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At least 1,567 records · Page 87Linked to original sources
PubMed2006

Fine mapping of the recessive genic male-sterile gene (Bnms1) in Brassica napus L.

A recessive genic male sterility (RGMS) system, S45 AB, has been developed from spontaneous mutation in Brassica napus canola variety Oro, and is being used for hybrid cultivar development in China. The male sterility of S45 was controlled by two duplicated recessive genes, named as Bnms1 and Bnms2. In this study, a NIL (near-isogenic line) population from the sib-mating of S45 AB was developed and used for the fine mapping of the Bnms1 gene, in which the recessive allele was homozygous at the second locus. AFLP technology combined with BSA (bulked segregant analysis) was used. From a survey of 2,560 primer combinations (+3/+3 selective bases), seven AFLP markers linked closely to the target gene were identified, of which four were successfully converted to sequence characterized amplified region (SCAR) markers. For further analysis, a population of 1,974 individuals was used to map the Bnms1 gene. On the fine map, Bnms1 gene was flanked by two SCAR markers, SC1 and SC7, with genetic distance of 0.1 cM and 0.3 cM, respectively. SC1 was subsequently mapped on linkage group N7 using doubled-haploid mapping populations derived from the crosses Tapidor x Ningyou7 and DH 821 x DHBao 604, available at IMSORB, UK, and our laboratory, respectively. Linkage of an SSR marker, Na12A02, with the Bnms1 gene further confirmed its location on linkage group N7. Na12A02, 2.6 cM away from Bnms1, was a co-dominant marker. These molecular markers developed from this research will facilitate the marker-assisted selection of male sterile lines and the fine map lays a solid foundation for map-based cloning of the Bnms1 gene.

Alleles↗
PubMed2006

Genetic mapping of the pear scab resistance gene Vnk of Japanese pear cultivar Kinchaku.

Pear scab (caused by Venturia nashicola) is one of the most harmful diseases of pears, especially Japanese and Chinese pear species. The molecular identification and early selection of resistant plants could greatly improve pear breeding. We have identified the position of the scab resistance gene, designated Vnk in an indigenous Japanese pear cultivar Kinchaku, within the pear genome by using simple sequence repeat (SSR) markers derived from pear and apple. The position of Vnk was identified in the central region of linkage group 1 of Kinchaku. Several amplified fragment length polymorphism (AFLP) markers linked to Vnk were obtained by bulked segregant analysis. Among them, the AFLP marker closest to Vnk was converted into a sequence tagged site (STS) marker. Four random amplified polymorphic DNA (RAPD) markers previously found to be loosely associated with Vnk (Iketani et al. 2001) were successfully converted into STS markers. Six markers (one SSR Hi02c07 and five STSs converted from AFLP and RAPD) showed tight linkages to Vnk, being mapped with distances ranging from 2.4 to 12.4 cM. The SSR CH-Vf2, which was isolated from a BAC clone of the contig containing the apple scab gene Vf, was mapped at the bottom of linkage group 1 in Kinchaku, suggesting that the Vnk and Vf loci are located in different genomic regions of the same homologous linkage group.

Ascomycota↗
PubMed2006

CAPs markers to assist selection for low vicine and convicine contents in faba bean (Vicia faba L.).

