The Genom of Homo sapiens.pdf

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α-SYNUCLEIN EXPRESSION AND PD 411Table 3. Sequence of the Different Alleles at the NACP-Rep1Locus in HumanDifferent variantsAllele size TC TT TC TA CA–1 (76 bp) NA0 (78 bp) 10 1 10 8 1010 1 11 7 1010 1 9 9 101 (80 bp) 10 1 10 8 1110 1 11 7 1111 1 10 8 1011 1 11 7 1011 1 9 9 102 (82 bp) 10 1 10 8 1210 1 11 7 123 (84 bp) 10 1 10 8 13Indicated are only the sequences of the variant alleles thatwere found more than once to date, based on sequencing of independentcloned PCR products at the NACP-Rep1 region(Chiba-Falek and Nussbaum 2001; Chiba-Falek et al. 2003).(NA) Not available.Chiba-Falek et al. 2003). Extended sequence analysis indicatesthat sequence variation also occurs at positionsother than within the CA repeat itself and that alleles ofthe same size can differ in their sequence combination.The intra-size sequence difference is contributed mainlyby variation in the (TC) y (TA) z component of the repeat.Where the number y + z is constant (=18) for a given allele,the most frequent combination is y = 10 and z = 8,followed by 11 and 7, with the least common being 9 and9 (Table 3) (Chiba-Falek et al. 2003). It is interesting tonote that allele size 1, which is the most frequent sizeamong the Caucasian population (Farrer et al. 2001), hasthe largest number of intra-sequence variations. Some ofthe allele size 1 variants demonstrate an even higher degreeof variation with n = 11 in the first (TC) n repeat andw = 10 in the last (CA) w dinucleotide vs. n = 10 and w =11 (Table 3).SNPs AT THE α-SYNUCLEIN PROMOTERREGION FAIL TO BE ASSOCIATEDWITH SPORADIC PDThree SNPs in the promoter region of α-synucleinwere tested for association with sporadic PD (Farrer et al.2001; Holzmann et al. 2003). Farrer et al. (2001) foundno significant association of –116C>G and –770C>Awith sporadic PD (p = 0.317 and 0.763, respectively) inCaucasian residents of the US. Recently, the –116C>GSNP was studied again in the Caucasian German populationas well as the –668T>C polymorphism. In this report,alleles and genotype frequencies of both loci alsodid not reveal significant differences between the groupsof sporadic PD patients and controls (Holzmann et al.2003).ASSOCIATION STUDIES BETWEENNACP-Rep1 AND SPORADIC PDSeveral association studies have shown that certain allelesof the NACP-Rep1 locus may confer an increasedrisk of sporadic PD in Caucasian (Kruger et al. 1999; Tanet al. 2000; Farrer et al. 2001) and Asian (Mizuta et al.2002; Tan et al. 2003) populations, but other studiesfailed to replicate these findings (Parsian et al. 1998;Izumi et al. 2001; Khan et al. 2001; Tan et al. 2003). Unfortunately,inconsistencies in the designation and namingof the NACP-Rep1 alleles in the literature make an attemptat a meta-analysis a great challenge. Thus, wedecided to perform our analysis separately for Caucasianand Asian populations (Table 4). Because differences inallele sizes reported in the different studies made crossstudycomparisons of particular alleles difficult, we attemptedto assign a uniform designation of allele 0, 1, 2,and 3 within each study based on the frequency of the allelerelative to the frequency of the other alleles withinthat same study. Overall, the distribution of alleles 0, 1,and 2+3 was significantly different among Caucasianswith PD and controls (p = 0.002, χ 2 = 12.05, 2 df); becauseallele 3 is so rare, we combined 2 and 3 together forchi-square analysis. There was a significantly lower frequencyof allele size 0 in sporadic Caucasian PD patientsas compared to controls (p = 0.0007, χ 2 = 11.25, 1 df), resultingin a reduced relative risk for PD for allele 0 carriersof 0.89 (95% C.I. 0.81–0.95). There is also a higherfrequency of allele 1 (p = 0.02, χ 2 = 5.14, 1 df) comparedto the other alleles, although the relative risk was only1.08 (95% C.I. 1.01–1.16). These results suggest a negativeassociation of allele 0 and a positive association withallele 1 with PD in the studies from Caucasian populations.In the case of reports based on studies among populationsin Asia, once again, the distribution of alleles 0, 1and 2, and 3 was significantly different between PD andcontrols (p = 0.0158, χ 2 = 10.33, 