共查询到20条相似文献,搜索用时 15 毫秒
1.
Niels Wedemeyer Andreas Lengeling Melanie Ronsiek Dirk Korthaus Kristin Baer Martina Wuttke Harald Jockusch 《Genomics》1996,32(3):447
Despite rapid progress in the physical characterization of murine and human genomes, little molecular information is available on certain regions, e.g., proximal mouse chromosome 11 (Chr 11) and human chromosome 2p (Chr 2p). We have localized thewobblerspinal atrophy genewrto proximal mouse Chr 11, tightly linked toRab1,a gene coding for a small GTP-binding protein, andGlns-ps1,an intronless pseudogene of the glutamine synthetase gene. We have now used these markers to construct a 1.3-Mb yeast artificial chromosome (YAC) contig of theRab1region on mouse Chr 11. Four YAC clones isolated from two independent YAC libraries were characterized by rare-cutting analysis, fluorescencein situhybridization (FISH), and sequence-tagged site (STS) isolation and mapping.Rab1andGlns-ps1were found to be only 200 kb apart. A potential CpG island near a methylatedNarI site and a trapped exon,ETG1.1,were found between these loci, and a new STS,AHY1.1,was found over 250 kb fromRab1.Two overlapping YACs were identified that contained a 150-kb region of human Chr 2p, comprising theRAB1locus,AHY1.1,and the human homologue ofETG1.1,indicating a high degree of conservation of this region in the two species. We mappedAHY1.1and thus humanRAB1on Chr 2p13.4–p14 using somatic cell hybrids and a radiation hybrid panel, thus extending a known region of conserved synteny between mouse Chr 11 and human Chr 2p. Recently, the geneLMGMD2Bfor a human recessive neuromuscular disease, limb girdle muscular dystrophy type 2B, has been mapped to 2p13–p16. The conservation between the mouseRab1and humanRAB1regions will be helpful in identifying candidate genes for thewobblerspinal muscular atrophy and in clarifying a possible relationship betweenwrandLMGMD2B. 相似文献
2.
Although the phenomenon of innate resistance to flaviviruses in mice was recognized many years ago, it was only recently that the genetic locus (Flv) controlling this resistance was mapped to mouse Chromosome (Chr) 5. Here we report the fine mapping of the Flv locus, using 12 microsatellite markers which have recently been developed for mouse Chr 5. The new markers were genotyped in 325 backcross mice of both (C3H/HeJxC3H/ RV)F1xC3H/HeJ and (BALB/cxC3H/RV)F1xBALB/c backgrounds, relative to Flv. The composite genetic map that has been constructed identifies three novel microsatellite loci, D5Mit68, D5Mit159, and D5Mit242, tightly linked to the Flv locus. One of those loci, D5Mit159, showed no recombinations with Flv in any of the backcross mice analyzed, indicating tight linkage (<0.3 cM). The other two, D5Mit68 and D5Mit242, exhibited two and one recombinations with Flv (0.6 and 0.3 cM) respectively, defining the proximal and distal boundaries of a 0.9-cM segment around this locus. The proximal flanking marker, D5Mit68, maps to a segment on mouse Chr 5 homologous to human Chr 4. This, together with the previous data produced by our group, locates Flv to a region on mouse Chr 5 carrying segments that are conserved on either human Chr 4, 12, or 7, but present knowledge does not allow precise identification of the syntenic element. 相似文献
3.
K. A. Mills K. D. Mathews T. Scherpbier-Heddema R. L. Schelper R. Schmalzel H. L. Bailey J. H. Nadeau K. H. Buetow J. C. Murray 《Mammalian genome》1995,6(4):278-280
Myodystrophy (myd), an autosomal recessive mutation of the mouse characterized by progressive weakness and dystrophic muscle histology, maps to the central portion of Chromosome (Chr) 8 (Lane et al. J. Hered 67, 135, 1976). This portion of Chr 8 contains the genes for a mitochondrial uncoupling protein (Ucp) and kallikrein (Kal3), which map to distal 4q in the human, providing evidence for a segment of homology. Characteristics of the myd phenotype coupled with this homology suggest that myd may be a mouse homolog of facioscapulohumeral muscular dystrophy (FSHD), which maps to human 4q35. We have confirmed and expanded the region of mouse 8-human 4 homology by generating a map of Chr 8 in an interspecific backcross of C57BL/6J and a partially inbred strain derived from M. spretus. The map is comprised of the genes for Ucp, coagulation factor XI (Cf11), and chloride channel 5 (Clc5), all of which have homologs on distal human 4q, 15 microsatellite loci, and the membrane cofactor protein pseudogene (Mcp-ps). To place myd in the genetic map, 75 affected progeny from an intersubspecific backcross of animals heterozygous for myd with Mus musculus castaneus were genotyped with Chr 8 microsatellite loci. The mutation maps between D8Mit30 and D8Mit75, an interval that is flanked by genes with human homologs at distal 4q. These results are consistent with the possibility that myd is the mouse homolog of FSHD. 相似文献
4.