The antinutritional factors (ANFs) present in Vicia spp. seeds are a major constraint to the wider utilization of these crops as grain legumes. In the case of faba bean (Vicia faba L.), a breeding priority is the absence vicine and convicine (v-c); responsible for favism in humans and for the reduced animal performance or low egg production in laying hens. The discovery of a spontaneous mutant allele named vc-, which induces a 10-20 fold reduction of v-c contents, may facilitate the process. However, the high cost and difficulty of the chemical detection of v-c seriously restricts the advances in breeding-selection. To identify random amplified polymorphic DNA (RAPD) markers linked to this gene, we have analysed an F(2 )population derived from a cross between a line with high v-c content (Vf6) and the vc- genotype (line 1268). Quantification of v-c was done by spectrophotometry on the parents and the F(2 )population (n = 136). By using bulked segregant analysis (BSA), two RAPD markers linked in coupling and repulsion phase to the allele vc- were identified and further converted into sequence characterized amplified regions (SCARs). Amplification of SCARS was more consistent, although the initial polymorphism between pools was lost. To recover the polymorphisms several approaches were explored. Restriction digestion with HhaI (for SCAR SCH01(620)) and RsaI (for SCAR SCAB12(850)) revealed clear differences between the parental lines. The simultaneous use of the two cleavage amplified polymorphism (CAP) markers will allow the correct fingerprinting of faba bean plants and can be efficiently used in breeding selection to track the introgression of the vc- allele to develop cultivars with low v-c content and improved nutritional value.

Animals↗
PubMed2006

Identification of AFLP markers linked to the male fertility restorer gene of CMS (Moricandia arvensis) Brassica juncea and conversion to SCAR marker.

We have developed a cytoplasmic male sterile (CMS) line of Brassica juncea through somatic hybridization with Moricandia arvensis and introgressed the fertility restorer gene into B. juncea. This fertility restorer locus is unique in that it is capable of restoring male fertility to two other alloplasmic CMS systems of B. juncea. As a first step toward cloning of this restorer gene we attempted molecular tagging of the Rf locus using the amplified fragment length polymorphism (AFLP) technique. A BC(1)F(1) population segregating for male sterility/fertility was used for tagging using the bulk segregant analysis method. Out of 64 primer combinations tested in the bulks, 5 combinations gave polymorphic amplification patterns. Further testing of these primers in individual plants showed four amplicons associated with the male fertility trait. Polymorphic amplicons were cloned and used for designing SCAR primers. One of the SCAR primers generated amplicons mostly in the fertile plants. Linkage analysis using MAPMAKER showed two AFLP and one SCAR markers linked to the male fertility gene with a map distance ranging from 0.6 to 2.9 cM. All the markers are located on one side of the Rf locus.

Fertility↗
PubMed2002

The relationship between homozygous and hemizygous transgene expression levels over generations in populations of transgenic rice plants.

Segregating T(1), T(2) and T(3) transgenic rice populations, derived from independent particle-bombardment-mediated transformation events were examined in order to assess the effect of gene dosage on transgene expression levels and stability. The expression level of the unselected beta-glucuronidase ( gusA) reporter gene was quantified in plants from these populations. The gusA gene dosage was determined by segregation analysis of progeny seedlings at the structural level (by PCR) and at the expression level. For some transformation events a gene dosage effect on transgene expression was observed, leading to higher transgene expression levels in homozygous progeny than in hemizygous progeny or primary transgenic plants. However, in many other transformation events, the homozygous state appears to be disadvantageous, being associated with lower transgene expression levels, gene silencing or counter-selection of homozygous plants across generations. Change of gene dosage is probably one of the key factors influencing transgene expression levels and stability in transgenic rice. This is particularly important when considering molecular genetic studies and crop improvement programmes. The possible influence of matrix attachment regions (MARs) in increasing the likelihood of an additive effect on transgene expression level is discussed.

Journal Article↗
PubMed2001

Low rate of proliferation in immature thymocytes of the non-obese diabetic mouse maps to the Idd6 diabetes susceptibility region.

AIMS/HYPOTHESIS: The non-obese diabetic (NOD) mouse spontaneously develops T-cell-dependent autoimmune diabetes. This mouse strain has a number of immune dysfunctions related to T-cell development but so far there are no available data on the proliferation of NOD immature thymocytes. We therefore studied the thymocyte proliferation in the NOD mouse in discrete stages of T-cell development. METHODS: We depleted thymocytes in vivo and analysed thymocyte proliferation during the thymus recovery from depletion. We used co-segregation analysis and quantitative loci trait analysis to investigate the genetic control of proliferation impairments in NOD thymocytes. RESULTS: Immature thymocytes of female NOD mice proliferate with a relatively low rate compared to non-autoimmune C57Bl/6 mice. This aberrant proliferation was most pronounced in CD4-/lo CD8+ cells differentiating from the CD4-CD8- to the CD4+CD8+ stage. A genetic mapping study using an F2 intercross between the NOD and the C57BL/6 strains showed that a major locus controlling this trait is linked to the insulin-dependent diabetes susceptibility locus Idd6. CONCLUSION/INTERPRETATION: Our results suggest that impairment of proliferation of immature thymocytes is one possible mechanism through which the Idd6 locus contributes to the pathogenesis of diabetes.

