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Characterization of the Rho GTPase-Activating Protein RhoGAP68F
남민엽,이승복 한국뇌신경과학회 2011 Experimental Neurobiology Vol.20 No.1
Rho small GTPases control multiple aspects of neuronal morphogenesis by regulating the assembly and organization of the actin cytoskeleton. Although they are negatively regulated by GTPase activating proteins (GAPs), the roles of RhoGAPs in the nervous system have not been fully investigated. Here we describe a characterization of Drosophila RhoGAP68F that is mainly expressed in the embryonic central nervous system. RNA in situ hybridization analysis showed that expression of RhoGAP68F is highly restricted to the embryonic brain and ventral nerve cord. Database search revealed that RhoGAP68F contains an N-terminal Sec14 domain and a C-terminal RhoGAP domain. Rho-GTP pull-down assay demonstrated that the RhoGAP domain of RhoGAP68F inactivates RhoA but not Rac1 or Cdc42 in HEK293 cells. In addition, expression of RhoGAP68F in NIH3T3 cells suppressed LPA-induced stress fiber formation, which is mediated by RhoA. Finally, neuronal overexpression of RhoGAP68F causes synaptic overgrowth at the larval neuromuscular junction (NMJ). Taken together, these results suggest that RhoGAP68F may play a role in synaptic growth regulation by inactivating RhoA.
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완두 엽록체 Fructose-1,6-Bisphosphatase 유전자의 특성에 관한 연구
남민엽,한태룡 경희대학교 생명자원과학연구원 1997 遺傳工學論文集 Vol.9 No.-
A gene encoding chloroplast fructose-1,6-bisphosphatase (EC 3.1.3.11, FBPase) was isolated from a pea genomic library with a pea chloroplast FBPase cDNA clone (1.2 kb) as a probe. Three positive clones were screened and analyzed by phage Southern blot method. A positive phage clone (pFHNl) was digested with restriction enzymes and subcloned. Nucleotide sequence analysis of the gene indicated that the pea chloroplast FBPase gene contained three introns and four exons. The structure of pea chloroplast FBPase gene was similar with that of wheat chloroplast FBPase gene, although the pea chloroplast FBPase gene has relatively longer introns. Light responsive cis-acting elements (GATA motif, AT-rich sequence, GT-1 site) were found in 5' upstream sequences of the pea chloroplast FBPase gene.
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허근정,임수민,남민엽,김영은,오기욱,박환태,기창석,김승현,이승복 한국뇌신경과학회 2018 Experimental Neurobiology Vol.27 No.6
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease that is frequently linked to microtubule abnormalities and mitochondrial trafficking defects. Whole exome sequencing (WES) of patient-parent trios has proven to be an efficient strategy for identifying rare de novo genetic variants responsible for sporadic ALS (sALS). Using a trio-WES approach, we identified a de novo RAPGEF2 variant (c.4069G>A, p.E1357K) in a patient with early-onset sALS. To assess the pathogenic effects of this variant, we have used patient-derived skin fibroblasts and motor neuron-specific overexpression of the RAPGEF2-E1357K mutant protein in Drosophila. Patient fibroblasts display reduced microtubule stability and defective microtubule network morphology. The intracellular distribution, ultrastructure, and function of mitochondria are also impaired in patient cells. Overexpression of the RAPGEF2 mutant in Drosophila motor neurons reduces the stability of axonal microtubules and disrupts the distribution of mitochondria to distal axons and neuromuscular junction (NMJ) synapses. We also show that the recruitment of the pro-apoptotic protein BCL2- associated X (BAX) to mitochondria is significantly increased in patient fibroblasts compared with control cells. Finally, increasing microtubule stability through pharmacological inhibition of histone deacetylase 6 (HDAC6) rescues defects in the intracellular distribution of mitochondria and BAX. Overall, our data suggest that the RAPGEF2 variant identified in this study can drive ALSrelated pathogenic effects through microtubule dysregulation.
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The Phosphoinositide Phosphatase Sac1 Is Required for Midline Axon Guidance
이성수,김성대,남민엽,김의재,김태일,윤진호,이승복 한국분자세포생물학회 2011 Molecules and cells Vol.32 No.5
Sac1 phosphoinositide (PI) phosphatases are important regulators of PtdIns(4)P turnover at the ER, Golgi, and plasma membrane (PM) and are involved in diverse cellu-lar processes including cytoskeletal organization and vesicular trafficking. Here, we present evidence that Sac1 regulates axon guidance in the embryonic CNS of Droso-phila. Sac1 is expressed on three longitudinal axon tracts that are defined by the cell adhesion molecule Fasciclin II (Fas II). Mutations in the sac1 gene cause ectopic midline crossing of Fas II-positive axon tracts. This phenotype is rescued by neuronal expression of wild-type Sac1 but not by a catalytically-inactive mutant. Finally, sac1 displays dosage-sensitive genetic interactions with mutations in the genes that encode the midline repellent Slit and its axonal receptor Robo. Taken together, our results suggest that Sac1-mediated regulation of PIs is critical for Slit/ Robo-dependent axon repulsion at the CNS midline.
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Tbc1d15-17 Regulates Synaptic Development at the Drosophila Neuromuscular Junction
이민정,이승복,장수연,남민엽,윤진호 한국분자세포생물학회 2013 Molecules and cells Vol.36 No.2
Members of the Tre-2/Bub2/Cdc16 (TBC) family of pro-teins are believed to function as GTPase-activating pro-teins (GAPs) for Rab GTPases, which play pivotal roles in intracellular membrane trafficking. Although membrane trafficking is fundamental to neuronal morphogenesis and function, the roles of TBC-family Rab GAPs have been poorly characterized in the nervous system. In this paper, we provide genetic evidence that Tbc1d15-17, the Drosophila homolog of mammalian Rab7-GAP TBC1d15, is required for normal presynaptic growth and postsynaptic organization at the neuromuscular junction (NMJ). A loss-of-function mutation in tbc1d15-17 or its presynaptic knock- down leads to an increase in synaptic bouton number and NMJ length. tbc1d15-17 mutants are also defective in the distribution of the postsynaptic scaffold Discs-large (Dlg) and in the level of the postsynaptic glutamate subunit GluRIIA. These postsynaptic phenotypes are recapitulated by postsynaptic knockdown of Tbc1d15-17. We also show that presynaptic overexpression of a constitutively active Rab7 mutant in a wild-type background causes a synaptic overgrowth phenotype resembling that of tbc1d15-17 mutants, while a dominant-negative form of Rab7 has the opposite effect. Together, our findings establish a novel role for Tbc1d15-17 and its potential substrate Rab7 in regulating synaptic development.
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