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A polymorphism, R653Q, in the trifunctional enzyme methylenetetrahydrofolate dehydrogenase/methenyltetrahydrofolate cyclohydrolase/formyltetrahydrofolate synthetase is a maternal genetic risk factor for neural tube defects: Report of the birth defects research group

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AMERICAN JOURNAL OF HUMAN GENETICS 2002年第5期71卷 1207-1215页

作者： Brody, LC Conley, M Cox, C Kirke, PN McKeever, MP Mills, JL Molloy, AM O'Leary, VB Parle-McDermott, A Scott, JM Swanson, DA Univ Dublin Trinity Coll Dept Biochem Dublin 2 Ireland Univ Dublin Trinity Coll Dept Clin Med Dublin 2 Ireland Univ Dublin Trinity Coll Child Hlth Epidemiol Div Hlth Res Board Dublin 2 Ireland NICHHD Genome Technol Branch NHGRI NIH Bethesda MD 20892 USA NICHHD Div Epidemiol Stat & Prevent Res NIH Bethesda MD 20892 USA

Women who take folic acid periconceptionally reduce their risk of having a child with a neural tube defect (NTD) by >50%. A variant form of methylenetetrahydrofolate reductase (MTHFR) (677C-->T) is a known risk factor for NTDs, but the prevalence of the risk genotype explains only a small portion of the protective effect of folic acid. This has prompted the search for additional NTD-associated variants in folate-metabolism enzymes. We have analyzed five potential single-nucleotide polymorphisms (SNPs) in the cytoplasmic, nicotinamide adenine dinucleotide phosphate-dependent, trifunctional enzyme methylenetetrahydrofolate dehydrogenase/methenyltetrahydrofolate cyclohydrolase/formyltetrahydrofolate synthetase (MTHFD1) for an association with NTDs in the Irish population. One SNP, R653Q, in this gene appears to be associated with NTD risk. We observed an excess of the MTHFD1 "Q" allele in the mothers of children with NTD, compared with control individuals. This excess was driven by the overrepresentation of QQ homozygotes in the mothers of children with NTD compared with control individuals (odds ratio 1.52 [95% confidence interval 1.16-1.99], P=.003). We conclude that genetic variation in the MTHFD1 gene is associated with an increase in the genetically determined risk that a woman will bear a child with NTD and that the gene may be associated with decreased embryo survival.

关键词：氨基水解酶类/遗传学甲酸-四氢叶酸连接酶/遗传学爱尔兰甲烷四氢叶酸环水解酶亚甲基四氢叶酸脱氢酶(NADP)/遗传学分子序列数据神经管缺损/遗传学多态性单核苷酸危险因素人类

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Zic2 regulates the kinetics of neurulation

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PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 2000年第4期97卷 1618-1623页

作者： Nagai, T Aruga, J Minowa, O Sugimoto, T Ohno, Y Noda, T Mikoshiba, K RIKEN Brain Sci Inst Dev Neurobiol Lab Wako Saitama 3510198 Japan RIKEN Tsukuba Life Sci Ctr Mol Neurobiol Lab Tsukuba Ibaraki 3050074 Japan Japanese Fdn Canc Res Inst Canc Dept Cell Biol Toshima Ku Tokyo 1708455 Japan Univ Tsukuba Div Res Facilitat Tsukuba Ibaraki 3058577 Japan Univ Tokyo Inst Med Sci Dept Mol Neurobiol Minato Ku Tokyo 1088639 Japan

Mutation in human ZIC2, a zinc finger protein homologous to Drosophila odd-paired, causes holoprosencephaly (HPE), which is a common, severe malformation of the brain in humans. However, the pathogenesis is largely unknown. Here we show that reduced expression (knockdown) of mouse Zic2 causes neurulation delay, resulting in HPE and spina bifida. Differentiation of the most dorsal neural plate, which gives rise to both roof plate and neural crest cells, also was delayed as indicated by the expression lag of a roof plate marker, Wnt3a, In addition the development of neural crest derivatives such as dorsal root ganglion was impaired. These results suggest that the Zic2 expression level is crucial for the timing of neurulation, Because the Zic2 knockdown mouse is the first mutant with HPE and spina bifida to survive to the perinatal period, the mouse will promote analyses of not only the neurulation but also the pathogenesis of human HPE.

