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1.
The Dombrock blood group system (DO) is a common polymorphism in Caucasians, represented by two red cell antigen alleles. In a linkage study in our family material
of 832 families from the Copenhagen area, we found a strong indication of tight linkage with the two flanking DNA polymorphisms
D12S358 (z = 7.66; at θ
M = 0.001, θ
F = 0.031) and D12S364 (z = 8.53; at θ
M = 0.068, θ
F = 0.031). DO is assigned to the region 12p13.2– 12p12.1 by physically localised markers.
Received: 18 April 1996 / Revised: 4 July 1996 相似文献
2.
B. Cormand Magda Montfort Amparo Chabás Lluïsa Vilageliu D. Grinberg 《Human genetics》1997,100(1):75-79
Mutations in the glucocerebrosidase (GBA) and prosaposin (PSAP) genes are responsible for Gaucher disease, the most prevalent sphingolipidosis. Somatic cell hybrid analysis and in situ
hybridization experiments have localized the GBA gene to 1q21 and the PSAP gene to 10q21-q22. We performed pairwise and multi-point linkage analyses between the two genes and several highly polymorphic
markers from the Généthon human linkage map. Our results show that six markers cosegregate with the GBA gene (Zmax = 8.73 at θ = 0.00 for marker D1S2714) and define a 3.2-cM interval between D1S305 and D1S2624 as the most probable location
for the gene. Three of these markers (D1S2777, D1S303, and D1S2140), as well as the gene encoding pyruvate kinase (PKLR), are contained in a single YAC clone together with the GBA gene. A new polymorphism was identified within the PSAP gene (C16045T) and used for linkage studies. The multi-point analysis places the gene in a 9.8-cM interval between D10S1688
and D10S607. The fine localization of these genes provides a useful tool for cosegregation analysis, indirect molecular diagnosis,
and population genetic studies.
Received: 22 October 1996 / Accepted: 4 February 1997 相似文献
3.
Plasma methylumbelliferyl tetra-N-acetylchitotetraoside hydrolase or chitinase (CHIT) might play a role in degrading the
chitin wall of some microorganisms. In about 6% of Caucasian people the enzyme shows pseudodeficiency (defined as very low
activity without apparent symptoms). We have mapped this locus by linkage analysis to the marker D1S306 (z = 4.00 at θ
M = F = 0.0) on chromosome 1q between the flanking markers D1S191 and D1S245 in the area of 1q31–1qter.
Received: 13 December 1996 / Accepted: 8 July 1997 相似文献
4.
A. Toutain Nathalie Ronce Benoît Dessay Laura Robb Christine Francannet Martine Le Merrer Marie-Louise Briard Josseline Kaplan Claude Moraine 《Human genetics》1997,99(2):256-261
Nance-Horan syndrome (NHS) is an X-linked disease characterized by severe congenital cataract with microcornea, distinctive
dental findings, evocative facial features and mental impairment in some cases. Previous linkage studies have placed the NHS
gene in a large region from DXS143 (Xp22.31) to DXS451 (Xp22.13). To refine this localization further, we have performed linkage
analysis in four families. As the maximum expected Lod score is reached in each family for several markers in the Xp22.31–p22.13
region and linkage to the rest of the X chromosome can be excluded, our study shows that NHS is a genetically homogeneous
condition. An overall maximum two-point Lod score of 9.36 (θ = 0.00) is obtained with two closely linked markers taken together,
DXS207 and DXS1053 in Xp22.2. Recombinant haplotypes indicate that the NHS gene lies between DXS85 and DXS1226. Multipoint
analysis yields a maximum Lod score of 9.45 with the support interval spanning a 15-cM region that includes DXS16 and DXS1229/365.
The deletion map of the Xp22.3–Xp21.3 region suggests that the phenotypic variability of NHS is not related to gross rearrangement
of sequences of varying size but rather to allelic mutations in a single gene, presumably located proximal to DXS16 and distal
to DXS1226. Comparison with the map position of the mouse Xcat mutation supports the location of the NHS gene between the GRPR and PDHA1 genes in Xp22.2.
Received: 14 June 1996 / Revised: 10 October 1996 相似文献
5.