Animals↗
PubMed2003

Molecular characterization of the pig C3 gene and its association with complement activity.

The complement system catalyzes direct lysis of micro-organisms and modulates phagocytosis, inflammation, humoral and cellular immune responses. Since the complement protein C3 is the central component within all pathways of complement activation, C3 is a candidate gene for complement activity and also for improved protection against many pathogens. The pig C3 gene was sequenced, screened for polymorphisms, and analyzed for association with hemolytic complement activity of the alternative and classical pathway (AH(50), CH(50)). C3c serum levels and haptoglobin (HP) serum concentrations were measured before and after vaccination against Mycoplasma hyopneumoniae, Aujeszky virus, and porcine reproductive and respiratory syndrome virus in F2 animals of a pig resource population based on crossbreeding of Duroc and Berlin Miniature Pig. The genomic C3 sequence covers 444 bp of promoter region, 41 exons and 40 introns, as well as 881 bp of the 3'-flanking region. The cDNA codes for a 1,661-amino acid precursor C3. Five polymorphic sites were detected in the 5'-UTR, intron 13, exon 15, exon 30, and the 3'-UTR. Within the resource population two haplotypes were found to segregate. Analysis of variance applying a repeated measures model revealed a significant effect of the interaction of C3 genotype and time of measurement relative to immunization on CH(50), AH(50,)and C3c that is likely to be due to variation of C3 expression. In contrast, the time course of the HP acute-phase reaction is not associated with C3 genomic variation. The association of C3 with complement activity indicates the importance of C3 as a candidate gene for natural resistance to micro-organisms, although the causative polymorphism modulating the expression of C3 remains to be delineated.

Alleles↗
PubMed2003

Physical and genetic mapping of the rainbow trout major histocompatibility regions: evidence for duplication of the class I region.

One of the most unexpected discoveries in MHC genetics came from studies dealing with the teleost MHC. Initially discovered in zebrafish, the MHC class I and II regions of all bony fish are not linked. Previous segregation analysis in trout suggested that the class I and II regions reside on completely different chromosomes. To learn more about MHC genomics in trout, we have isolated BAC clones harboring class Ia and Ib loci, a single BAC clone containing an MH class II gene ( DAB), as well as BAC clones containing the ABCB2 gene. Upon PCR and sequence confirmation, BAC clones were labeled and used as probes for in situ hybridization on rainbow trout metaphase chromosomes for determination of the physical locations of the trout MH regions. Finally, SNPs, RFLPs, and microsatellites found within the BAC clones allowed for these regions to be assigned to specific linkage groups on the OSU x Hotcreek (HC) and OSU x Arlee (ARL) genetic linkage maps. Our data demonstrate that the trout MH regions are located on at least four different chromosomes and the corresponding linkage groups, while also providing direct evidence for the partial duplication of the MH class I region in trout.

Animals↗
PubMed1999

Identification and genetic mapping of Xenopus TAP2 genes.