Maree L. Overall Nigel J. Parker Deborah L. Scarcella Peter J. Smith Marie Dziadek 《Mammalian genome》1998,9(8):657-659
STIM1 (GOK) maps to a region of human Chromosome (Chr) 11p15.5 that is implicated in several embryonal tumors, and some evidence
indicates that STIM1 may have a growth suppressor role in rhabdomyosarcoma. In this study we have mapped the murine homolog,
Stim1, to the same position as Hbb on distal mouse Chr 7. This region is separated by 20 cM from the region of distal Chr 7 that contains Igf2, H19, and other imprinted genes. Using strain-specific polymorphisms, we have shown that Stim1 is expressed from both parental alleles in fetal and neonatal mouse tissues. Similar analyses of human Wilms' tumor and normal
kidney tissues demonstrated biallelic expression of STIM1 in the majority of samples. These data demonstrate that Stim1 expression is not regulated by genomic imprinting in either mouse or human tissues. Thus, if STIM1 is a tumor suppressor
at 11p15.5, loss of expression is not due to imprinting effects.
Received: 23 January 1998 / Accepted: 10 April 1998 相似文献
5.
N. Janicic E. Soliman Z. Pausova M. F. Seldin M. Rivière J. Szpirer C. Szpirer G. N. Hendy 《Mammalian genome》1995,6(11):798-801
The calcium-sensing receptor (CASR), a member of the G-protein coupled receptor family, is expressed in both parathyroid and kidney, and aids these organs in sensing extracellular calcium levels. Inactivating mutations in the CASR gene have been described in familial hypocalciuric hypercalcemia (FHH) and neonatal severe hyperparathyroidism (NSHPT). Activating mutations in the CASR gene have been described in autosomal dominant hypoparathyroidism and familial hypocalcemia. The human CASR gene was mapped to Chromosome (Chr) 3q13.3-21 by fluorescence in situ hybridization (FISH). By somatic cell hybrid analysis, the gene was localized to human Chr 3 (hybridization to other chromosomes was not observed) and rat Chr 11. By interspecific backcross analysis, the Casr gene segregated with D16Mit4 on mouse Chr 16. These findings extend our knowledge of the synteny conservation of human Chr 3, rat Chr 11, and mouse Chr 16. 相似文献
6.
Sonja Fuchs Karin Resch Cora Thiel Michael Ulbrich Matthias Platzer Harald Jockusch Thomas Schmitt-John 《BMC genetics》2002,3(1):40
Background
To support the positional cloning of the mouse mutation wobbler (wr ) the corresponding regions on human Chr2p13-14 and mouse Chr11 were analyzed in detail and compared with respect to gene content, order, and orientation. 相似文献7.
Guylaine Bouchard Heather M. Nelson Frank Lammert Lucy B. Rowe Martin C. Carey Beverly Paigen 《Mammalian genome》1999,10(11):1070-1074
The Lith1 region on Chromosome (Chr) 2 contains a gene that markedly affects the prevalence of cholesterol gallstones in inbred mice.