关键词：骨和骨组织/胚胎学骨和骨组织/病理学细胞分化中枢神经系统/胚胎学中枢神经系统/病理学疾病模型动物胚胎和胎儿发育基因表达调控发育期基因打靶前脑无裂畸形/胚胎学原位杂交原位缺口末端标记小鼠基因敲除突变神经管缺损/遗传学核蛋白质类蛋白质类/遗传学椎管闭合不全/胚胎学转录因子/遗传学转录因子/药理学 Wnt蛋白质类 Wnt3蛋白质 Wnt3A蛋白质锌指动物人类小鼠

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Investigation of folate pathway gene polymorphisms and the incidence of neural tube defects in a Texas Hispanic population

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MOLECULAR GENETICS AND METABOLISM 2000年第1期70卷 45-52页

作者： Barber, R Shalat, S Hendricks, K Joggerst, B Larsen, R Suarez, L Finnell, R Univ Nebraska Med Ctr Ctr Human Mol Genet Nebraska Med Ctr 985455 Omaha NE 68198 USA Texas A&M Univ Ctr Environm & Rural Hlth College Stn TX USA Rutgers State Univ UMDNJ Environm & Occupat Hlth Sci Inst Piscataway NJ USA Texas Dept Hlth Texas Neural Tube Defect Project Austin TX 78756 USA

Neural tube defects (NTDs) are multifactorial in their etiology, having both genetic and environmental factors contributing to their development. Recent evidence demonstrates that periconceptional supplementation of the maternal diet with a multivitamin containing folic acid significantly reduces the occurrence and recurrence risk for having a pregnancy complicated by NTDs. Unfortunately, the mechanism underlying the beneficial effects of folic acid remains unknown. NTD surveillance data from the Texas-Mexico border show that the high NTD rate (28/10,000 live births) noted during the 1990-1991 Cameron county NTD cluster was superimposed on a background Cameron county NTD rate (16/10,000 five births) which is considerably higher than that generally noted in the United States (8-10/10,000 live births). These data suggest that genetic factors as well as transient environmental factors may contribute to the etiology of the NTDs. Furthermore, clinical and experimental evidence imply that allelic forms of genes involved with folate metabolism and/or transport may explain some of the observed variation in the NTD rates found across different populations. Two folate pathway genes were selected for evaluation in this study. The loci investigated included two known alleles of the 5,10-methylenetetrahydrofolate reductase (MTHFR) gene, as well as the promoter region of the folate receptor-alpha (FR-alpha) gene. Odds ratios (ORs) for the C677T polymorphism in the MTHFR gene were 1.8 (CI 0.47-6.8) for heterozygosity and 1.8 (CI 0.35-9.4) for homozygosity for the mutant 677T allele, relative to wildtype homozygotes. The odds ratio for the heterozygosity for the A1298C polymorphism in the same gene was 1.1 (CI 0.09-14). No individuals homozygous for the 1298C allele were observed. The OR for heterozygosity of FR-cy gene polymorphisms detected at nucleotide 762 and at nucleotides 610/631 was 1.4 and 0.7, respectively. Neither of the FR-alpha polymorphisms was observed in the homozyg

关键词：载体蛋白质类/遗传学家庭卫生叶酸/代谢杂合子西班牙裔美国人/遗传学发病率亚甲基四氢叶酸还原酶(NADPH) 神经管缺损/流行病学神经管缺损/遗传学神经管缺损/代谢作用于CH-NH族供体的氧化还原酶类/遗传学点突变多态现象遗传妊娠并发症启动区(遗传学) 受体细胞表面得克萨斯/流行病学成年人儿童女(雌)性人类男(雄)性妊娠

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Ribonucleotide reductase subunit R1: A gene conferring sensitivity to valproic acid-induced neural tube defects in mice

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TERATOLOGY 2000年第4期61卷 305-313页