3 df); however, the particularalleles and their effect on PD susceptibility are differentand appear to contradict the results from Caucasianpopulations. No significant reduced risk was seen for allele0 carriers versus noncarriers in Asian populations (p= 0.3, χ 2 = 1.02, 1 df), giving a relative risk of 1.044 (95%C.I. 0.96–1.14). There also appeared to be a reduced riskfor carriers of allele 1 versus other alleles (p = 0.0018, χ 2= 9.64, 1 df), resulting in a lower relative risk for PD forallele 1 carriers of 0.86 (95% C.I. 0.78–0.95). However,it should be noted that the allele frequencies of the four allelesamong the controls are vastly different between theCaucasian and Asian populations. Restricting our analysisto control populations only, the allele frequencies foralleles 0, 1, 2, and 3 among Caucasians were reportedly28%, 65%, 7%, and
412 CHIBA-FALEK AND NUSSBAUMTable 4. Association Studies of NACP-Rep1 with Sporadic PDStudy χ 2 Population Allele a –1 a 0 a 1 a 2 a 3 aFarrer et al. (2001) p = 0.005 Caucasian PD 1(0.2) 126(20.6) 430(70.3) 54(8.8) 1(0.2)(European) control 3(0.8) 110(29.1) 236(62.4) 28(7.4) 1(0.3)Kruger et al. (1999) p = 0.16 Caucasian PD 33(20.2) 113(69.1) 17(10.7) 0German control 44(22.8) 139(72.0) 10(5.2) 0Tan et al. (2000) p = 0.009 Caucasian PD 42(21) 140(70) 18(9) 0control 56(28) 139(69.5) 5(2.5) 0Parsian et al. (1998) p = 0.19 Caucasian PD 118(27.3) 275(63.7) 39(9) 0control 114(32.8) 203(58.3) 31(8.9) 0Khan et al. (2001) p = 0.64 UK PD 77(25.1) 212(69.4) 17(5.5) 0control 86(26.1) 216(65.5) 28(8.4) 0TOTAL p = 0.0007 Caucasian PD 396(23.1) 1170(68.3 145(8.5) 1control 410(28.3) 933(64.5) 102(7) 1Izumi et al. (2001) p = 0.14 Japanese PD 1(0.25) 163(40.75) 99(24.75) 132(33) 5(1.25)control 1(0.2) 195(39) 160(32) 136(27.2) 6(1.2)Mizuta et al. (2002) p = 0.017 Japanese PD 171(51.8) 84(25.5) 66(20) 6(1.8)control 126(40.6) 110(35.5) 65(21) 5(1.6)Tan et al. (2003) p = 0.20 Singaporean PD 148(36) 115(28) 140(34)control 169(41) 119(29) 115(28)TOTAL p = 0.0158 Asian PD 482(42.7) 298(26.4) 338(30) 11(0.9)control 490(40.6) 389(32.2) 316(26.2) 11(0.9)a Alleles as defined by size using Xia et al. (1996) original designation. The results are presented in each row as follows: numberof chromosomes (% of chromosomes).NACP-Rep1 AS A TRANSCRIPTIONALFUNCTIONAL ELEMENTTo determine whether the genetic association studiescorrelated with biological function, we examined the activityof the entire 10.7-kb upstream region of SNCA in aluciferase reporter assay in 293T and SH-SY5Y cells todetermine the role of the NACP-Rep1 repeat and its variousalleles on SNCA promoter function (Chiba-Falek andNussbaum 2001). Luciferase expression levels variedvery significantly among the different alleles over a 3-fold range in the human neuroblastoma SH-SY5Y cellsbut showed little or no significant variation in the 293Tcells (Fig. 1). In SH-SY5Y cells, the highest promoter activitywas seen with the construct containing the repeatwith 11 CA (allele size 1), leading to a 3-fold increase inthe expression relative to the allele carrying 10 CA (allelesize 0) (Fig. 1) (Chiba-Falek and Nussbaum 2001). Itshould be noted that allele 1 and allele 0, respectively,confer the most significant increased and decreased relativerisk for PD in Caucasian populations. The constructcontaining the largest repeat (13 CA- size 3) resulted in a2.5-fold increase in activity over that seen with the constructcontaining 10 CA (size 0) repeats. The promoteractivity was suppressed as the length of the repeat decreasedto 12 CA (size 2), resulting in only a 1.5-fold increasein activity as compared to the shortest repeat.Figure 1. The ratio of fold expression of luciferase activity derived by the full-length pASP constructs harboring different NACP-Rep1 alleles to pASP-10.7 in SH-SY5Ycells. The fold expression for each pASP was determined by dividing the average relative activityof each construct to that of the average obtained with the empty pGL 3-Basic. Then, the ratio in percentage of the fold expressionfor each of the pASP-1, 2, and 3 relative to pASP-10.7 was determined. The average of the ratios of four to five independentexperiments performed on separate days was calculated. The fold expression of pASP-10.7 is arbitrarily assigned 100%. The datarepresented here are the average ratios in percentage ± 1 S.E.M. for the pASP-1, 2, and 3 constructs relative to pASP-10.7. Student’st-test comparing the “fold expression” of each of the pASP-1, 2, and 3 constructs to pASP-10.7 revealed p = 5 x 10 –6 , 0.002, and 5x 10 –9 , respectively, in SH-SY5Y cells. (Adapted, with permission, from Chiba-Falek and Nussbaum 2001.)