We report the high-resolution genetic and radiation hybrid maps of the chromosomal region surrounding Lith1, using three resources: a DNA panel from 188 progeny from two reciprocal backcrosses between C57BL/6 and Mus spretus inbred strains; 423 progeny of an N4 generation from backcrossing the susceptible C57L/J alleles at Lith1 into the resistant AKR/J strain; and the newly developed hamster–mouse T31 radiation hybrid panel. We mapped 17 microsatellite
markers in the D2Mit182 to D2Mit14 region and two candidate genes for Lith1, the canalicular bile salt export pump (Bsep) also known as sister of P-glycoprotein (Spgp) and the low-density-lipoprotein-receptor-related gene megalin (Gp330). Both genetic maps were in agreement and ordered the microsatellite markers into a 10.4 ± 1.5 cM region. The high-resolution
physical map revealed ordering of microsatellite markers and relative distances between markers in almost complete agreement
with the genetic maps. Mapping of Bsep revealed its location on Chr 2, homologous to the human chromosomal position (Nature Genet 20, 233–238, 1998). The radiation
hybrid results also provided the highest resolution of the area containing the two candidate genes, which both mapped in the
Lith1 region with close linkage, being separated by a distance of only 15 cR3000. The total radiation hybrid map length of the region between D2Mit182 and D2Mit14 was 326 cR3000, suggesting that 31 cR3000 is equivalent to 1 cM in this region of Chr 2.
Received: 29 April 1999 / Accepted: 21 July 1999 相似文献
8.
P. A. Baldacci M. Cohen-Tannoudji C. Kress S. Pournin C. Babinet 《Mammalian genome》1996,7(2):114-116
The locus Om (ovum mutant) identified in the mouse strain DDK affects the viability of (DDK |m~ non-DDK)F1 preimplantation embryos. We previously located this locus on Chromosome (Chr) 11 close to Scya2 (Baldacci et al. Mamm. Genome 2, 100–105, 1992). Here we report a high-resolution map of the region around Om based on a large number of backcross individuals. The same region has been analyzed on the EUCIB backcross, and the two maps
have been compared. The results define the proximal and distal boundaries for the Om mutation as Scya2 and D11Mit36 respectively. The distance between these two markers is about 2 cM. These data should facilitate the positional cloning and
molecular characterization of Om.
Received: 10 July 1995 / Accepted: 11 September 1995 相似文献
9.
James Lund Bruce Roe Feng Chen Marcia Budarf Naomi Galili Roy Riblet Robert D. Miller Beverly S. Emanuel Roger H. Reeves 《Mammalian genome》1999,10(5):438-443
Proximal mouse Chromosome (Chr) 16 shows conserved synteny with human Chrs 16, 8, 22, and 3. The mouse Chr 16/human Chr 22
conserved synteny region includes the DiGeorge/Velocardiofacial syndrome region of human Chr 22q11.2. A physical map of the
entire mouse Chr 16/human Chr 22 region of conserved synteny has been constructed to provide a substrate for gene discovery,
genomic sequencing, and animal model development. A YAC contig was constructed that extends ca. 5.4 Mb from a region of conserved
synteny with human Chr 8 at Prkdc through the region conserved with human Chr 3 at DVL3. Sixty-one markers including 37 genes are mapped with average marker
spacing of 90 kb. Physical distance was determined across the 2.6-Mb region from D16Mit74 to Hira with YAC fragmentation. The central region from D16Jhu28 to Igl-C1 was converted into BAC and PAC clones, further refining the physical map and providing sequence-ready template. The gene
content and borders of three blocks of conserved linkage between human Chr 22q11.2 mouse Chr 16 are refined.
Received: 4 November 1998 / Accepted: 21 December 1998 相似文献
10.
Helona Havelková Marcela Kosařová Magdalena Krulová Peter Demant Marie Lipoldová 《Mammalian genome》1999,10(7):670-674
Lymphocytes of mouse strains BALB/cHeA (BALB/c) and STS/A (STS) differ in their response to CD3 antibody (anti-CD3). We analyzed
the genetic basis of this strain difference, using the Recombinant Congenic Strains (RCS) of the BALB/c-c-STS/Dem (CcS/Dem)
series. Each of the 20 CcS/Dem strains carries a different, random combination of 12.5% genes from the nonresponding strain
STS and 87.5% genes of the intermediate responder strain BALB/c. Differences in the magnitude of anti-CD3-induced response
among CcS/Dem strains indicated that in addition to Fcγ receptor 2 (Fcgr2) other genes are involved in the control of this response as well, and we have already mapped loci Tria1 (T cell receptor-induced activation 1), Tria2, and Tria3. In order to map additional Tria genes, we tested F2 hybrids between the high responder RC strain CcS-9 and the low responder strain CcS-11. Proliferation in complete RPMI medium
without anti-CD3 is controlled by locus Sprol1 (spontaneous proliferation 1) linked to the marker D4Mit23 on Chr 4. At concentration 0.375 μg/ml anti-CD3 mAb, the response was controlled by a locus Tria4, which maps to the marker D7Mit32 on Chr 7. The response to the higher concentration of mAb, 3 μg/ml, was controlled by Tria5, which mapped to the marker D9Mit15 on Chr 9. Anti-CD3 is being used for modulation of lymphocyte functions in transplantation reactions and in cancer treatment.