作者： Craig, JC Bennett, GD Miranda, RC Mackler, SA Finnell, RH Texas A&M Univ Dept Vet Anat & Publ Hlth College Stn TX 77843 USA Texas A&M Univ Ctr Environm & Rural Hlth College Stn TX 77843 USA Texas A&M Univ Dept Human Anat & Neurobiol College Stn TX 77843 USA Univ Penn Sch Med Dept Psychiat Philadelphia PA 19104 USA Univ Penn Sch Med Dept Med Philadelphia PA 19104 USA VAMC Med Res Serv Philadelphia PA 19104 USA

Pleural tube defects (NTDs), although prevalent and easily diagnosed, are etiologically heterogeneous, rendering mechanistic interpretation problematic. To date, there is evidence that mammalian neural tube closure (NTC) initiates and fuses intermittently at four discrete locations. Disruption of this process at any of these four sites may lead to a region-specific NTDs, possibly arising through closure site-specific genetic mechanisms. Although recent efforts have focused on elucidating the genetic components of NTDs, a void persists regarding gene identification in closure site-specific neural tissue. To this end, experiments were conducted to identify neural tube closure site-specific genes that might confer regional sensitivity to teratogen-induced NTDs. Using an inbred mouse strain (SWV/Fnn) with a high susceptibility to VPA-induced NTDs that specifically targets and disrupts NTC between the prosencephalon and mesencephalon region (future fore/midbrain;neural tube closure site II), we identified a VPA-sensitive closure site Ii-specific clone. Sequencing of this clone from an SWV neural tube cDNA library confirmed that it encodes the r1 subunit of the cell cycle enzyme ribonucleotide reductase (RNR). The abundance of rnr-r1 mRNA was significantly increased in response to VPA drug treatment. This upregulated expression was accompanied by a significant decrease in cellular proliferation in the closure site II neural tube region of the embryos, as determined by ELISA cellular proliferation assays performed on BrdU-pulsed neuroepithelial cells in vivo. We hypothesize that mr-r1 plays a critical role in the development of VPA-induced exencephaly. (C) 2000 Wiley-Liss, Inc.

关键词：抗惊厥药/毒性胚胎和胎儿发育基因表达调控发育期基因表达调控酶学基因文库疾病遗传易感性小鼠近交系神经管缺损/化学诱导神经管缺损/酶学神经管缺损/遗传学 RNA 信使/遗传学核苷酸还原酶类/遗传学致畸剂转录遗传丙戊酸/毒性动物女(雌)性小鼠妊娠

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Characterization and targeted disruption of murine Nup50, a p27^Kip1-interacting component of the nuclear pore complex

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MOLECULAR AND CELLULAR BIOLOGY 2000年第15期20卷 5631-5642页

作者： Smitherman, M Lee, K Swanger, J Kapur, R Clurman, BE Fred Hutchinson Canc Res Ctr Div Clin Res Seattle WA 98109 USA Fred Hutchinson Canc Res Ctr Human Biol Div Seattle WA 98109 USA Univ Washington Dept Med Seattle WA 98104 USA Univ Washington Dept Pathol Seattle WA 98104 USA Chonnam Natl Univ Hormone Res Ctr Kwangju 500757 South Korea

p27(Kip1) is a member of the Cip-Kip family of cyclin-dependent kinase (Cdk) inhibitors that binds to cyclin-Cdk complexes and inhibits their catalytic activity in response to antiproliferative stimuli. p27(Kip1) is regulated by several posttranscriptional mechanisms, including subcellular localization. We have identified a component of the nuclear pore complex (NPC), termed Nup50, through its two-hybrid interactions with p27(Kip1). Nup50 is a nucleoplasmically oriented component of the nuclear pore complex with a role in protein export (T. Guan, R. H. Kehlenbach, E. C. Schirmer, A. Kehlenbach, F. Fan, B. E. Clurman, N. Arnheim, and L. Gerace, Mol. Cell. Biol, 20:5619-5630, 2000). We found that murine Nup50 is a widely expressed nucleoporin and that Nup50 expression is highest in the developing neural tube and adult testes. We have also examined interactions between Nup50 and the NPC and found specific two-hybrid interactions between Nup50 and several well-defined components of the NPC, as well as coimmunoprecipitation of Nup50 with the nucleoporin Nup153 from transfected mammalian cells. In order to study Nup50 function in vivo, we cloned the mouse Nup50 genomic locus and created a targeted Nup50 deletion in the mouse germ line. Nup50 disruption resulted in a complex phenotype characterized by late embryonic lethality, neural tube defects, and intrauterine growth retardation. Although Nup50-null mouse embryo fibroblasts exhibited no defects in either cell cycle control or p27(Kip1) regulation, Nup50 deletion was associated with abnormalities in p27(Kip1) expression and cell proliferation in the developing neuroepithelium. We conclude that Nup50 is a nucleoporin with essential functions during mouse development.