The locus (RP1) for one form of autosomal dominant retinitis pigmentosa (adRP) was mapped on chromosome 8q11-q22 between
D8S589 and D8S285, which are about 8 cM apart, by linkage analysis in an extended family ascertained in the USA. We have studied
a multigeneration Australian family with adRP and found close linkage without recombination between the disease locus and
D8S591, D8S566, and D8S166 (Zmax = 1.137– 4.650 at θ = 0.00), all mapped in the region known to harbor RP1. Assuming that the mutation of the same gene is
responsible for the disease in both families, the analysis of multiply informative meioses in the American and Australian
families places the adRP locus between D8S601 and D8S285, which reduces the critical region to about 4 cM, corresponding to
approximately 4 Mb, which is completely covered by a yeast artificial chromosome contig assembled recently.
Received: 23 April 1996 / Accepted: 3 July 1996 相似文献
6.
Illarioshkin S. N. Rakhmonov R. A. Ivanova-Smolenskaya I. A. Brice A. Markova E. D. Miklina N. I. Klyushnikov S. A. Limborska S. A. 《Russian Journal of Genetics》2002,38(12):1447-1451
Essential tremor (ET) is the most common extrapyramidal disorder of the central nervous system with autosomal dominant transmission in the majority of cases and age-dependent penetrance of the mutant gene. In a number of cases, it shares some phenotypic features with autosomal dominant idiopathic torsion dystonia (locusDYT1on chromosome 9q32–34) and is genetically heterogeneous: distinct variants of ET were mapped to chromosomes 3q13 (ETM1) and 2p22–25 (ETM2). We performed studies of candidate loci in a group of Slavonic (11 patients) and Tajik (19 patients) families with ET. Mutational analysis of the DYT1 gene in probands did not reveal the major deletion 946–948delGAG characteristic of idiopathic torsion dystonia, which allows one to genetically distinguish the studied hereditary forms of ET and torsion dystonia. Based on analysis of genetic linkage in informative Tajik pedigrees with ET, linkage to locus ETM1 on chromosome 3q13 was established in four families. Maximum pairwise Lod score was 2.46 at recombination fraction of = 0.00; maximum combined multipoint Lod score was 3.35 for marker D3S3515 and a common mutant haplotype for markers D3S3620, D3S3576, and D3S3720 allowed us to locate a mutant gene in a relatively narrow chromosome region spanning 2 cM. In one informative pedigree with ET, both candidate loci ETM1 and ETM2 were definitely excluded on the basis of negative Lod scores obtained by linkage estimations, which testifies to the existence of another distinct gene for autosomal dominant ET. 相似文献
7.
Suggestive evidence for linkage of schizophrenia to markers on chromosome 13 in Caucasian but not Oriental populations 总被引:5,自引:0,他引:5
M.-W. Lin P. Sham Hai-Gwo Hwu David Collier Robin Murray John F. Powell 《Human genetics》1997,99(3):417-420
Previously we reported suggestive evidence for linkage of schizophrenia to markers on chromosome 13q14.1–q32. We have now
studied an additional independent sample of 44 pedigrees consisting of 34 Taiwanese, 9 English and 1 Welsh family in an attempt
to replicate this finding. Narrow and broad models based on Research Diagnostic Criteria or the Diagnostic and Statistical
Manual of Mental Disorders, third edition, revised, were used to define the schizophrenia phenotype. Under a dominant genetic
model, two-point lod scores obtained for most of the markers were negative except that marker D13S122 gave a total lod score
of 1.06 (θ = 0.2, broad model). As combining pedigrees from different ethnic origins may be inappropriate, we combined this replication
sample and our original sample, and then divided the total sample into Caucasian (English and Welsh pedigrees) and Oriental
(Taiwanese and Japanese pedigrees) groups. The Caucasian pedigrees produced maximized admixture two-point lod scores (A-lod)
of 1.41 for the marker D13S119 (θ = 0.2, α = 1.0) and 1.54 for D13S128 (θ = 0, α = 0.3) with nearby markers also producing positive A-lod scores. When five-point model-free linkage analysis was applied
to the Caucasian sample, a maximum lod score of 2.58 was obtained around the markers D13S122 and D13S128, which are located
on chromosome 13q32. The linkage results for the Oriental group were less positive than the Caucasian group. Our results again
suggest that there is a potential susceptibility locus for schizophrenia on chromosome 13q14.1–q32, especially in the Caucasian
population.
Received: 13 September 1996 相似文献
8.
