共查询到20条相似文献,搜索用时 31 毫秒
1.
The genes for insulin-like growth factor 1 receptor (IGF1R), aggrecan (AGC1), β2-microglobulin (B2M), and an H6-related gene have been mapped to a single chicken microchromosome by genetic linkage analysis.
In addition, a second H6-related gene was mapped to chicken macrochromosome 3. The Igf1r and Agc1 loci are syntenic on mouse Chr 7, together with Hmx3, an H6-like locus. This suggests that the H6-related locus, which maps to the chicken microchromosome in this study, is the
homolog of mouse Hmx3. The IGF1R, AGC1, and B2M loci are located on human Chr 15, probably in the same order as found for this chicken microchromosome.
This conserved segment, however, is not entirely conserved in the mouse and is split between Chr 7 (Igf1r-Agc) and 2 (B2m). This comparison also predicts that the HMX3 locus may map to the short arm of human Chr 15. The conserved segment defined
by the IGF1R–AGC1–HMX3—B2M loci is approximately 21–35 Mb in length and probably covers the entire chicken microchromosome.
These results suggest that a segment of human Chr 15 has been conserved as a chicken microchromosome. The significance of
this result is discussed with reference to the evolution of the avian and mammalian genomes.
Received: 7 December 1996 / Accepted: 7 February 1997 相似文献
2.
Haruhiko Koseki Jochen Zachgo Yoko Mizutani Dominique Simon-Chazottes Jean-Louis Guénet Rudi Balling Achim Gossler 《Mammalian genome》1993,4(6):324-327
Danforth's short tail (Sd) is a semidominant mutation of the mouse with effects on the skeleton and the urogenital system. In view of its phenotype and its position in the proximal part of Chromosome (Chr) 2, three genes qualified as possible candidates: Pax-8, a paired box-containing gene; Midkine (Mdk), a retinoic acid-responsive gene; and a new locus (Etl-4) identified by enhancer trapping with a lacZ reporter gene which showed expression in the notochord, the mesonephric mesenchyme, and the apical ectodermal ridge. Three different backcrosses involving all three genes in different combinations were set up and analyzed. From our results we conclude that Sd, Etl-4, Pax-8, and Mdk are independent loci, with Etl-4 being the closest genetic marker (1.1±1.4 cM) to the Danforth's short tail (Sd) gene. 相似文献
3.
Nearly all F1 male mice with Dh/+ genotype between DDD female and DH–Dh/+ male die within a few days after birth; however, this is not observed in the reciprocal cross. The F1
Dh/+ males usually exhibit growth retardation prior to death. To identify the putative genetic locus or loci in DDD genome that
cause the abnormalities in the presence of the Dh, a linkage analysis was carried out in backcross progeny of a cross of (DDD female × DH–+/+ male) F1 female × DH–Dh/+ male. Appearance of growth retardation was examined from the day of birth, and both growth-retarded and normally weaned
Dh/+ males were genotyped for microsatellite marker loci spanning autosomes and the X Chromosome (Chr). Significant evidence
for linkage was identified on the distal edge of the X Chr, near the microsatellite marker of DXMit135. Furthermore, among mice from DDD female × reciprocal F1
Dh/+ male produced between DH–Dh/+ and progenitor strains (C57BL/6J, C3H/HeJ and BALB/cA), only the progeny from ♀DDD ×♂(♀DH–Dh/+×♂C3H/HeJ) F1
Dh/+ male did not show any lethality and/or growth retardation. Thus, the lethality in F1
Dh/+ males accompanied by growth retardation is caused by the interactions between the Dh gene, X Chr, and Y Chr. Based on the CAG repeat sequence length polymorphism among Mus musculus musculus Sry gene, C3H/HeJ was different from C57BL/6J, BALB/cA, and DH. These data suggest that there are at least two functional types
of Y Chr in Mus musculus musculus.
Received: 22 January 1999 / Accepted: 5 April 1999 相似文献
4.