关键词：氨基酸序列细胞周期蛋白质类细胞核/代谢细胞核/超微结构克隆分子周期素依赖激酶抑制剂p27 死胎/遗传学胎儿生长迟缓/遗传学成纤维细胞基因缺失基因表达调控发育期小鼠近交C57BL 小鼠突变型微管相关蛋白质类/代谢分子序列数据神经管缺损/遗传学核孔复合蛋白质类核蛋白质类/遗传学核蛋白质类/代谢孔蛋白质类/遗传学孔蛋白质类/代谢沉淀素试验肿瘤抑制蛋白质类动物小鼠

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The X-linked mouse mutation Bent tail is associated with a deletion of the Zic3 locus

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HUMAN MOLECULAR GENETICS 2000年第13期9卷 1937-1942页

作者： Carrel, T Purandare, SM Harrison, W Elder, F Fox, T Casey, B Herman, GE Baylor Coll Med Dept Pathol Houston TX 77030 USA Univ Texas Hlth Sci Ctr Dept Pathol Houston TX 77030 USA Ohio State Univ Childrens Res Inst Columbus OH 43221 USA Ohio State Univ Dept Pediat Columbus OH 43221 USA Ohio State Univ Dept Pathol Columbus OH 43221 USA

Bent tail (Bn) is a spontaneous, semi-dominant mutation on the mouse X chromosome that produces tail deformities and, rarely, open neural tube defects. Analysis of 292 normal male and affected male and female progeny from an intraspecific back-cross involving Bn supports a gene order of cen-DXMit89-18.5 +/- 2.3 cM-DXMit166-1.4 +/- 0.7 cM-Bn-1.0 +/- 0.6 cM-DXMit140-4.8 +/- 1.3 cM-DXBay6-tel. A high frequency of sex chromosomal non-disjunction, unrelated to the Bn mutation, was also identified in the background strain. Refined genetic and physical mapping of the Bn critical region demonstrate that the mutation is associated with a <170 kb submicroscopic deletion that includes the anonymous microsatellite marker DXMit208 as well as the entire Zic3 locus. Human mutations in ZIC3 are associated with left-right axis malformations (MIM 306955, 208530, 207100). Abnormalities of abdominal and thoracic situs were also detected in viable Bn males and females. The presence of anal and spinal abnormalities in some of the human patients and the deletion of Zic3 in Bn mice support a key role for this gene in neural tube development and closure.

关键词：印迹法 DNA 交叉遗传基因缺失同源盒结构域蛋白质类小鼠近交C3H 小鼠近交C57BL 分子序列数据神经管缺损/遗传学表型物理染色体图聚合酶链反应性染色体畸变尾/畸形转录因子/遗传学内脏/畸形 X染色体/遗传学动物女(雌)性人类男(雄)性小鼠

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Mouse models for neural tube closure defects

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HUMAN MOLECULAR GENETICS 2000年第6期9卷 993-1000页

作者： Juriloff, DM Harris, MJ Univ British Columbia Dept Med Genet Vancouver BC V6T 1Z3 Canada