Connexin 50 mutation in a family with congenital "zonular nuclear" pulverulent cataract of Pakistani origin 总被引:16,自引:0,他引:16
Vanita Berry Donna Mackay Shagufta Khaliq Peter J. Francis Abdul Hameed Khalid Anwar S. Qasim Mehdi Richard J. Newbold Alex Ionides Alan Shiels Tony Moore Shomi S. Bhattacharya 《Human genetics》1999,105(1-2):168-170
Inherited cataract is a clinically and genetically heterogeneous disease that most often presents as a congenital autosomal
dominant trait. Here we report linkage of a three-generation family of Pakistani origin with autosomal dominant cataract "zonular
nuclear" pulverulent type (CZNP) on chromosome 1q21.1. Genome wide-linkage analysis excluded all the known cataract loci except
on chromosome 1q. Significantly positive 2-point lod score values (Z=3.01 at θ=0) were obtained for markers D1S305 and D1S2721, which are known to flank the gene for connexin 50 (Cx50) or gap
junction protein alpha-8 (Gja8). Previously a mutation in this gene has been reported in a British family with zonular pulverulent cataract (CZP).Here we
describe a second mutation (E48K) in connexin 50 that confirms the involvement of this gene in cataractogenesis.
Electronic Publication 相似文献
9.
Rinki Ratnapriya Joseph Vijai Jayaram S. Kadandale Rajesh S. Iyer Kurupath Radhakrishnan Anuranjan Anand 《Human genetics》2010,128(2):123-130
We performed a whole genome linkage analysis in a three-generation south Indian family with multiple members affected with
juvenile myoclonic epilepsy (JME). The maximum two-point LOD score obtained was 3.32 at recombination fraction (θ) = 0 for
D2S2248. The highest multipoint score of 3.59 was observed for the genomic interval between D2S2322 and D2S2228 at the chromosomal
region 2q33–q36. Proximal and distal boundaries of the critical genetic interval were defined by D2S116 and D2S2390, respectively.
A 24-Mb haplotype was found to co-segregate with JME in the family. While any potentially causative variant in the functional
candidate genes, SLC4A3, SLC23A3, SLC11A1 and KCNE4, was not detected, we propose to examine brain-expressed NRP2, MAP2, PAX3, GPR1, TNS1 and DNPEP, and other such positional candidate genes to identify the disease-causing gene for the disorder. 相似文献
10.
Linkage between atopy and the IgE high-affinity receptor gene at 11q13 in atopic dermatitis families 总被引:9,自引:0,他引:9
R. Fölster-Holst Hans W. Moises L. Yang Wolfgang Fritsch Jean Weissenbach Enno Christophers 《Human genetics》1998,102(2):236-239
Atopic dermatitis is a common skin disease frequently associated with allergic disorders such as allergic rhinitis and asthma.
Controversial linkage findings between atopy and markers at chromosome 11q13 led us to search chromosome 11 for genes conferring
susceptibility to atopic dermatitis and atopy. Twelve families were investigated using highly polymorphic markers and a powerful
model-free linkage test. Two markers gave evidence for linkage, D11S903 (P = 0.02) and FCER1B (P = 0.005). A two-point lod-score analysis between these two markers revealed significant evidence for linkage (z
max = 4.02 at (θ = 0.0). In regard to model-dependent lod-score analyses between atopic disorders and FCER1B, two-point analysis gave a lod
score of z = 0.78 whereas two-locus analysis using a recessive-dominant mode of inheritance displayed a significant lod score of z = 3.55. Only 2 of 12 families showed evidence for linkage using the latter oligogenic model. In conclusion, the results of
our study map the FCER1B gene in close proximity to D11S903, support the finding of Cookson et al. implicating the IgE high-affinity
receptor gene (FCER1B) at 11q13, and furthermore suggest an oligogenic mode of inheritance as well as heterogeneity in the
genetic susceptibility to atopy and atopic dermatitis.
Received: 6 November 1995 / Accepted: 1 October 1997 相似文献
11.