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ForewordIn 2001, as we considered t
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The Finished Genome Sequence of Hom
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4 ROGERSFigure 2. Accumulation of h
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6 ROGERSFigure 4. Sequencing center
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8 ROGERSabcFigure 5. Ensembl view o
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10 ROGERS2000. Analysis of vertebra
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The Human Genome: Genes, Pseudogene
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VARIATION ON CHROMOSOME 7 15rived f
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VARIATION ON CHROMOSOME 7 17DNAs an
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VARIATION ON CHROMOSOME 7 19expecte
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VARIATION ON CHROMOSOME 7 21Drosoph
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Mutational Profiling in the Human G
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HUMAN MUTATIONAL PROFILING 25Anothe
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HUMAN MUTATIONAL PROFILING 27Figure
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HUMAN MUTATIONAL PROFILING 29Rieder
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32 SCHMUTZ ET AL.algorithm itself,
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34 SCHMUTZ ET AL.Figure 2. Genomic
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36 SCHMUTZ ET AL.compared. Some of
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Human Subtelomeric DNAH. RIETHMAN,
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HUMAN SUBTELOMERIC SEQUENCES 41The
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HUMAN SUBTELOMERIC SEQUENCES 43cate
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HUMAN SUBTELOMERIC SEQUENCES 45Figu
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HUMAN SUBTELOMERIC SEQUENCES 47pres
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50 COLLINSand expand the genomics r
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52 COLLINSFigure 2. A public-sector
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54 COLLINSdefine all the parts of t
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56 BENTLEYmon over many generations
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58 BENTLEYTable 1. Genetic Disease
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60 BENTLEY(Clark et al. 1998; Reich
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62 BENTLEYACKNOWLEDGMENTSThe author
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SNP Genotyping and Molecular Haplot
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GENETIC ANALYSIS OF DNA POOLS 67gen
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70 FAN ET AL.matrix is then mated t
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72 FAN ET AL.Figure 3. Views of gen
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74 FAN ET AL.including 32 duplicate
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76 FAN ET AL.Figure 7. Allele-speci
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78 FAN ET AL.microsphere-based assa
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80 BERTRANPETIT ET AL.function, may
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82 BERTRANPETIT ET AL.diversity in
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84 BERTRANPETIT ET AL.gree of block
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86 BERTRANPETIT ET AL.Figure 1. Dec
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88 BERTRANPETIT ET AL.1999. Populat
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90 WINDEMUTH ET AL.Expression data.