Study of mechanisms of action of different Tria loci could lead to better understanding of genetic regulation of these reactions.
Received: 28 October 1998 / Accepted: 17 March 1999 相似文献
11.
A novel mouse gene, provisionally named Lx1, has been cloned and sequenced. Lx1 most likely represents the mouse homolog of the rat gene OCT1, which encodes a polyspecific transmembrane transporter that is possibly involved in drug elimination. The LX1 predicted protein
is highly hydrophobic, possesses twelve putative transmembrane domains, and also shares significant homology with members
of the sugar transporter family, particularly the novel liver-specific transporter NLT. Lx1 mRNA is expressed at high levels in mouse liver, kidney, and intestine, and at low levels in the adrenals and in lactating
mammary glands. The Lx1 gene maps very close to the imprinted Igf2r/Mpr300 gene on mouse Chromosome (Chr) 17, in a region that is syntenic to human Chr 6q. Chr 6q has been previously associated with
transient neonatal diabetes mellitus and breast cancer.
Received: 11 March 1996 / Accepted: 5 June 1996 相似文献
12.
J. Michael Salbaum 《Mammalian genome》1999,10(2):107-111
The mouse gene Punc encodes a member of the immunoglobulin superfamily of cell surface proteins. It is highly expressed in the developing embryo
in nervous system and limb buds. At mid-gestation, however, expression levels of Punc decrease sharply. To allow investigation of such a regulatory mechanism, the genomic locus encompassing the Punc gene was cloned, characterized, and mapped. Fluorescent in situ hybridization was used to determine the chromosomal location
of the Punc gene of mouse and human. Mouse Punc maps to Chromosome (Chr) 9 in the region D-E1, whereas the human PUNC gene is localized to Chr 15 at 15q22.3-23, a region
known to be syntenic to mouse 9D-E1. The human PUNC gene therefore maps close to a genetic locus that is linked to Bardet-Biedl
Syndrome, an autosomal recessive human disorder. Confirmation for the location of human PUNC was obtained through sequence
relationships between mouse Punc cDNA, human PUNC cDNA, genomic sequence upstream of the murine Punc gene, and human STS markers that had been previously mapped on Chr 15. The STS sequence WI-14920 is in fact derived from
the 3′-untranslated region of the human PUNC gene. WI-14920 had been placed at 228cR from the top of the Chr 15 linkage group,
which provided positional information for the human PUNC gene at high resolution. Thus, this study identifies PUNC as the
gene corresponding to a previously anonymous marker and serves as a basis to investigate its role in genetic disorders.
Received: 8 July 1998 / Accepted: 14 October 1998 相似文献
13.
High-resolution mapping of mouse Chromosome 8 identifies an evolutionary chromosomal breakpoint 总被引:3,自引:0,他引:3
Prabhjit K. Grewal Daniel J. Bolland Laura Carim Todd Jane E. Hewitt 《Mammalian genome》1998,9(8):603-607
The central region of mouse Chromosome (Chr) 8, containing the myodystrophy (myd) locus, is syntenic with human Chr 4q28-qter. The human neuromuscular disorder facioscapulohumeral muscular dystrophy (FSHD)
maps to Chr 4q35, and myd has been proposed as a mouse homolog of FSHD. We have employed a comparative mapping approach to investigate this relationship
further by extending the mouse genetic map of this region. We have ordered 12 genes in a single cross, 8 of which have human
homologs on 4q28-qter. The results confirm a general relationship between the most distal genes on human 4q and the most proximal
genes in the mouse 8 syntenic region. Despite chromosomal rearrangements of syntenic groups in this region, conservation of
gene order is maintained between the group of genes in the human telomeric region of 4q35 and MMU8. Furthermore, this conserved
telomeric HSA4q35 syntenic group maps proximal to the myd mutation and is flanked by genes with homologs on HSA8p22. At the proximal boundary of the MMU8 linkage group we have identified
a single 300-kb YAC containing the genes Frgl and Pcml, which have human homologs on 4q35 and 8p22, respectively. Thus, this YAC spans an evolutionary chromosomal breakpoint. As
well as providing clues about chromosomal evolution, this map of the FSHD syntenic mouse region should prove invaluable in
the isolation of candidate genes for this disease.
