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Solh, the mouse homologue of the Drosophila melanogaster small optic lobes gene:: Organization, chromosomal mapping, and localization of gene product to the olfactory bulb

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GENOMICS 2000年第1期64卷 82-89页

作者： Kamei, M Webb, GC Heydon, K Hendry, IA Young, IG Campbell, HD Australian Natl Univ RSBS Ctr Mol Struct & Funct Canberra ACT 2601 Australia Australian Natl Univ Mol Genet & Evolut Grp Res Sch Biol Sci Canberra ACT 2601 Australia Australian Natl Univ Div Neurosci Canberra ACT 2601 Australia Australian Natl Univ John Curtin Sch Med Res Div Biochem & Mol Biol Canberra ACT 2601 Australia Univ Adelaide Queen Elizabeth Hosp Dept Obstet & Gynaecol Woodville SA 5011 Australia Univ Adelaide Queen Elizabeth Hosp Dept Anim Sci Woodville SA 5011 Australia

The Drosophila melanogaster small optic lobes gene (sol) is required for normal development of the neuropiles of the medulla and lobula complexes of the adult optic lobes, The predicted protein products of sol and its human homologue SOLH contain zinc-finger-like repeats, a calpain-like protease domain, and a C-terminal domain of unknown function, Long-distance PCR was used to amplify genomic DNA for Solh, the mouse homologue of sol, following the identification of mouse Solh expressed sequence tags. The nucleotide sequence of the Solh coding region (6.0 kb) was determined. The predicted Solh protein of 1095 amino acid residues shows 89% identity (93% similarity) to the human homologue. Solh was localized by in situ hybridization to band A3.3 on mouse Chromosome 17, in a region of maintained homology with human 16p13.3, Antipeptide antibodies were prepared and verified by demonstration of specific reactivity with recombinant human SOLH protein prepared by in vitro transcription/translation and expression in insect cells using the baculovirus system, The antibodies were used to show that the Solh protein localizes to the olfactory bulb in mouse and rat brain, suggesting that it could have an analogous role in development of sensory system neurons in Drosophila and in mammals. (C) 2000 Academic Press.

关键词：氨基酸序列碱基序列卡配因染色体图克隆分子 DNA 互补果蝇蛋白质类黑腹果蝇/遗传学表达的序列标记昆虫蛋白质类/遗传学小鼠近交BALBC 小鼠近交C57BL 分子序列数据神经组织蛋白质类/遗传学嗅球视叶非哺乳动物蛋白质类/遗传学序列同源性氨基酸中脑顶盖锌指动物人类小鼠

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(Over)correction of FMR1 deficiency with YAC transgenics: behavioral and physical features

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HUMAN MOLECULAR GENETICS 2000年第8期9卷 1145-1159页

作者： Peier, AM McIlwain, KL Kenneson, A Warren, ST Paylor, R Nelson, DL Baylor Coll Med Dept Mol & Human Genet Houston TX 77030 USA Emory Univ Sch Med Dept Chem Atlanta GA 30322 USA Emory Univ Sch Med Howard Hughes Med Inst Atlanta GA 30322 USA

Fragile X syndrome is a common cause of mental retardation involving loss of expression of the FMR1 gene. The role of FMR1 remains undetermined but the protein appears to be involved in RNA metabolism. Fmr1 knock-out mice exhibit a phenotype with some similarities to humans, such as macroorchidism and behavioral abnormalities. As a step toward understanding the function of FMR1 and the determination of the potential for therapeutic approaches to fragile X syndrome, yeast artificial chromosome (YAC) transgenic mice were generated in order to determine whether the Fmr1 knockout mouse phenotype could be rescued. Several transgenic lines were generated that carried the entire FMR1 locus with extensive amounts of flanking sequence. We observed that the YAC transgene supported production of the human protein (FMRP) which was present at levels 10 to 15 times that of endogenous protein and was expressed in a cell- and tissue-specific manner. Macroorchidism was absent in knockout mice carrying the YAC transgene indicating functional rescue by the human protein. Given the complex behavioral phenotype in fragile X patients and the mild phenotype previously reported for the Fmr1 knockout mouse, we performed a more thorough evaluation of the Fmr1 knockout phenotype using additional behavioral assays that had not previously been reported for this animal model. The mouse displayed reduced anxiety-related responses with increased exploratory behavior. FMR1 YAC transgenic mice overexpressing the human protein did produce opposing behavioral responses and additional abnormal behaviors were also observed. These findings have significant implications for gene therapy for fragile X syndrome since overexpression of the gene may harbor its own phenotype.