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92 WINDEMUTH ET AL.Table 1. A Summa
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94 WINDEMUTH ET AL.Table 2. Signifi
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96 WINDEMUTH ET AL.Table 3. Summary
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98 WINDEMUTH ET AL.Table 6. List of
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100 WINDEMUTH ET AL.Table 6. (Conti
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102 WINDEMUTH ET AL.Table 6. (Conti
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104 WINDEMUTH ET AL.much of a surpr
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106 WINDEMUTH ET AL.Given our resul
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Genetic Variation and the Control o
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GENETIC CONTROL OF TRANSCRIPTION 11
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GENETIC CONTROL OF TRANSCRIPTION 11
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Genome-wide Detection and Analysis
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RECENT SEGMENTAL DUPLICATIONS 117Fi
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RECENT SEGMENTAL DUPLICATIONS 119St
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RECENT SEGMENTAL DUPLICATIONS 121Co
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RECENT SEGMENTAL DUPLICATIONS 123Ho
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The Effects of Evolutionary Distanc
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EVOLUTIONARY DISTANCE AND GENE PRED
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EVOLUTIONARY DISTANCE AND GENE PRED
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Lineage-specific Expansion of KRAB
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EVOLUTION OF ZNF GENES 133Figure 2.
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EVOLUTION OF ZNF GENES 135Figure 4.
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EVOLUTION OF ZNF GENES 137get gene,
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EVOLUTION OF ZNF GENES 139Y., Goodw
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Sequence Organization and Functiona
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CENTROMERE ANNOTATION 143THE CENTRO
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CENTROMERE ANNOTATION 145Figure 4.
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CENTROMERE ANNOTATION 147CONCLUSION
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CENTROMERE ANNOTATION 149Schueler M
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152 PARKHILL AND THOMSONFigure 1. T
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154 PARKHILL AND THOMSONshow very h
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156 PARKHILL AND THOMSONGene Loss a
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158 PARKHILL AND THOMSONYersinia ad
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160 MCKAY ET AL.Choosing Candidate
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162 MCKAY ET AL.new comparative too
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164 MCKAY ET AL.rich. Based on a th
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166 MCKAY ET AL.Embryonic Muscle an
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168 MCKAY ET AL.native polyadenylat
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Building Comparative Maps Using 1.5
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HUMAN CHROMOSOME 1p IN THE DOG 1731
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HUMAN CHROMOSOME 1p IN THE DOG 175(
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HUMAN CHROMOSOME 1p IN THE DOG 177l
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180 GEORGES AND ANDERSSON5. There i
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182 GEORGES AND ANDERSSONplied to r
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184 GEORGES AND ANDERSSONbe common
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186 GEORGES AND ANDERSSONin humans
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Evolving Methods for the Assembly o
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ASSEMBLING LARGE GENOMES 191Figure
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ASSEMBLING LARGE GENOMES 193tant ad
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Mouse Genome Encyclopedia ProjectY.
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MOUSE GENOME ENCYCLOPEDIA PROJECT 1
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DNA Sequence Assembly and Multiple
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EULERIAN ASSEMBLY AND MULTIPLE ALIG
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Ensembl: A Genome InfrastructureE.
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ENSEMBL 215projects often submit th
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218 ZHANGthe majority of these are
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220 ZHANGFigure 2. Demonstration of
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222 ZHANG(G.X. Chen et al., in prep
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224 ZHANGWe are waiting for experim
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Ontologies for Biologists: A Commun
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ONTOLOGIES FOR BIOLOGISTS 229al. 20
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ONTOLOGIES FOR BIOLOGISTS 231TOPIC
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ONTOLOGIES FOR BIOLOGISTS 233a.b.Fi
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ONTOLOGIES FOR BIOLOGISTS 2352003.
