcartilages comprise cartilage tissue of outer ear and tracheal cartilage. In case of articularcartilage tissue regeneration, ACT is the best approach, and autologous articularchondrocytes are isolated from the articular cartilage tissue of non-load bearing site.However, for elastic cartilage regeneration, it is hard to get donor cartilage tissue withoutcompromising external shape or function of elastic cartilage. We histologically analyzedthe xiphoid process and found that xiphoid process is comprised of hyaline cartilage atthe proximal part and elastic cartilage at the distal part. The elastic chondrocytes isolatedfrom distal part of xiphoid process (XCs) showed superior in vitro expansion and colonyforming efficiency. When XCs-based cell mass were subcutaneously transplanted tonude mice, the resultant tissues formed were characteristic of elastic cartilage based onthe presence of elastic fiber, large lacunae, and narrow pericellular matrix. These resultsindicate that the XCs can be used for elastic cartilage reconstruction. A grant supportfrom Korean Ministry of Health & Welfare (A040003).E-17-15Transcriptional regulation of osteoblast differentiation from adiposetissue derived mesenchymal stem cellMi-Kyung Choi, Sun-Ah Kang, Jae-Sang KimDivision of Life and Pharmaceutical Sciences and Center for Cell Signaling & Drug DiscoveryResearch, Ewha Womans University, Seoul 120-750, KoreaAs the stem cells derived from adipose tissues (ADSCs) are capable of differentiating intomultiple cellular lineages, they have drawn broad interest as the potential source forregenerative medicine. We searched for transcription factors whose gene expressionlevel changed significantly during osteoblast differentiation using microarray. We found 12genes whose expression increased by more than 5 fold and 5 genes that showed over 5fold decrease. As we were interested in identifying ‘stemness’transcription factors, wechose to focus on the latter group. For the functional analysis, we generated retrovirusesthat led to over-expression of each of the transcription factors. ADSCs were infected withthe retroviruses and were induced to differentiate into osteoblast for 14 days. After thisperiod, we measured the level of osteoblast differentiation by von kossa staining andalizarin red staining. Here, we show that ectopic expression of Sox11 blockeddifferentiation of mouse ADSCs to osteoblast. As Sox11 maintained stem cell propertiesof mADSCs under the differentiation condition. We are currently investigating the ‘knockdown’effectof Sox11 using virally mediated RNA interference to explore the possibilitythat Sox11 is the factor responsible for maintaining ‘stemness’of ADSCs.E-17-18Tbx2 and Tbx3 specify epidermis by the inhibition of FGF signaling inthe ventral ectodermGun-Sik Cho and Jin-Kwan HanDivision of Molecular and Life Sciences, Pohang University of Science and Technology, San 31,Hyoja-dong, Nam-gu, Pohang, Kyungbuk 790-784, KoreaDuring vertebrate early development, ectoderm becomes differentiated into epidermisand neural tissue. In neural default model, the activation of BMP signaling is essential forepidermis specification. However, the inhibition mechanism of neural fate by theactivation of BMP signaling has not identified well. We report here that the Xenopus T-box protein Tbx2 and Tbx3 are required at epidermis specification. They are induced byBMP signaling in the ventral ectoderm at gastrula stage. The ectopic expression of Tbx2and Tbx3 induces epidermis, and inhibits neural tissue and mesoderm formation. On thecontrary, neural tissue and mesoderm are dramatically expanded to the ventral ectodermregion by the depletion of Tbx2 and Tbx3. In addition, over-expression of Tbx2 and Tbx3inhibit FGF signaling. Thus, BMP signaling inhibits FGF signaling in the ventral ectodermby the induction of Tbx2 and Tbx3 for epidermis specification.232 Korean Society for Biochemistry and Molecular Biology