Diana Valverde Mònica Bayés Immaculada Martínez Daniel Grinberg Lluïsa Vilageliu Susana Balcells Roser Gonzàlez-Duarte Montserrat Baiget 《Human genetics》1994,94(2):193-194
Arrestin is a component of the light transduction cascade that takes place in the outer segment of retinal rods. In situ hybridization and linkage analysis have localized the arrestin gene to a region of 50 cM between CRYG and D2S23/D2S55 on chromosome 2q24–37. We have performed pairwise and multipoint linkage analysis between arrestin and four highly polymorphic markers from this region. The results indicate tight linkage between the gene and the microsatellite D2S172 (Z
max
= 9.25 at =0.038). This fine localization of the gene should provide a useful tool for cosegregation analyses involving the arrestin gene. 相似文献
12.
Rinki Ratnapriya Parthasarthy Satishchandra S. Dilip Girish Gadre Anuranjan Anand 《Human genetics》2009,126(5):677-683
Hot water epilepsy is a reflex or sensory epilepsy in which seizures are triggered by the stimulus of bathing in hot water.
Although there is evidence of a genetic basis to its etiology, no gene associated with this disorder has so far been found.
In order to identify the genetic locus involved in the pathophysiology of hot water epilepsy, we performed a genome-wide linkage
analysis in a four-generation family manifesting the disorder in an autosomal dominant manner. Significant linkage was detected
on chromosome 4q24-q28, with the highest two-point LOD score of 3.50 at recombination value (θ) of 0 for the marker D4S402. Centromere-proximal and centromere-distal boundaries of this locus were defined by the markers
D4S1572 and D4S2277, respectively. The critical genetic interval spans 22.5 cM and corresponds to about 24 megabases of DNA.
The genes NEUROG2, ANK2, UGT8 and CAMK2D, which are known to be expressed in human brain, are strong positional candidates and we propose to examine these and other
genes in the locus to identify the causative gene for this intriguing form of epilepsy. 相似文献
13.
Localisation of a gene for Papillon-Lefèvre syndrome to chromosome 11q14–q21 by homozygosity mapping
Martin Walter Laass Hans Christian Hennies Sabine Preis Howard P. Stevens Martin Jung Irene M. Leigh Thomas F. Wienker André Reis 《Human genetics》1997,101(3):376-382
Papillon-Lefèvre syndrome is an autosomal recessively inherited palmoplantar keratoderma of unknown aetiology associated
with severe periodontitis leading to premature loss of dentition. Three consanguineous families, two of Turkish and one of
German origin, and three multiplex families, one of Ethiopian and two of German origin, with 11 affected and 6 unaffected
siblings in all were studied. A targeted genome search was initially attempted to several candidate gene regions but failed
to demonstrate linkage. Therefore a genome-wide linkage scan using a combination of homozygosity mapping and traditional linkage
analysis was undertaken. Linkage was obtained with marker D11S937 with a maximum two-point lod score of Z
max = 6.1 at recombination fraction θ = 0.00 on chromosome 11q14–q21 near the metalloproteinase gene cluster. Multipoint likelihood calculations gave a maximum
lod score of 7.35 between D11S901 and D11S1358. A 9.2-cM region homozygous by descent in the affected members of the three
consanguineous families lies between markers D11S1989 and D11S4176 harbouring the as yet unknown Papillon-Lefèvre syndrome
gene. Haplotype analyses in all the families studied support this localisation. This study has identified a further locus
harbouring a gene for palmoplantar keratoderma and one possibly involved in periodontitis.
Received: 19 July 1997 / Accepted: 22 August 1997 相似文献
14.
Localized aggressive periodontitis (LAP; previously known as localized juvenile periodontitis) is one of the rapidly progressive periodontal diseases. Certain forms of familial LAP show a simple Mendelian pattern of transmission. However, no gene mutation has been identified to be responsible for the LAP phenotype. As an initial step to identify a gene mutation associated with LAP, we have performed genetic linkage analysis with four multigenerational families exhibiting the LAP phenotype. Affected individuals in the families were identified based on clinical and laboratory criteria in an attempt to define a homogeneous phenotype, since the clinical presentation of LAP may represent a manifestation of a heterogeneous group of diseases. The LAP phenotype is linked to a DNA marker, D1S492, with LOD score 3.48, =0.00. The haplotype analysis of the chromosome interval associated with D1S492 indicates that a LAP locus is located between D1S196 and D1S533 on chromosome 1, covering about 26 million DNA basepairs. We have also examined the DNA sequence of prostaglandin-endoperoxide synthase 2 (PTGS2 or cyclooxygenase 2, COX2) since prostaglandin 2 (PGE2), the product of COX2, is upregulated in LAP patients and COX2 is located between D1S196 and D1S533. No mutation in COX2 was identified in the patients. 相似文献
15.