T. Agui T. Miyamoto C.-G. Jung T. Tsumagari K. Masuda T. Manabe 《Mammalian genome》2000,11(10):862-865
The LEC rat has been reported to exhibit X-ray hypersensitivity and deficiency in DNA double-strand break (DSB) repair. The
present study was performed to map the locus responsible for this phenotype, the xhs (X-ray hypersensitivity), as the first step in identifying the responsible gene. Analysis of the progeny of (BN × LEC)F1× LEC backcrosses indicated that the X-ray hypersensitive phenotype was controlled by multiple genetic loci in contrast to
the results reported previously. Quantitative trait loci (QTL) linkage analysis revealed two responsible loci located on Chromosomes
(Chr) 4 and 1. QTL on Chr 4 exhibited very strong linkage to the X-ray hypersensitive phenotype, while QTL on Chr 1 showed
weak linkage. The Rad52 locus, mutation of which results in hypersensitivity to ionizing radiation and impairment of DNA DSB repair in yeast, was
reported to be located on the synteneic regions of mouse Chr 6 and human Chr 12. However, mapping of the rat Rad52 locus indicated that it was located 23 cM distal to the QTL on Chr 4. Furthermore, none of the radio-sensitivity-related
loci mapped previously in the rat chromosome were identical to the QTL on Chrs 4 and 1 in the LEC rat. Thus, it seems that
X-ray hypersensitivity in the LEC rat is caused by mutation(s) in as-yet-undefined genes.
Received: 14 February 2000 / Accepted: 17 May 2000 相似文献
5.
Fernando Pardo-Manuel de Villena Elena de la Casa-Esperón Andrei Verner Kenneth Morgan Carmen Sapienza 《Mammalian genome》1999,10(5):492-497
The DDK syndrome is a polar, early embryonic lethal phenotype caused by incompatibility between a maternal factor of DDK
origin and a paternal gene of non-DDK origin. Both maternal factor and paternal gene have been mapped to the Om locus on mouse Chromosome (Chr) 11. The paternal contribution to the syndrome has been shown to segregate as a single locus.
Although the inheritance of the maternal contribution has not been characterized in depth, it as been assumed to segregate
as a single locus. We have now characterized the segregation of the DDK fertility phenotype in over 240 females. Our results
demonstrate that females require at least one DDK allele at Om to manifest the syndrome. However, the DDK syndrome inter-strain cross-fertility phenotype of heterozygous females is highly
variable and spans the gamut from completely infertile to completely fertile. Our results indicate that this phenotypic variability
has a genetic basis and that the modifiers of the DDK syndrome segregate independently of Om.
Received: 24 November 1998 / Accepted: 19 January 1999 相似文献
6.
Michael C. Rule Raye J. Mutcherson II Andrew D. Foss Tien K.-X. Nguyen Kenute A. Myrie Thomas R. King 《Mammalian genome》1999,10(5):447-450
The recessive male sterility and histoincompatibility (mshi) mutation in the mouse generates pleiotropic effects on graft transplantation and male reproduction. Previous analysis of
backcross mice typed for mshi either by testicular morphology or by allograft rejection has located each trait to a 20-cM region on proximal mouse Chr
10. Here we present the microsatellite polymorphism analysis of a new 276-member intraspecific backcross panel—including a
set of 135 males typed for sterility and histoincompatibility—that places both features controlled by mshi within a 1.7-cM interval between markers D10Mit51/168/212 and D10Mit213. In addition, this analysis has allowed an explicit test of a two-gene model for the mshi locus and has provided a measurement of the penetrance of the mshi-generated histogenic phenotype in both male (88.4 ± 3.9%) and female (91.0 ± 3.5%) mutants. The fine-structure map presented
should facilitate a chromosome walk across this region and, ultimately, the molecular identification of the gene or genes
affected by this interesting mutation.
Received: 28 August 1998 / Accepted 18 December 1998 相似文献
7.
Structural variants of the mouse Chr 17-specific t complex, known as t haplotypes, express factors that alter the ability of sperm to carry out their roles in the normal fertilization process.