Received: 20 January 1998 / Accepted: 10 April 1998 相似文献
14.
T. R. Devereux R. W. Wiseman N. Kaplan S. Garren J. F. Foley C. M. White C. Anna M. A. Watson A. Patel S. Jarchow R. R. Maronpot M. W. Anderson 《Mammalian genome》1994,5(12):749-755
Previous studies have hypothesized that at least three genetic loci contribute to differences in pulmonary adenoma susceptibility between mouse strains A/J and C57BL/6J. One gene that may confer susceptibility to lung tumorigenesis is the Kras protooncogene. To identify other relevant loci involved in this polygenic trait, we determined tumor multiplicity in 56 randomly chosen N-ethyl-N-nitrosourea-treated (A/J×C57BL/6J) N1×C57BL/6 backcross (AB6N2) progeny and correlated it with genotypes at 77 microsatellite markers spanning the genome. A correlation of lung tumor multiplicity phenotypes with genotypes of microsatellite markers on distal Chromosome (Chr) 6 in the Kras region (Pas1) was confirmed, and a new region on Chr 19 (designated Pas3) was identified that also contributes to susceptibility. Linkage analysis on Chr 19 with 270 AB6N2 mice localized the region flanked by D19Mit42 and D19Mit19 that is most closely associated with lung tumor susceptibility. The Pas3 locus may be an enhancer of the susceptibility locus on Chr 6. 相似文献
15.
The positions of 12 simple sequence repeat markers relative to reference loci on mouse Chromosome 16
The genetic map positions of 12 simple sequence repeat (SSR) markers spanning mouse Chromosome (Chr) 16 were determined relative to reference markers on that chromosome. Interval mapping data were obtained with a panel of DNAs from two intersubspecific backcrosses. All but one of the markers were typed by use of nonradioactive polymerase chain reaction (PCR) products analyzed on agarose gels. The marker order was determined to be Prm-1, D16Mit9, Igl-1, D16Mit29, D16Mit1/D16Mit2, Smst, D16Mit4, D16Mit11, Gap43, D16Mit14, D16Mit30, D16Mit5, Pit-1, D16Mit27, D16H21S16 (formerly D21S16h), D16Mit19, App, D16Mit7, Sod-1. Two of these markers mapped to the known human Chr 21 (HSA21)/Chr 16 conserved linkage group. Nine additional SSR markers could not be typed because they were not polymorophic (four markers), did not amplify MOLD/Rk DNA (three markers), or failed to give PCR products under a range of conditions (two markers). A subset of the most robust SSRs provide a useful marker set for the analysis of previously unmapped crosses. 相似文献
16.
The linkage map of sheep Chromosome 6 compared with orthologous regions in other species 总被引:9,自引:0,他引:9
E. A. Lord J. M. Lumsden K. G. Dodds H. M. Henry A. M. Crawford H. A. Ansari P. D. Pearce D. W. Maher R. T. Stone S. M. Kappes C. W. Beattie G. W. Montgomery 《Mammalian genome》1996,7(5):373-376
The genetic linkage map of sheep Chromosome (Chr) 6 has been extended to include 35 loci with the addition of 11 RFLP and
12 microsatellite loci. The sex-averaged linkage map now spans 154 cM from phosphodiesterase cyclic GMP beta polypeptide (PDE6B) to OarCP125, an anonymous sheep microsatellite. The male and female map lengths, at 180 cM and 132 cM respectively, did not differ significantly.
The physical assignment of PDE6B to Chr 6q33-qter orientates the linkage map on sheep Chr 6 with PDE6B near the telomere and OarCP125 towards the centromere. The order and genetic distances between loci are similar for the sheep Chr 6 and cattle Chr 6 maps,
except for the position of the casein genes. The sheep Chr 6 linkage map is also comparable to portions of human Chr 4, mouse
Chrs 5 and 3, and pig Chr 8. The synteny between sheep Chr 6 and human Chr 4 has been extended from PDE6B (4p16.3) to epidermal growth factor (EGF, 4q25-q27). However, a region from platelet-derived growth factor receptor α polypeptide (PDGFRA) to bone morphogenetic protein 3 (BMP3), which spans 19 cM on sheep Chr 6, appears to be inverted with respect to the human and mouse loci. Other differences in
the gene order between sheep, pig, and mouse suggest more complex rearrangements.