Autosomal dominant retinitis pigmentosa: a new multi-allelic marker (D3S621) genetically linked to the disease locus (RP4) 总被引:2,自引:0,他引:2
Rajendra Kumar-Singh Daniel G. Bradley G. Jane Farrar Mark Lawler Siobhan A. Jordan Peter Humphries 《Human genetics》1991,86(5):502-504
Summary We report the characterization of a new eightallele microsatellite (D3S621) isolated from a human chromosome 3 library. Two-point and multi-locus genetic linkage analysis have shown D3S621 to co-segregate with the previously mapped RP4 (
m=0.12, Z
m=4.34) and with other genetic markers on the long arm of the chromosome, including D3S14 (R208) (
m=0.00, Z
m= 15.10), D3S47 (C17) (
m=0.11, Z
m=4.95), Rho (
m= 0.07, Z
m=1.37), D3S21 (L182) (
m=0.07, Z
m=2.40) and D3S19 (U1) (
m=0.13, Z
m=2.78). This highly informative marker, with a polymorphic information content of 0.78, should be of considerable value in the extension of linkage data for autosomal dominant retinitis pigmentosa with respect to locii on the long arm of chromosome 3. 相似文献
16.
Helge Klungland Luis Gomez-Raya Chris John Howard Robert Alan Collins Sissel Rogne Sigbjorn Lien 《Mammalian genome》1997,8(8):573-577
Polymorphic sites within the bovine FcγRI (FCGR1), FcγRII (FCGR2), and FcγRIII (FCGR3) genes were used for proximal mapping of these genes to bovine Chromosome (Chr) 3 (BTA3) with paternal half-sib families
from Norwegian Cattle. A fine-structure genetic map of the region was obtained by the analysis of 288 sperm cells from three
bulls that were heterozygous for the loci included in the study. No recombinants were observed between FCGR2 and FCGR3 (242 sperm cells). Considering FCGR2 and FCGR3 as a single locus, a three-point linkage analysis for [FCGR2/FCGR3], FCGR1, and INRA003 was carried out. The best-supported order of the loci was found to be INRA003–FCGR1–[FCGR2/FCGR3]. Map distances in a two-point linkage analysis were 10.3 cM between [FCGR2/FCGR3] and FCGR1, and 25.5 cM between FCGR1 and INRA003, respectively. This linkage mapping of the bovine FCGR gene family resembles the human situation where all FCGR genes are located at Chr 1 (HSA1), at position q21-q24. Moreover,
the results locate the evolutionary breakpoint between HSA1q and BTA3 within the human 1q24 region.
Received: 27 January 1997 / Accepted: 1 April 1997 相似文献
17.
B. Edman Ahlbom Muhammad Yaqoob Agne Larsson Adam Ilicki Göran Annerén C. Wadelius 《Human genetics》1997,99(2):186-190
Congenital hypothyroidism affects 1/3000– 4000 newborns. The causes of this group of disorders are still largely unknown.
Although most cases are sporadic, some families have several affected children and/or consanguineous parents, suggesting autosomal
recessive inheritance. Furthermore, there is a murine strain (hyt) with congenital hypothyroidism and autosomal recessive
inheritance, whose phenotype appears to be identical with the corresponding human disease. In the hyt mouse, the disease is
caused by a mutation in the thyroid-stimulating hormone receptor (TSHR) gene, making this gene a likely candidate also for
the human disease. The human TSHR gene was mapped on radiation hybrid panels and closely linked flanking markers D14S287 and
D14S616 were identified. On the Genebridge 4 panel, D14S287 was found to be located 8.5 cR (corresponding to 2.3 cM) proximal
to the TSHR gene, and D14S616 was found to be located 4.4 cR (1.2 cM) distal to the TSHR gene. These markers were analyzed
in 23 families, most of them with two or more children affected by congenital hypothyroidism and some with appreciable consanguinity
of the parents. Assuming homogeneity, the two-point lod score at θ = 0.1 was –4.8 for D14S287 and –5.8 for D14S616, and thus
linkage to the TSHR gene was excluded. Even when the data were analyzed with allowance for heterogeneity, there was no evidence
of linkage. Our conclusion is that if mutation of the TSHR gene causes familial congenital hypothyroidism in humans, it affects
only a small proportion of the cases.