Neural tube closure defects (NTDs), in particular anencephaly and spina bifida, are common human birth defects (1 in 1000), their genetics is complex and their risk is reduced by periconceptional maternal folio acid supplementation. There are >60 mouse mutants and strains with NTDs, many reported within the past 2 years. Not only are NTD mutations at loci widely heterogeneous in function, but also most of the mutants demonstrate variable low penetrance and some show complex inheritance patterns (e.g. SELH/Bc, Abl/Arg, Mena/ Profilin1). In most of these mouse models, the NTDs are exencephaly (equivalent to anencephaly) or spina bifida or both, reflecting failure of neural fold elevation in well defined, mechanistically distinct elevation zones. NTD risk is reduced in various models by different maternal nutrient supplements, including folic acid (Pax3,Cart1, Cd mutants), inositol (ct) and methionine (Axd). Lack of de novo methylation in embryos (Dnmt3b-null) leads to NTD risk, and we suggest a potential link between methylation and the observed female excess among cranial NTDs in several models. Some surprising NTD mutants (Gadd45a, Terc, Trp53) suggest that genes with a basic mitotic function also have a function specific to neural fold elevation. The genes mutated in several mouse NTD models involve actin regulation (Abl/Arg, Macs, Mena/Profilin1, Mlp, Shrm, Vcl), support the postulated key role of actin in neural fold elevation, and may be a good candidate pathway to search for human NTD genes.

关键词：肌动蛋白类/遗传学疾病模型动物叶酸/投药和剂量突变神经管缺损/遗传学神经管缺损/预防和控制性别因素动物女(雌)性人类男(雄)性小鼠

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Collagen XVIII, containing an endogenous inhibitor of angiogenesis and tumor growth, plays a critical role in the maintenance of retinal structure and in neural tube closure (Knobloch syndrome)

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HUMAN MOLECULAR GENETICS 2000年第13期9卷 2051-2058页

作者： Sertié, AL Sossi, V Camargo, AA Zatz, M Brahe, C Passos-Bueno, MR Univ Sao Paulo Dept Biol BR-05508900 Sao Paulo Brazil Catholic Univ Inst Med Genet Rome Italy Ludwig Inst Canc Res Sao Paulo Brazil

Knobloch syndrome (KS) is an autosomal recessive disorder defined by the occurrence of high myopia, vitreoretinal degeneration with retinal detachment, macular abnormalities and occipital encephalocele. The KS causative gene had been assigned to a 4.3 cM interval at 21q22.3 by linkage analysis of a large consanguineous Brazilian family. We reconstructed the haplotypes of this family with ten additional markers (five were novel) and narrowed the candidate interval to a region of <245 kb, which contains 24 expressed sequence tags, the KIAA0958 gene and the 5' end of the COL18A1 gene, We identified a homozygous mutation at the AG consensus acceptor splice site of COL18A1 intron 1 exclusively among the 12 KS patients, which was not found among 140 control chromosomes. This mutation predicts the creation of a stop codon in exon 4 and therefore the truncation of the alpha 1(XVIII) collagen short form, which was expressed in human adult retina. These findings provide evidence that KS is caused by mutations in COL18A1 which, therefore, has a major role in determining the retinal structure as well as in the closure of the neural tube. Therefore, we show for the first time that the absence of a collagen isoform impairs embryonic cell proliferation and/or migration as a primary or secondary effect.

关键词：畸形多发性/遗传学等位基因血管生成抑制剂/遗传学染色体人 21对胶原/遗传学胚胎哺乳动物/细胞学胚胎哺乳动物/代谢眼畸形/遗传学遗传标记单倍型内含子肿瘤/遗传学新生血管化病理性神经管缺损/遗传学器官特异性系谱物理染色体图多态现象单链构象 RNA剪接逆转录聚合酶链反应综合征成年人女(雌)性人类男(雄)性

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A genetic risk factor for mouse neural tube defects: defining the embryonic basis

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HUMAN MOLECULAR GENETICS 2000年第4期9卷 575-581页

作者： Fleming, A Copp, AJ UCL Inst Child Hlth Neural Dev Unit London WC1N 1EH England