关键词：脑/代谢染色体人工酵母外显子脆性X智力低下蛋白质脆性X综合征/遗传学脆性X综合征/治疗基因疗法精神障碍/遗传学小鼠基因敲除小鼠转基因运动活动神经组织蛋白质类/缺乏神经组织蛋白质类/遗传学神经组织蛋白质类/生理学表型 RNA结合蛋白质类重组蛋白质类/生物合成睾丸/代谢动物人类男(雄)性小鼠

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Molecular and cellular genetics of fragile X syndrome

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AMERICAN JOURNAL OF MEDICAL GENETICS 1999年第1期88卷 11-24页

作者： Kaufmann, WE Reiss, AL Johns Hopkins Univ Sch Med Dept Pathol Baltimore MD 21205 USA Johns Hopkins Univ Sch Med Dept Neurol Baltimore MD 21205 USA Johns Hopkins Univ Sch Med Dept Pediat Baltimore MD 21205 USA Johns Hopkins Univ Sch Med Dept Psychiat Baltimore MD 21205 USA Stanford Univ Dept Psychiat Sch Med Div Child & Adolescent Psychiat & Child Dev Stanford CA 94305 USA Stanford Univ Dept Pediat Sch Med Div Child & Adolescent Psychiat & Child Dev Stanford CA 94305 USA

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G protein modulation of recombinant P/Q-type calcium channels by regulators of G protein signalling proteins

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JOURNAL OF PHYSIOLOGY-LONDON 2000年第1期528卷 65-77页

作者： Mark, MD Wittemann, S Herlitze, S Univ Tubingen Dept Physiol 2 D-72074 Tubingen Germany

1. Fast synaptic transmission is triggered by the activation of presynaptic Ca2+ channels which can be inhibited by G beta gamma subunits via G protein-coupled receptors (GPCR). Regulators of G protein signalling (RGS) proteins are GTPase-accelerating proteins (GAPs), which are responsible fur >100-fold increases in the GTPase activity of G proteins and might be involved in the regulation of presynaptic Ca2+ channels. In this study we investigated the effects of RGS2 on G protein modulation of recombinant P/Q-type channels expressed in a human embryonic kidney (HEK293) cell line using whole-cell recordings. 2. RGS2 markedly accelerates transmitter-mediated inhibition and recovery from inhibition of Ba2+ currents (I-Ba) through P/Q-type channels heterologously expressed with the muscarinic acetylcholine receptor M2 (mAChR M2). 3. Both RGS2 and RGS4 modulate the prepulse facilitation properties of P/Q-type Ca2+ channels. G protein reinhibition is accelerated, while release from inhibition is slowed. Those kinetics depend on the availability of G protein alpha and beta gamma subunits which is altered by RGS proteins. 4. RGS proteins unmask the Ca2+ channel beta subunit modulation of Ca2+ channel G protein inhibition. In the presence of RGS2, P/Q-type channels containing the beta (2a) and beta (3) subunit;reveal significantly altered kinetics of G protein modulation and increased facilitation compared to Ca2+ channels coexpressed with the beta (1b) or beta (4) subunit.

关键词：钡/药理学钙通道/遗传学钙通道/代谢钙通道 N型钙通道 P型/药物作用钙通道 P型/遗传学钙通道 P型/代谢钙通道 Q型/药物作用钙通道 Q型/遗传学钙通道 Q型/代谢细胞系 GTP结合蛋白质类/代谢 GTP结合蛋白质类/药理学鸟苷5'-O-(3-硫代三磷酸)/药理学离子通道闸门/药物作用肾/细胞学肾/代谢神经组织蛋白质类/遗传学神经组织蛋白质类/代谢膜片钳术磷蛋白类/生物合成蛋白质亚单位 RGS蛋白质类/代谢 RGS蛋白质类/药理学反应时间/药物作用受体毒蕈碱M2 受体毒蕈碱/代谢重组蛋白质类/药物作用重组蛋白质类/遗传学重组蛋白质类/代谢信号传导/药物作用人类

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Kinetics of synaptotagmin responses to Ca²⁺ and assembly with the core SNARE complex onto membranes

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NEURON 1999年第2期24卷 363-376页

作者： Davis, AF Bai, JH Fasshauer, D Wolowick, MJ Lewis, JL Chapman, ER Univ Wisconsin Sch Med Dept Physiol Madison WI 53706 USA Max Planck Inst Biophys Chem Dept Neurobiol D-37077 Gottingen Germany