The amphibian Xenopus laevis is one non-mammalian vertebrate in which the major histocompatibility complex (MHC) has been analyzed extensively. Class IIbeta, class Ia, LMP2, LMP7, HSP70, C4, Factor B, and Ring3 genes have been identified and mapped to the MHC. Here, we report the isolation of a transporter associated with antigen processing (TAP) gene, TAP2, and demonstrate its linkage to the MHC. While the ATP-binding region of Xenopus TAP2 is highly conserved in evolution, amino acid identity to other vertebrate TAP proteins was not detected in the N-terminal region. Segregation analysis of 34 individuals from two families showed exact restriction fragment length polymorphism matching between the MHC class Ia gene and the one TAP2 gene demonstrating linkage conservation since the mammalian/amphibian divergence approximately 350 million years ago. In addition, one non-MHC-linked TAP2-hybridizing fragment was detected in approximately half of the individuals tested. Interestingly, TAP2 allelic lineages appear to match those of LMP7 and classical class I, which previously were categorized into two highly divergent groups that emerged at least 60 million years ago. Similar to LMP7 and class Ia,TAP2 is expressed ubiquitously with highest levels in intestine and spleen.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2003

Meiotic behavior of a supernumerary chromosome in Magnaporthe oryzae.

A 1.2-Mb DNA band from an isolate of Magnaporthe oryzae was detected in a pulsed-field gel. A chromosomal entity corresponding to this band was observed at the mitotic metaphase stage. This minichromosome, carrying many transposable elements and two telomeres, was transmitted to ascosporic F(1) cultures in a non-Mendelian manner with frequent changes in its size and number. Segregation analysis with RFLP markers indicated that the minichromosome underwent structural rearrangements, such as deletion and duplication, not only during meiosis but also after meiosis. An ectopic sister chromatid recombination may cause the size variation of the minichromosomes.

Blotting, Southern↗
PubMed1998

Genetic mapping of telomeric DNA sequences in the maize pathogen Cochliobolus heterostrophus.

Numerous polymorphic bands were observed when genomic DNA of Cochliobolus heterostrophus was cut with restriction enzymes and hybridized with a telomere-specific probe. Bal31 digestion demonstrated that the majority of the bands were from the chromosome termini and thus constitute telomeres. However, numerous hybridizing sequences in the strain B30.A3.R.45 were Bal31 exonuclease-insensitive and thus located at least 600 bases internal to the chromosome ends. Segregation analysis of the polymorphic bands identified nine telomeres; seven were linked to other markers and thus permitted the proper orientation of linkage groups with respect to their chromosome ends. Three internal, telomere-homologous sequences, at least one of which may be subtelomeric, were also mapped.

Ascomycota↗
PubMed2004

Agrobacterium-mediated transformation of bottle gourd (Lagenaria siceraria Standl.).

We describe a procedure for producing transgenic bottle gourd plants by inoculating cotyledon explants with Agrobacterium tumefaciens strain AGL1 that carries the binary vector pCAMBIA3301 containing a glufosinate ammonium-resistance (bar) gene and the beta-D-glucuronidase (GUS) reporter gene. The most effective bacterial infection was observed when cotyledon explants of 4-day-old seedlings were co-cultivated with Agrobacterium for 6-8 days on co-cultivation medium supplemented with 0.1-0.001 mg/l L-alpha-(2-aminoethoxyvinyl) glycine (AVG). The putatively transformed shoots directly emerged at the proximal end of cotyledon explants after 2-3 weeks of culturing on selection medium containing 2 mg/l DL-phosphinothricin. These shoots were rooted after 3 weeks of culturing on half-strength MS medium containing 0.1 mg/l indole acetic acid and 1 mg/l DL-phosphinothricin. Transgenic plants were obtained at frequencies of 1.9%. Stable integration and transmission of the transgenes in T1 generation plants were confirmed by a histochemical GUS assay, polymerase chain reaction and Southern blot analyses. Genetic segregation analysis of T1 progenies showed that transgenes were inherited in a Mendelian fashion. To our knowledge, this study is the first to show Agrobacterium-mediated transformation in bottle gourd.

Agrobacterium tumefaciens↗
PubMed2005

Characterization of Pisrt1/Foxl2 in Ellobius lutescens and exclusion as sex-determining genes.