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238 JOSHI-TOPE ET AL.Figure 1. The
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240 JOSHI-TOPE ET AL.state of knowl
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242 JOSHI-TOPE ET AL.and co-immunop
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The Share of Human Genomic DNA unde
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DNA UNDER SELECTION FROM HUMAN-MOUS
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Detecting Highly Conserved Regions
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DETECTING MULTISPECIES CONSERVED SE
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266 ROE ET AL.noncoding regions. On
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268 ROE ET AL.a48 hpf embryos in Mi
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270 ROE ET AL.aNovel gene KIAA0819[
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272 ROE ET AL.aMouseRatAP00354.2 Hu
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274 ROE ET AL.Tautz D. and Pfeifle
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276 JAILLON ET AL.Detection of Evol
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278 JAILLON ET AL.Table 1. Distribu
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280 JAILLON ET AL.Table 3. Distribu
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282 JAILLON ET AL.ecotig is a resul
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284 OVCHARENKO AND LOOTSdivergent r
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286 OVCHARENKO AND LOOTSmodulation
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288 OVCHARENKO AND LOOTSsequencing
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290 OVCHARENKO AND LOOTSments of cl
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Evolution of Eukaryotic Gene Repert
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EVOLUTION OF EUKARYOTIC GENES AND I
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304 PENNACCHIO, BAROUKH, AND RUBINA
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306 PENNACCHIO, BAROUKH, AND RUBINh
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308 PENNACCHIO, BAROUKH, AND RUBINA
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High-Throughput Mouse Knockouts Pro
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314 FRIDDLE ET AL.screen to lines o
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Identification of Novel Functional
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100 bp ladder68G1168G1168H1168H6100
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FUNCTIONAL ELEMENTS IN HUMAN DNA 32
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High-resolution Human Genome Scanni
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HUMAN GENOME SCANNING 325false-posi
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HUMAN GENOME SCANNING 327affecting
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HUMAN GENOME SCANNING 329methods fo
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332 MALEK ET AL.Figure 1. The bacte
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334 MALEK ET AL.J., Vincent S., and
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336 HARDISON ET AL.reflect blocks o
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338 HARDISON ET AL.plain the region
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340 HARDISON ET AL.CALIBRATION OF T
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342 HARDISON ET AL.PositionRP2.3noE
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344 HARDISON ET AL.cific chromosoma
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346 WESTON ET AL.these differences
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348 WESTON ET AL.els controlled by
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350 WESTON ET AL.ures prominently i
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352 WESTON ET AL.nal and Bop, which
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354 WESTON ET AL.ablp 1466 bopbcrtB
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356 WESTON ET AL.like fold (Fig. 6)
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Implications of Genomics for Public
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Page 378: PTC TASTE GENETICS 371the emergence
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Page 390 and 391: Genetics of Schizophrenia and Bipol
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Page 402 and 403: The Genetics of Common Diseases: 10
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Page 416 and 417: Regulation of α-Synuclein Expressi
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Page 422: α-SYNUCLEIN EXPRESSION AND PD 415g
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Novel Transcriptional Units and Unc
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TRANSCRIPTIONAL UNITS AND GENE PAIR
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mtDNA Variation, Climatic Adaptatio
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mtDNA VARIATION 473Figure 3. Region
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ANALYSIS OF ADAPTIVE SELECTION FORR
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mtDNA VARIATION 477Figure 8. Temper
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Positive Selection in the Human Gen
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HUMAN-SPECIFIC EVOLUTIONARY CHANGES
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488 UNDERHILLorigin episodes, each
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490 UNDERHILLhaplogroups C through
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492 UNDERHILLO (Fig. 2e) that share
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The New Quantitative BiologyM.V. OL
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NEW QUANTITATIVE BIOLOGY 497alone.
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NEW QUANTITATIVE BIOLOGY 499There w
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NEW QUANTITATIVE BIOLOGY 501ceded,
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