In previous studies of males carrying heterospecific combinations of the t complex, we discovered a unique M. spretus/t haplotype phenotype of male sterility. In additional studies with mice carrying a series of M. spretus–M. m. domesticus recombinant Chr 17 homologs and a complete t haplotype (S-+/t), we monitored physiological aspects of sperm function to map a locus (Hst6) responsible for expression of the t-specific ``curlicue' sperm flagellar curvature phenotype to 1 cM within the fourth inversion of the t complex. In the present report, we quantitatively analyze the in vitro capability of sperm from mice with similar S-+/t Chr 17 genotypes to fertilize zona pellucida-free mouse eggs. The results identify a locus, Stop1, mapping distal to Pim1, with acute effects on the ability of sperm to penetrate the oolemma. The data suggest that Stop1 is a complex locus consisting of at least two genetic elements, a proximal one overlapping the Hst6 locus, and another, distal to the Hst6 locus. Further quantitative analyses of the ``curlicue' phenotype produced by sperm derived from these same animals indicate
that expression of this chronic flagellar curvature phenotype also derives from at least two elements, both mapping within
the Hst6 locus. Thus, these studies provide higher resolution mapping of the molecular basis of t haplotype-specific sperm dysfunction emanating from In(17)4.
Received: 22 May 1998 / Accepted: 17 June 1998 相似文献
8.
Pluridigite (Pdt) is a semi-dominant mutation obtained after a mutagenesis experiment with ethyl-nitroso-urea (ENU). The mutant exhibits abnormal skeletal pattern formation characterized by the formation of extra digits (polydactyly) in the preaxial (anterior) part of the hindlimbs. The phenotype shows incomplete penetrance, depending on the genetic background. In an F2 cross with C57BL/6, the phenotype could not be associated with a single locus. Strong linkage was observed with markers located on Chromosome (Chr) 12, in a 2-cM interval between D12Mit136 and D12Mit153. This region contains the Twist gene, and we show that the [Pdt] phenotype is dependent upon a new allele of Twist. We further identified that the whole Chr 4 is associated with the [Pdt] phenotype. The Pluridigite phenotype thus results from the combination of a Twist mutant allele and at least two additional loci. 相似文献
9.
We found a new X-linked dominant mouse mutation. This mouse has the same phenotype as Td, which exhibits hyperkeratotic skin, reduced viability in affected females, a tendency to be smaller, lighter weight than
the normal sibs during weaning age, and prenatal lethality in affected males. To map the locus, we tested 267 progeny from
an intraspecific backcross between affected females and wild-origin strain males. Polymerase chain reaction (PCR) was performed
with microsatellite markers of the proximal region of the mouse X Chromosome (Chr). This mutant showed no recombination with
DXMit 123, DXMit 55, or DXMit 26. The gene position and phenotype of this mutant were very similar to those of Td. Therefore, it is speculated that the new mutant gene is a multiple allele of Td, and we designated it Tattered-Hokkaido (Td
ho
). Linkage analysis of these animals suggested a possible gene order of cen-(Td
ho
, DXMit123, DXMit55, DXMit26)–DXMit161–DXMit54–DXMit103–DXMit52–DXMit190–DXMit138) in the X Chr. Prenatal lethality of male mutants was also investigated, with 12.5 to 16.5 embryonic day (E) backcrossed
embryos from affected F1 females. It was found that the male mutants died between E12.5 and E14.5. The cause of death of male mutants is discussed
in relation with the other proximal genes of the X Chr.
Received: 15 December 1997 / Accepted: 1 April 1997 相似文献
10.
The btm (brachyury-interacting tail length modifier) mutation was discovered in strain MOL-NIS derived from Japanese wild mice (Mus musculus molossinus) as an autosomal recessive mutation. Homozygotes for this mutation show a short tail phenotype and, moreover, this mutation causes the tailless character by interacting with the T (brachyury) gene on Chromosome (Chr) 17. Our linkage tests and RFLP analyses suggest that btm is located within the t complex on Chr 17 and represents a new partial t haplotype. 相似文献
11.