The synaptic vesicle protein synaptotagmin I binds Ca2+ and is required for efficient neurotransmitter release. Here, we measure the response time of the C2 domains of synaptotagmin to determine whether synaptotagmin is fast enough to function as a Ca2+ sensor for rapid exocytosis. We report that synaptotagmin is "tuned" to sense Ca2+ concentrations that trigger neuronal exocytosis. The speed of response is unique to synaptotagmin I and readily satisfies the kinetic constraints of synaptic vesicle membrane fusion. We further demonstrate that Ca2+ triggers penetration of synaptotagmin into membranes and simultaneously drives assembly of synaptotagmin onto the base of the ternary SNARE (soluble N-ethylmaleimide-sensitive fusion protein [NSF] attachment receptor) complex, near the transmembrane anchor of syntaxin. These data support a molecular model in which synaptotagmin triggers exocytosis through its interactions with membranes and the SNARE complex.

关键词：钙/生理学钙结合蛋白质类动力学膜融合/生理学膜糖蛋白类/化学膜糖蛋白类/遗传学膜糖蛋白类/代谢膜蛋白质类/代谢膜/代谢神经组织蛋白质类/化学神经组织蛋白质类/遗传学神经组织蛋白质类/代谢重复序列核酸 SNARE蛋白质类序列同源性突触小泡/代谢突触结合蛋白质Ⅰ 突触结合蛋白质类膜泡运输蛋白质类动物大鼠

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Developmental profiles of growth-associated protein (Gap43), Ngfb, Bndf and Ntf4 mRNA levels in the rat forebrain after exposure to 60 Hz magnetic fields

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RADIATION RESEARCH 2000年第5期153卷 642-647页

作者： Harry, GJ Bartenbach, M Haines, W Bruccoleri, A NIEHS Neurotoxicol Grp Res Triangle Pk NC 27709 USA

Fischer 344 rats were exposed to 60 Hz magnetic fields (EMFs) during gestation and lactation. Rats received continuous exposure to 2-, 200- or 1000-mu T magnetic fields for 18.5 h per day, 7 days a week, or sham exposure (sham controls). During postnatal development, on postnatal days 1, 3, 6, 9, 15 and 20, forebrain tissue from male pups was examined for alterations in mRNA level for developmentally regulated central nervous system-specific proteins. Alterations in these factors during critical periods of development could result in alterations in the final neural network. Gap43 (growth-associated protein 43) mRNA was measured by Northern hybridization as a developmental indicator of axonal growth during the development of the neuron. Between postnatal days 1 and 9, detectable levels of Gap43 mRNA displayed a similar pattern across all sham control and exposure groups. In addition to Gap43, mRNA levels for the nervous system-specific growth factors ciliary neurotrophic factor (Cntf), brain-derived neurotrophic factor (Bdnf), beta nerve growth factor (Ngfb), neurotrophin-3 (Ntf3), and neurotrophin-4 (Ntf4) were examined by RNase protection assay. While there is public concern for developmental neurotoxicity associated with exposure to EMFs, these data, generated from animals exposed to 2-, 200 or 1000-mu T magnetic fields during both gestational and lactational periods of development, suggest that under these conditions no significant alterations in these critical factors for brain development occur. (C) 2000 by Radiation Research Society.

关键词：动物新生动物吮乳期脑源性神经营养因子/遗传学脑源性神经营养因子/代谢剂量效应关系辐射电磁场/副作用环境暴露/副作用 GAP-43蛋白/遗传学 GAP-43蛋白/代谢胶质细胞源性神经营养因子母亲暴露/副作用神经生长因子/遗传学神经生长因子/代谢神经生长因子类/遗传学神经生长因子类/代谢神经组织蛋白质类/遗传学神经组织蛋白质类/代谢神经营养因子3/遗传学神经营养因子3/代谢前脑/生长和发育前脑/代谢前脑/辐射效应 RNA 信使/分析大鼠近交F344 大鼠 Sprague-Dawley 核糖核酸酶类/代谢动物女(雌)性男(雄)性大鼠

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Developmental exposure to polychlorinated biphenyls exerts thyroid hormone-like effects on the expression of RC3/neurogranin and myelin basic protein messenger ribonucleic acids in the developing rat brain

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ENDOCRINOLOGY 2000年第1期141卷 181-189页

作者： Zoeller, RT Dowling, ALS Vas, AA Univ Massachusetts Dept Biol Morrill Sci Ctr Amherst MA 01003 USA