The rodent Ellobius lutescens is an exceptional mammal which determines male sex constitutively without the SRY gene and, therefore, may serve as an animal model for human 46,XX female-to-male sex reversal. It was suggested that other factors of the network of sex-determining genes determine maleness in these animals. However, some sex-determining genes like SOX9 and SF1 have already been excluded by segregation analysis as primary sex-determining factors in E. lutescens. In this work, we have cloned and characterized two genes of the PIS (polled intersex syndrome) gene interval, which were reported as candidates in female-to-male sex reversal in hornless goats recently. The genes Foxl2 and Pisrt1 from that interval were identified in E. lutescens DNA and mapped to Chromosome 8. We have excluded linkage of Foxl2 and Pisrt1 loci with the sex of the animals. Hence, the involvement of this gene region in sex determination may be specific for goats and is not a general mechanism of XX sex reversal or XX male sex determination.

Amino Acid Sequence↗
PubMed1996

A rat homolog of the mouse deafness mutant jerker (je).

An autosomal recessive deafness mutant was discovered in our colony of Zucker (ZUC) rats. These mutants behave like shaker-waltzer deafness mutants, and their inner ear pathology classifies them among neuroepithelial degeneration type of deafness mutants. To determine whether this rat deafness mutation (-) defines a unique locus or one that has been previously described, we mapped its chromosomal location. F2 progeny of (Pbrc:ZUC x BN/Crl) A/a B/b H/h +/- F1 rats were scored for coat color and behavioral phenotypes. Segregation analysis indicated that the deafness locus might be loosely linked with B on rat Chromosome (Chr) 5 (RNO5). Therefore, 40 -/- rats were scored for BN and ZUC alleles at four additional loci, D5Mit11, D5Mit13, Oprd1, and Gnb1, known to map to RNO5 or its homolog, mouse Chr 4 (MMU4). Linkage analysis established the gene order (cM distance) as D5Mit11-(19.3)-B-(17.9)-D5Mit13-(19. 2)-Oprd1-(21.5) - (1.2) Gnb1, placing the deafness locus on distal RNO5. The position of the deafness locus on RNO5 is similar to that ofjerker (je) on MMU4; the phenotypes and patterns of inheritance of the deafness mutation and je are also similar. It seems likely that the mutation affects the rat homolog of je. The rat deafness locus should, therefore, be named jerker and assigned the gene symbol Je.

Animals↗
PubMed1996

Identification and genetic mapping of random amplified polymorphic DNA (RAPD) markers to the sheep genome.

The random amplified polymorphic DNA (RAPD) assay utilizes the polymerase chain reaction (PCR) and short primers of arbitrary nucleotide sequence to amplify DNA. In this study, the RAPD assay was used to identify and map polymorphic markers in the AgResearch International Mapping Flock (IMF) sheep pedigrees. Sires and dams of eight of the full-sib IMF pedigrees were screened with 131 different 10-mer oligonucleotide primers. An average of 85 RAPD polymorphisms was identified between each parental pair, and 53 markers were contributed to the AgResearch IMF collaboration. Forty-five of the RAPD markers were mapped in the AgResearch IMF genetic linkage map, and at least one marker was located on 17 of the 26 autosomes and both sex chromosomes. Three lines of evidence were used to check for the homology of scored polymorphisms in different pedigrees, pedigree evaluation, segregation analysis, and Southern blot analysis. These results demonstrate that the RAPD assay is a powerful approach for identifying polymorphisms that can be used as markers for constructing a sheep genetic linkage map.

Animals↗
PubMed1999

BB rat diabetes susceptibility and body weight regulation genes colocalize on chromosome 2.