Localization of the locus causing Spider Lamb Syndrome to the distal end of ovine Chromosome 6 总被引:7,自引:0,他引:7
N.E. Cockett T.L. Shay J.E. Beever D. Nielsen J. Albretsen M. Georges K. Peterson A. Stephens W. Vernon O. Timofeevskaia S. South J. Mork A. Maciulis T.D. Bunch 《Mammalian genome》1999,10(1):35-38
Spider Lamb Syndrome (SLS) is a semi-lethal congenital disorder, causing severe skeletal abnormalities in sheep. The syndrome
has now been disseminated into several sheep breeds in the United States, Canada, and Australia. The mode of inheritance for
SLS is autosomal recessive, making the identification and culling of carrier animals difficult due to their normal phenotype.
Two large pedigrees segregating for the SLS mutation were established, and a genome scan with genetic markers from previously
published genome maps of cattle and sheep was used to map the locus causing SLS. Genetic linkage between SLS and several microsatellite
markers, OarJMP8, McM214, OarJMP12, and BL1038, was detected, thereby mapping the SLS locus to the telomeric end of ovine Chromosome (Chr) 6. Alignment of ovine Chr 6 with
its evolutionary ortholog, human Chr 4, revealed a positional candidate gene, fibroblast growth factor receptor 3 (FGFR3).
Received: 10 June 1998 / Accepted: 23 September 1998 相似文献
12.
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
13.
Yuka Namiki Yasuhiro Kon Katsuyuki Kazusa Atsushi Asano Nobuya Sasaki Takashi Agui 《Mammalian genome》2005,16(2):96-102
The MRL/MpJ mouse has previously been reported to possess an interesting phenotype in which spermatocytes are resistant to the abdominal temperature heat shock. In this study genetic analysis for it was performed. The phenotypes of F2 progenies produced by mating MRL/MpJ and control strain C57BL/6 mice were not segregated into two types as parental phenotypes, suggesting that the phenotype is controlled by multiple genetic loci. Thus, quantitative trait loci (QTL) analysis was performed using 98 microsatellite markers. The weight ratio of the cryptorchid testis to the intact testis (testis weight ratio) and the Sertoli cell index were used for quantitative traits. QTL analysis revealed two significant QTLs located on Chrs 1 and 11 for testis weight ratio and one significant QTL located in the same region of Chr 1 for the Sertoli cell index. A microsatellite marker locus located in the peak of the QTL on Chr 1 did not recombine with the exonuclease 1 (Exo1) gene locus in 140 F2 progenies. Mutation of the Exo1 gene was previously reported to be responsible for metaphase-specific apoptosis (MSA) of spermatocytes in the MRL/MpJ mouse. These results raise the possibility that mutation of the Exo1 gene is responsible for both MSA and heat stress resistance of spermatocytes in the MRL/MpJ mouse. 相似文献
14.
Johannes Becker-Follmann Andreas Gaa Elke Baùsch Ernst Natt Gerd Scherer Otto von Deimling 《Mammalian genome》1997,8(3):172-177
We have performed a high-resolution linkage analysis for the conserved segment on distal mouse Chromosome (Chr) 8 that is
homologous to human Chr 16q. The interspecific backcross used involved M. m. molossinus and an M. m. domesticus line congenic for an M. spretus segment from Chr 8 flanked by phenotypic markers Os (oligosyndactyly) and e, a coat colormarker. From a total of 682 N2 progeny, the 191 animals revealing a recombination event between these phenotypic markers were typed for 23 internal loci.
The following locus order with distances in cM was obtained: (centromere)–Os–4.1–Mmp2–0.2–Ces1,Es1, Es22–1.2–Mt1,D8Mit15–2.2–Got2, D8Mit11–3.7–Es30–0.3–Es2, Es7–0.9–Ctra1,Lcat–0.3–Cdh1, Cadp, Nmor1, D8Mit12–0.2–Mov34–2.5–Hp,Tat–0.2–Zfp4–1.6–Zfp1,Ctrb–10.9–e. In a separate interspecific cross involving 62 meioses, Dpep1 was mapped together with Aprt and Cdh3 at 12.9 cM distal to Hp, Tat, to the vicinity of e. Our data give locus order for markers not previously resolved, add Mmp2 and Dpep1 as new markers on mouse Chr 8, and indicate that Ctra1 is the mouse homolog for human CTRL. Comparison of the order of 17 mouse loci with that of their human homologs reveals that
locus order is well conserved and that the conserved segment in the human apparently spans the whole long arm of Chr 16.