Polychlorinated biphenyls (PCBs) are a class of industrial compounds consisting of paired phenyl rings with various degrees of chlorination. They are now ubiquitous, persistent environmental contaminants that are routinely found in samples of human and animal tissues and are known to affect brain development. The effects of PCBs on brain development may be attributable, at least in part, to their ability to reduce circulating levels of thyroid hormone. However, the developmental effects of PCB exposure are not fully consistent with hypothyroidism. Because some individual PCB congeners interact strongly with various thyroid hormone binding proteins, several investigators have speculated that these congeners may be producing thyroid hormone-like effects on brain development. Therefore, we tested whether a mixture of PCBs, Aroclor 1254 (A1254), would pro-duce an antithyroid or thyromimetic effect on the expression of known thyroid hormone-responsive genes in the developing brain. Pregnant female rats were fed various doses of A1254 (0, 1, 4, and 8 mg/kg) from gestational day 6 to weaning on postnatal day (P) 21. Pups derived from these dams were sampled on P5, P15, and P30. Total T-4 was reduced by A1254 in a dose-dependent manner, but body weight of the pups or dams was not affected. The expression of RC3/Neurogranin and myelin basic protein was not affected by A1254 on P5 or P30. However, on P15, RC3/Neurogranin was elevated by A1254 in a dose-dependent manner, and myelin basic protein expression followed this general pattern. These data clearly demonstrate that the developmental effects of PCB exposure are not simply a function of PCB-induced hypothyroidism.

关键词：放射自显影术体重/药物作用脑/药物作用脑/胚胎学脑/生长和发育脑/代谢钙调蛋白结合蛋白质类/生物合成钙调蛋白结合蛋白质类/遗传学基因表达调控/药物作用原位杂交髓磷脂碱性蛋白质类/生物合成髓磷脂碱性蛋白质类/遗传学神经组织蛋白质类/生物合成神经组织蛋白质类/遗传学神经颗粒素多氯联苯化合物/毒性 RNA探针 RNA 信使/生物合成放射免疫测定大鼠 Sprague-Dawley 受体甲状腺激素/生物合成受体甲状腺激素/药物作用受体甲状腺激素/生理学信号传导/生理学甲状腺激素类/药理学动物女(雌)性妊娠大鼠

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Molecules of the brain

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HOSPITAL PRACTICE 2000年第2期35卷 41-+页

作者： Levey, AI Emory Univ Sch Med Atlanta GA 30322 USA

Progress against a range of brain disorders is being sustained by the use of genetic research techniques to identify specific molecules involved in brain disease, and by the realization that the identified molecules may disclose novel therapeutic targets. Both strategies are illustrated by recent insights and interventions in Alzheimer's disease and Parkinson's disease.

关键词：阿尔茨海默病/药物疗法阿尔茨海默病/遗传学阿尔茨海默病/代谢淀粉样β蛋白前体/遗传学脑化学/遗传学脑化学/生理学遗传学医学膜蛋白质类/遗传学分子生物学突变/遗传学神经组织蛋白质类/遗传学帕金森病/药物疗法帕金森病/遗传学帕金森病/代谢遗传药理学早老素1 受体胆碱能/药物作用受体胆碱能/遗传学受体多巴胺/药物作用受体多巴胺/遗传学受体谷氨酸/药物作用受体谷氨酸/遗传学突触核蛋白类人类

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p38 mitogen-activated protein kinase can be involved in transforming growth factor β superfamily signal transduction in Drosophila wing morphogenesis

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MOLECULAR AND CELLULAR BIOLOGY 1999年第3期19卷 2322-2329页

作者： Adachi-Yamada, T Nakamura, M Irie, K Tomoyasu, Y Sano, Y Mori, E Goto, S Ueno, N Nishida, Y Matsumoto, K Nagoya Univ Grad Sch Sci Div Biol Sci Dev Biol LabChikusa Ku Nagoya Aichi 4648602 Japan Japan Sci & Technol Corp CREST Chikusa Ku Nagoya Aichi 4648602 Japan Natl Inst Basic Biol Dept Dev Biol Div Morphogenesis Okazaki Aichi 4448585 Japan Natl Inst Genet Genet Strains Res Ctr Invertebrate Genet Lab Mishima Shizuoka 4118540 Japan