Received: 16 August 1995 / Accepted: 12 December 1995 相似文献
17.
Christine Ambrose Shirley Cheng Bertrand Fontaine Joseph H. Nadeau Marcy MacDonald James F. Gusella 《Mammalian genome》1992,3(3):151-155
Recent evidence suggests that the human neuromuscular disorders, hyperkalemic periodic paralysis and paramyotonia congenita, are both caused by genetic defects in the -subunit of the adult skeletal muscle sodium channel, which maps near the growth hormone cluster (GH) on Chromosome (Chr) 17q. In view of the extensive homology between this human chromosome and mouse Chr 11, we typed an interspecies backcross to determine whether the murine homolog (Scn4a) of this sodium channel gene mapped within the conserved chromosomal segment. The cytosolic thymidine kinase gene, Tk-1, was also positioned on the genetic map of Chr 11. Both Scn4a and Tk-1 showed clear linkage to mouse Chr 11 loci previously typed in this backcross, yielding the map order: Tr
J-(Re, Hox-2, Krt-1)-Scn4a-Tk-1. No mouse mutant that could be considered a model of either hyperkalemic periodic paralysis or paramyotonia congenita has been mapped to the appropriate region of mouse Chr 11. These data incorporate an additional locus into the already considerable degree of homology observed for these human and mouse chromosomes. These data are also consistent with the view that the conserved segment region may extend to the telomere on mouse Chr 11 and on human 17q. 相似文献
18.
The genes for orosomucoid (ORM-1 and ORM-2), delta-aminolevulinate dehydratase (ALAD), and hexabrachion or tenascin (HXB) all map to the q31-qter region of human Chromosome (Chr) 9. The mouse homolog of each of these genes has been mapped to Chr 4, but hexabrachion has not previously been mapped by linkage analysis. We have now ordered Orm-1, Lv (the mouse homolog of ALAD), and Hxb in an interspecific backcross panel, by use of tyrosinase related protein-1, Tyrp-1, whose human homolog maps to 9p13-pter (Abbott et al., Genomics 1991) as a reference locus. No recombinants were identified in 124 animals between Lv and Orm-1. Hxb was found to be 1.6 cM distal to Lv and Orm-1, and 4.8 cM proximal to Tyrp-1, or b. These data therefore contribute to our knowledge of the conserved synteny between HSA 9q and MMU 4. 相似文献
19.
Mapping of the structural gene for S-adenosyl homocysteine hydrolase to mouse Chromosome 2, and related sequences to Chromosomes 8 and X 总被引:1,自引:0,他引:1
Alison Pilz Paul Le Tissier Heather Moseley Jo Peters Cathy Abbott 《Mammalian genome》1992,3(11):633-636
Comparative mapping studies in human and mouse have shown that, to date, human Chromosome (Chr) 20 is completely syntenic with distal mouse Chr 2. The structural locus for S-adenosyl-l-homocysteine hydrolase (EC 3.3.1.1) in human, AHCY, maps to 20 qterq13.1, and we report here that the homologous locus in the mouse, Ahcy, maps to distal mouse Chr 2 with gene order Pcna-Ahcy-Ada. Analysis of 123 progeny of an interspecific backcross between a laboratory stock, AN, and Mus spretus using a rat cDNA probe revealed the presence of at least two other Ahcy-related sequences segregating independently in the mouse genome. One, Ahcy-rs1, was mapped to Chr 8 in the BXH recombinant inbred strains, and the other, Ahcy-rs2, shows a pattern of inheritance consistent with X-linkage. 相似文献
20.
We have mapped the gene encoding the murine RYK growth factor receptor protein tyrosine kinase by genetic linkage analysis with recombinant inbred strains of mouse. Two distinct Ryk loci (Ryk-1 and Ryk-2) were identified. Ryk-1 mapped to Chromosome (Chr) 9, whereas Ryk-2 mapped to Chr 12. A similar arrangement of RYK-related loci was previously determined in the human. Synteny has already been established between murine Chr 9 in the region of Ryk-1, and human chromosome 3q11–12, the location of the human RYK-1 gene. However, the Ryk-2/RYK-2 loci on murine Chr 12 and human chr 17p13.3 define a new region of synteny. 相似文献