Received: 8 July 1996 相似文献
18.
Sfar S Abid A Mahfoudh W Ouragini H Ouechtati F Abdelhak S Chouchane L 《Molecular biology reports》2009,36(4):661-667
Hereditary multiple exostoses (HME) is an autosomal dominant orthopaedic disorder most frequently caused by mutations in the
EXT1 gene. The aim of the present study is to determine the underlying molecular defect of HME in two multigenerational Tunisian
families with 21 affected members and to examine the degree of intrafamilial variability. Linkage analysis was performed using
three microsatellite markers encompassing the EXT1 locus and mutation screening was carried out by direct sequencing. In family 1, evidence for linkage to EXT1 was obtained on the basis of a maximum LOD score of 4.26 at θ = 0.00 with D8S1694 marker. Sequencing of the EXT1 revealed a heterozygous G > T transversion (c.1019G>T) in exon 2, leading to a missense mutation at the codon 340 (p.Arg340Leu).
In family 2 we identified a novel heterozygous 1 bp deletion in the exon 1 (c.529_531delA) leading to a premature codon stop
and truncated EXT1 protein expression (p.Lys177LysfsX15). This mutation was associated with the evidence of an intrafamilial
clinical variability and considered to be a novel disease-causing mutation in the EXT1 gene. These findings provide additional support for the involvement of EXT1 gene in the HME disease. 相似文献
19.
P. Krajči T. Gedde-Dahl Jr B. Høyheim S. Rogde B. Olaisen P. Brandtzaeg 《Human genetics》1992,90(3):215-219
The human transmembrane secretory component (SC or poly-Ig receptor, PIGR) is expressed basolaterally on glandular epithelial cells and is responsible for the external translocation of polymeric IgA and IgM. SC is hence a key molecule in antibody protection of mucosal surfaces. The human SC gene (locus PIGR) is located on chromosome 1 (1q31–q41). Here we present the first genetic linkage study of PIGR versus syntenic markers, including D1S58 and F13B, which have been previously regionalized to 1q31–q32 and 1q31–q32.1, respectively. We found that PIGR is closely linked to D1S58 (lods + 5.06 at
max = 0.06, without sex difference). PIGR versus F13B showed + 1.46 at
max = 0.25 for both sexes combined. A recombination of 0.06 between F13B and D1S58 (lods + 2.24) was in contrast to a previously published study giving
max = 0.22 (lods + 3.9), the combined lods being 5.6 at
max = 0.20. The progeny of a triply heterozygotic female indicated that PIGR is the flanking locus, therefore suggesting a cen-F13B-D1S58-PIGR-qter gene sequence on human chromosome 1. Only negative lod scores to RH, C8@, and PGM1 on 1p, and FY on proximal 1q, were found. Current combined Norwegian allele frequencies were estimated for PIGR to be A1 = 0.63, A2 = 0.37 (370 chromosomes), and for D1S58 to be A1 = 0.44, A2 = 0.56 (218 chromosomes). 相似文献
20.
Jens Michael Hertz Torben A. Kruse Anette Thomsen Edwin S. Spencer 《Human genetics》1991,88(2):157-161
Summary In order to localize the gene for the X-linked form of Alport syndrome (ATS) more precisely, we performed restriction fragment length polymorphism analysis with nine different X-chromosomal DNA markers in 107 members of twelve Danish families segregating for classic ATS or progressive hereditary nephritis without deafness. Two-point linkage analysis confirmed close linkage to the markers DXS17(S21) (Z
max = 4.44 at = 0.04), DXS94(pXG-12) (Z
max=8.07 at =0.04), and DXS101(cX52.5) (Z
max=6.04 at =0.00), and revealed close linkage to two other markers: DXS88(pG3-1) (Z
max =6.36 at =0.00) and DXS11(p22–33) (z
max=3.45 at =0.00). Multipoint linkage analysis has mapped the gene to the region between the markers DXS17 and DXS94, closely linked to DXS101. By taking into account the consensus map and results from other studies, the most probable order of the loci is: DXYS1(pDP34)-DXS3(p19-2)-DXS17-(ATS, DXS101)-DXS94-DXS11-DXS42(p43-15)-DXS51(52A). DXS88 was found to be located between DXS17 and DXS42, but the order in relation to the ATS locus and the other markers used in this study could not be determined. 相似文献