p38 mitogen-activated protein kinase (p38) has been extensively studied as a stress-responsive kinase, but its role in development remains unknown. The fruit fly, Drosophila melanogaster, has two p38 genes, D-p38a and D-p38b. To elucidate the developmental function of the Drosophila p38's, we used various genetic and pharmacological manipulations to interfere with their functions: expression of a dominant-negative form of D-p38b, expression of antisense D-p38b RNA, reduction of the D-p38 gene dosage, and treatment with the p38 inhibitor SB203580. Expression of a dominant-negative D-p38b in the wing imaginal disc caused a decapentaplegic (dpp)-like phenotype and enhanced the phenotype of a dpp mutant. Dpp is a secretory ligand belonging to the transforming growth factor beta superfamily which triggers various morphogenetic processes through interaction with the receptor Thick veins (Tkv). Inhibition of D-p38b function also caused the suppression of the wing phenotype induced by constitutively active Tkv (Tkv(CA)). Mosaic analysis revealed that D-p38b regulates the Tkv-dependent transcription of the optomotor-blind (omb) gene in non-Dpp-producing cells, indicating that the site of D-p38b action is downstream of Tkv. Furthermore, forced expression of Tkv(CA) induced an increase in the phosphorylated active form(s) of D-p38(s). These results demonstrate that p38, in addition to its role as a transducer of emergency stress signaling, may function to modulate Dpp signaling.

关键词：碱基序列钙-钙调素依赖性蛋白激酶类/遗传学钙-钙调素依赖性蛋白激酶类/代谢 DNA结合蛋白质类/遗传学果蝇蛋白质类黑腹果蝇/遗传学黑腹果蝇/生长和发育黑腹果蝇/代谢昆虫蛋白质类/遗传学昆虫蛋白质类/代谢小鼠转基因丝裂原激活蛋白激酶类分子序列数据形态发生神经组织蛋白质类/遗传学表型蛋白质丝氨酸苏氨酸激酶/遗传学蛋白质丝氨酸苏氨酸激酶/代谢受体细胞表面/遗传学受体细胞表面/代谢信号传导 T盒域蛋白质类转录遗传转化生长因子β/遗传学转化生长因子β/代谢 p38丝裂原活化蛋白激酶类动物小鼠

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Cooperative assembly of an hnRNP complex induced by a tissue-specific homolog of polypyrimidine tract binding protein

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MOLECULAR AND CELLULAR BIOLOGY 2000年第20期20卷 7463-7479页

作者： Markovtsov, V Nikolic, JM Goldman, JA Turck, CW Chou, MY Black, DL Univ Calif Los Angeles Dept Microbiol & Mol Genet Los Angeles CA 90095 USA Univ Calif Los Angeles Howard Hughes Med Inst Los Angeles CA 90095 USA Univ Calif San Francisco Dept Med Howard Hughes Med Inst San Francisco CA 94143 USA Univ Calif San Francisco Cardiovasc Res Inst San Francisco CA 94143 USA

Splicing of the c-src N1 exon in neuronal cells depends in part on an intronic cluster of RNA regulatory elements called the downstream control sequence (DCS). Using site-specific cross-linking, RNA gel shift, and DCS RNA affinity chromatography assays, we characterized the binding of several proteins to specific sites along the DCS RNA. Heterogeneous nuclear ribonucleoprotein (hnRNP) H, polypyrimidine tract binding protein (PTB), and KH-type splicing-regulatory protein (KSRP) each bind to distinct elements within this sequence. We also identified a new 60-kDa tissue-specific protein that binds to the CUCUCU splicing repressor element of the DCS RNA. This protein was purified, partially sequenced, and cloned. The new protein (neurally enriched homolog of PTB [nPTB]) is highly homologous to PTB. Unlike PTB, nPTB is enriched in the brain and in some neural cell lines. Although similar in sequence, nPTB and PTB show significant differences in their properties. nPTB binds more stably to the DCS RNA than PTB does but is a weaker repressor of splicing in vitro. nPTB also greatly enhances the binding of two other proteins, hnRNP H and KSRP, to the DCS RNA. These experiments identify specific cooperative interactions between the proteins that assemble onto an intricate splicing-regulatory sequence and show how this hnRNP assembly is altered in different cell types by incorporating different but highly related proteins.

关键词：氨基酸序列碱基序列细胞系色谱法亲和克隆分子核不均一核糖核蛋白F-H组核不均一核糖核蛋白类模型遗传学分子序列数据神经组织蛋白质类/化学神经组织蛋白质类/遗传学神经组织蛋白质类/分离和提纯神经组织蛋白质类/代谢核蛋白质类/化学核蛋白质类/遗传学核蛋白质类/分离和提纯核蛋白质类/代谢器官特异性种系发生多聚嘧啶区结合蛋白质蛋白质结合 RNA剪接/遗传学 RNA 核不均一/代谢 RNA 信使/遗传学 RNA 信使/代谢 RNA结合蛋白质类/化学 RNA结合蛋白质类/遗传学 RNA结合蛋白质类/分离和提纯 RNA结合蛋白质类/代谢调控序列核酸核糖核蛋白类/化学核糖核蛋白类/遗传学核糖核蛋白类/分离和提纯核糖核蛋白类/代谢序列同源性氨基酸反式激活因子类人类

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