The genetic etiology of Type 1 (insulin-dependent) diabetes mellitus is complicated by the apparent presence of several diabetes susceptibility genetic regions. Type 1 diabetes in the inbred BioBreeding (BB) rat closely resembles the human disorder and was previously shown to involve two genes: the lymphopenia (lyp) region on Chromosome (Chr) 4 and RT1(u) in the major histocompatibility complex (MHC) on Chr 20. In addition, a segregation analysis of an F(2) intercross between the diabetes-prone congenic BB DR(lyp/lyp, u/u) and F344(+/+,)(lv/lv) rats indicated that at least one more genetic factor was responsible for Type 1 diabetes. In this study, we generated F(2)N(2) progeny in a cross between non-diabetic F(2)(DR(lyp/lyp,u/u) x F344)(lyp/lyp,u/u) and diabetic DR(lyp/lyp, u/u) rats. In a subsequent total genome scan, a third factor was mapped to the 21.3-cM region on Chr 2 between D2Mit14 and D2Mit15 (peak LOD score 4.7 with 67% penetrance). Interestingly, the homozygosity of the BB allele (b/b) for the Chr 2 region was significantly associated with a greater weight reduction after fasting than the homozygosity of the F344 allele (f/f, p < 0.008). In conclusion, the development of Type 1 diabetes in the congenic DR(lyp/lyp) rat is controlled by at least three genes: lymphopenia, MHC, and a third factor that may play a role in metabolism and body weight regulation.

Animals↗
PubMed1999

Characterization and chromosomal mapping of a mouse ortholog of the late-infantile ceroid-lipofuscinosis gene CLN2.

Late-infantile ceroid-lipofuscinosis (CLN2) is an autosomal recessively inherited, neurodegenerative disease in humans. The CLN2 locus has been mapped to Chromosome (Chr) 11p15, and its sequence and genomic organization have recently been reported. In the present study, the cDNA sequence, exon/intron organization, and chromosomal localization of a mouse ortholog of the CLN2 gene are described. The mouse cDNA contains an open reading frame that predicts a protein product of 562 amino acids. The mouse and human coding regions are 86% and 88% identical at the nucleic acid and amino acid levels, respectively. One less codon appears in the mouse cDNA when compared with the human ortholog. The mouse gene (Cln2) spans more than 6 kb and consists of 13 exons separated by introns ranging in size from 111 to 1259 bp. Length polymorphism in an (AC)(n) microsatellite in intron 3 of the mouse Cln2 gene was used to perform segregation analysis with The Jackson Laboratory DNA Panel Mapping Resource. On the basis of this analysis, the Cln2 gene was localized to a region of mouse Chr 7 that corresponds to human Chr 11p15. Characterization of the mouse Cln2 gene will facilitate generation of a mouse model for late-infantile ceroid-lipofuscinosis by gene targeting and identification of functionally important regions of the Cln2 protein.

Amino Acid Sequence↗
PubMed2007

Systemic lupus erythematosus: a genetic epidemiology study of 695 patients from China.

Our purpose was to explore potential genetic models for systemic lupus erythematosus (SLE) and analyze genetic epidemiologic characteristics of SLE in a Chinese population. Data for 695 patients with SLE were obtained by using a uniform questionnaire. Patients, clinical characteristics and their family history were analyzed using software. A complex segregation analysis was conducted to propose potential genetic models for SLE. The mean +/- SD age of onset were 30.2 +/- 10.5 years and mean time to progression to SLE was 32.5 +/- 44.4 months. The most frequent initial manifestations were malar rash (61.3%). During the evolution of the disease, the main clinical features were arthritis in 73.6% of our patients, followed by malar rash (68.1%), and renal involvement (56.7%). As the first symptom, the late-onset group (onset of disease beyond the age of 50 years) less often showed malar rash (45% vs. 63.4% in the early-onset group; p = 0.001). There were no significant differences in the other cumulative clinical symptoms between late-onset and early-onset group, except for a lower prevalence of malar rash, photosensitivity and alopecia and a higher prevalence of mucosal ulcers in the late-onset group. A positive family history of SLE was obtained in 50 patients (7.2%). There were no statistical differences in clinical characteristics between familial SLE and sporadic SLE patients. The heritability of SLE was 43.6%, the genetic model of SLE could be polygenetic model and major gene mode is the best fitted one. SLE could be a multifactorial disease with polygenetic model.

Adolescent↗