Received: 30 July 1996 / Accepted: 15 November 1996 相似文献
15.
Quantitative trait loci for baseline erythroid traits 总被引:1,自引:0,他引:1
Luanne L. Peters Amy J. Lambert Weidong Zhang Gary A. Churchill Carlo Brugnara Orah S. Platt 《Mammalian genome》2006,17(4):298-309
A substantial genetic contribution underlies variation in baseline peripheral blood counts. We performed quantitative trait
locus/loci (QTL) analyses to identify chromosome (Chr) regions harboring genes influencing the baseline erythroid parameters
in F2 intercrosses between NZW/LacJ, SM/J, and C57BLKS/J inbred mice. We identified multiple significant QTL for red blood cell
(RBC) count, hemoglobin (Hgb) and hematocrit (Hct) levels, mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH),
and mean cell hemoglobin concentration (CHCM). We identified four RBC count QTL: Rbcq1 (Chr 1, peak LOD score at 62 cM,), Rbcq2 (Chr 4, 60 cM), Rbcq3 (Chr 11, 34 cM), and Rbcq4 (Chr 10, 60 cM). Three MCV QTL were identified: Mcvq1 (Chr 7, 30 cM), Mvcq2 (Chr 11, 6 cM), and Mcvq3 (Chr 10, 60 cM). Single significant loci for Hgb (Hgbq1, Chr 16, 32 cM), Hct (Hctq1, Chr 3, 42 cM), and MCH (Mchq1, Chr 10, 60 cM) were identified. The data support the existence of a common RBC/MCH/MCV locus on Chr 10. Two QTL for CHCM
(Chcmq1, Chr 2, 48 cM; Chcmq2, Chr 9, 44 cM) and an interaction between Chcmq2 with a locus on Chr 19 were identified. These analyses emphasize the genetic complexity underlying the regulation of erythroid
peripheral blood traits in normal populations and suggest that genes not previously recognized as significantly impacting
normal erythropoiesis exist. 相似文献
16.
Ilya Ruvinsky Olga Chertkov Xenia V. Borue Sergei I. Agulnik Jeremy J. Gibson-Brown Stephen R. Lyle Lee M. Silver 《Mammalian genome》2002,13(12):675-679
Mutations in the mouse Brachyury (T) gene are characterized by a dominant reduction of tail length and recessive lethality.
Two quantitative trait loci, Brachyury-modifier 1 and 2 (Brm1 and Brm2) are defined by alleles that enhance the short-tail
Brachyury phenotype. Here we report on a genetic analysis of a visible dominant mutation Abnormal feet and tail (Aft) located
in the vicinity of Brm1. Affected animals display kinky tails and syndactyly in the hindlimbs, both likely resulting from
a defect in apoptosis. We observed an unusual genetic incompatibility between Aft and certain genetic backgrounds. We show
that Aft and T are likely to interact genetically, since some double heterozygotes are tailless. In addition to the tail and
hindlimb phenotypes, Aft-bearing mutants display characteristic late-onset skin lesions. We therefore tested for allelism
between Aft and a closely linked recessive mutation rough coat (rc) and found that these two mutations are likely nonallelic.
Our results provide a valuable resource for the study of mammalian skin development and contribute to the genetic analysis
of Brachyury function. 相似文献
17.
Caspase-2 is a member of the caspase family of cystein proteases involved in programmed cell death or apoptosis. Functional
and genetic data suggest it as a candidate gene for lymphopenia (Lyp)—a susceptibility gene for rat diabetes—which is responsible for the T-cell lymphopenia in the diabetes–prone BB rat. Firstly,
there is a higher frequency of apoptosis among recent thymic emigrants in the diabetes-prone BB rat than in the non-lymphopenic
diabetes-resistant BB rat. Secondly, caspase-2 maps close to Tcrb on mouse Chromosome (Chr) 6, while Lyp is closely linked to Tcrb on the homologous rat Chr 4. In this paper, we report genetic fine-positioning and radiation hybrid mapping of caspase-2
in the rat. Both methods positioned caspase-2 to rat Chr 4 between markers Prss1 and D4Mit5. Since Lyp maps distally to D4Mit5, between markers D4Rat75 and Npy, we exclude caspase-2 as a candidate gene for Lyp.