Genetic polymorphisms are thought to play an important role in determining susceptibility to neural tube defects (NTDs), for example between different ethnic groups, but the embryonic manifestation of these polymorphic genetic influences is unclear, We have used a mouse model to test experimentally whether polymorphic variations in the pattern of cranial neural tube closure can influence susceptibility to NTDs, The site at which cranial neural tube closure begins (so-called closure 2) is polymorphic between inbred mice. Strains with a caudal location of closure 2 (e.g. DBA/2) are relatively resistant to NTDs, whereas strains with a rostrally positioned closure 2 (e.g, NZW) exhibit increased susceptibility to NTDs, We tested experimentally whether altering the position of closure 2 can affect susceptibility to cranial NTDs, by backcrossing the splotch (Sp(2H)) mutant gene onto the DBA/2 background, As a control, Sp(2H) was transferred onto the NZW background, which resembles splotch mice in its closure pattern. Approximately 80% of Sp(2H) homozygotes develop NTDs, both cranial (exencephaly) and spinal (spina bifida), After transfer to the DBA/2 background, the frequency of cranial NTDs was reduced significantly in Sp(2H) homozygotes, confirming a protective effect of caudal closure 2, In contrast, Sp(2H) homozygotes on the NZW background had a persistently high frequency of cranial NTDs, The frequency of spina bifida was not altered in either backcross, emphasizing the specificity of this genetic effect for cranial neurulation. These findings demonstrate that variation in the pattern of cranial neural tube closure is a genetically determined factor influencing susceptibility to cranial NTDs.

关键词：交叉遗传培养技术中脑/胚胎学小鼠近交C3H 小鼠近交CBA 小鼠近交DBA 小鼠近交NZB 神经管缺损/胚胎学神经管缺损/遗传学前脑/胚胎学危险因素颅骨/胚胎学脊柱/胚胎学动物女(雌)性男(雄)性小鼠

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A deletion encompassing Zic3 in Bent tail, a mouse model for X-linked neural tube defects

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HUMAN MOLECULAR GENETICS 2000年第11期9卷 1615-1622页

作者： Klootwijk, R Franke, B van der Zee, CEEM de Boer, RT Wilms, W Hol, FA Mariman, ECM Univ Nijmegen Med Ctr Dept Human Genet Nijmegen Netherlands Univ Nijmegen Med Ctr Dept Cell Biol Nijmegen Netherlands Univ Nijmegen Med Ctr Dept Anat Nijmegen Netherlands Cent Anim Lab NL-6500 HB Nijmegen Netherlands

Bent tail is a mouse model for human neural tube defects. Bent tail mice are characterized by a shortened, kinked tail, We have observed numerous aberrations in Bent tail embryos including exencephaly, rotation defects and occasionally omphalocele, orofacial schisis and situs abnormalities. Exencephaly was seen in >10% of all embryos and resulted from a closure defect of the hindbrain, Bent fail maps to the proximal part of the X chromosome. By haplotype analysis we have appointed the Bent tail locus to a 1.1 cM interval between markers DXMit159 and DXMit143, Subsequent analysis has revealed the presence of a deletion in all affected animals. The deletion is similar to 1 Mb in size and encompasses the gene for Zic3, a zinc finger transcription factor expressed in murine neuroectoderm and dorsal axial mesoderm during neurulation, Zic3 is a homolog of the Drosophila segmentation gene odd-paired. Although the Bent tail phenotype probably is the result of the deletion of several genes, combining data on Zic3 expression and function of Zic genes in the mouse shows that deletion of Zic3 alone is compatible with a major role of this gene in the congenital malformations of the Bent tail mouse. In man, mutations in ZIC3 are associated with situs abnormalities. These patients occasionally also show spina bifida, indicating that genetic variation in human ZIC3 may contribute to other congenital malformations, including neural tube defects.

关键词：染色体图 DNA/遗传学疾病模型动物胚胎哺乳动物/畸形胚胎哺乳动物/代谢基因缺失鸟嘌呤核苷酸交换因子类同源盒结构域蛋白质类/遗传学连锁(遗传学) 小鼠近交BALBC 小鼠近交C57BL 小鼠近交CBA 小鼠近交DBA 小鼠近交系神经管缺损/遗传学表型原癌基因蛋白质类/遗传学尾/畸形尾/胚胎学转录因子/遗传学 X染色体/遗传学动物女(雌)性人类男(雄)性小鼠

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