Received: 13 March 1998 / Accepted: 28 October 1998 相似文献
18.
Kumud Majumder William Shawlot Gabriele Schuster Wilbur Harrison Frederick F.B. Elder Paul A. Overbeek 《Mammalian genome》1998,9(11):863-868
Mice with mutations at the downless (dl) locus have defects in hair follicle, tooth, sweat gland, preputial gland, Meibomian gland, and tail development. The dl phenotype is analogous to the human genetic disorder termed autosomal hypohidrotic (or anhidrotic) ectodermal dysplasia (HED).
On the basis of the identification of two related transgenic insertional mutations in the downless gene, yeast artificial
chromosomes (YACs) were identified that map to the critical region of mouse Chromosome (Chr) 10. To determine which of the
YACs contain the dl gene, we generated YAC transgenic mice by mouse embryo microinjections. The 200-kb YAC B25.D9 was found to rescue all of
the downless defects. In addition, the transgenic YAC rescued the dominant Sleek (Dl
slk
) allele. Since the sequences within the YAC are entirely deleted in one of the transgenic mutants, our results establish
that Sleek encodes a dominant-negative protein whose effects can be reversed by expression of extra copies of the wild-type
locus.
Received: 26 June 1998 / Accepted: 17 July 1998 相似文献
19.
A missense mutation in the bovine MGF gene is associated with the roan phenotype in Belgian Blue and Shorthorn cattle 总被引:5,自引:0,他引:5
Jeffrey J. Seitz Sheila M. Schmutz Tracey D. Thue Fiona C. Buchanan 《Mammalian genome》1999,10(7):710-712
The Roan locus is responsible for the coat coloration of Belgian Blue and Shorthorn cattle. The solid-colored and white animals
are homozygotes, and the roan animals, with intermingled colored and white hairs, are heterozygous. The roan phenotype was
mapped to cattle Chromosome (Chr) 5 with microsatellites, and a candidate gene was proposed (Charlier et al. Mamm Genome 7,
138, 1996). PCR primers to the exons of this candidate gene, the steel locus or mast cell growth factor (MGF) were designed. Solid-colored and white animals were sequenced. A missense mutation at 654 bp (amino acid 193, Ala → Asp)
was detected in these two groups. A PCR-RFLP was designed to this single base pair change, and 143 animals in total (Belgian
Blue, Shorthorn, and various other breeds) were screened. In addition, the Canadian Beef Cattle Reference Herd (http://skyway.usask.ca/∼schmutz)
was used to verify Mendelian inheritance of this marker with the phenotypic inheritance of roan. Our data suggest that this
mutation in the bovine MGF gene is responsible for the roan phenotype.
Received: 10 December 1998 / Accepted: 26 February 1998 相似文献
20.
Serge Alonso Xavier Montagutelli Dominique Simon-Chazottes Jean-Louis Guénet Margaret Buckingham 《Mammalian genome》1993,4(1):15-20
We present here the genetic mapping of the -skeletal actin locus (Actsk-1) on mouse Chromosome (Chr) 8, on the basis of the PCR analysis of a microsatellite in an interspecific backcross. Linkage and genetic distances were established for four loci by analysis of 192 (or 222) meiotic events and indicated the following gene order: (centromere)-Es-1-11.7 cM-Tat-8.3 cM-Actsk-1-0.5 cM-Aprt. Mapping of ACTSK to human Chr 1 and of TAT and APRT to human Chr 16 demonstrates the existence of a new short region of homology between mouse Chr 8 and human Chr 1. Intermingling on this scale between human and mouse chromosomal homologies that occurred during evolution creates disorders in comparative linkage studies. 相似文献