Prospects for introgressing tomato chromosomes into the potato genome: An assessment through GISH analysis

Genome ◽  
1999 ◽  
Vol 42 (2) ◽  
pp. 282-288 ◽  
Author(s):  
F Garriga-Calderé ◽  
D J Huigen ◽  
E Jacobsen ◽  
M S Ramanna
Keyword(s):  
Low Frequency ◽  
Chromosome 8 ◽  
Chromosome 1 ◽  
Crossing Over ◽  
Homoeologous Pairing ◽  
Potato Genome ◽  
Somatic Fusion ◽  
Tomato Chromosome ◽  
Genomic In Situ Hybridisation ◽  
Monosomic Addition

With a view to assess the possibility of homoeologous pairing and crossing-over between the chromosomes of potato (Solanum tuberosum) and tomato (Lycopersicon esculentum), a somatic fusion hybrid and two monosomic alien tomato addition genotypes were investigated through genomic in situ hybridisation (GISH). The somatic fusion hybrid, C31-17-51, was near hexaploid (2n = 6x - 4 = 68) possessing 46 potato chromosomes + 20 tomato chromosomes + 2 translocated chromosomes. The two alien addition genotypes were near tetraploids (2n = 4x + 1 = 49) and consisted of monosomic alien additions for tomato chromosome 1 in genotype 2103-1, and tomato chromosome 8 in genotype 2301-2. In the fusion hybrid the tomato pachytene chromosome identification revealed that the chromosomes 1, 2, 5, 6, 7, 10, and 12 were in diploid condition whereas among those that were in haploid condition, three could be identified viz., 4, 9, and 11. The remaining three chromosomes could not be cytologically identified. Although the chromosomes with translocated segments could not be identified at the pachytene stage due to technical difficulties, there was clear evidence for the presence of a reciprocal translocation observed at diakinesis and metaphase I stages. Because of autosyndetic pairing of the translocated segments, it gave a false impression as if there was a high frequency (86.0%) of allosyndetic pairing. In contrast to the fusion hybrid, the two alien monosomic addition genotypes showed a very low frequency of allosyndetic pairing, namely 1.1 and 1.3% respectively for the monosomic additions 1 and 8. In the genotype 2301-2, monosomic addition for tomato chromosome 8, crossing-over between the homoeologous chromosomes was estimated to occur in 0.8% of the meiotic cells investigated. Despite this low frequency of homoeologous pairing and crossing-over, there is a possibility for introgressing tomato chromosomal DNA into the potato genome through intergenomic recombination.Key words: Solanum, Lycopersicon, chromosome additions, GISH, introgression.

DETERMINATION OF BREAKPOINT POSITIONS IN BARLEY TRANSLOCATIONS BY KARYOTYPE ANALYSIS OF PERMANENT RINGS OF SIX CHROMOSOMES

1974 ◽  
Vol 16 (3) ◽  
pp. 539-548 ◽  
Author(s):  
N. A. Tuleen ◽  
J. H. Gardenhire
Keyword(s):  
Karyotype Analysis ◽  
Chromosome 1 ◽  
Crossing Over ◽  
Differential Segment

Five T1-5 and 10 T1-6 barley translocations were crossed with the translocation T1-7f. Plants in which the T1-5 and T1-6 translocations had been combined with T1-7f due to crossing over in the differential segment were selected in the F2 generation. One of the chromosomes present in plants carrying the translocations in the combined form is made up of parts of the three chromosomes involved in the two translocations, and the segmental arrangement of this tripartite chromosome is determined by the position of the breakpoints in chromosome 1. The karyotypes of these stocks were analyzed and the breakpoints in seven of the translocations were assigned to the same arm and eight to the opposite arm of chromosome 1 relative to the position of the breakpoint in T1-7f.

scholarly journals The M26 Hotspot of Schizosaccharomyces pombe Stimulates Meiotic Ectopic Recombination and Chromosomal Rearrangements

Genetics ◽  
1998 ◽  
Vol 149 (3) ◽  
pp. 1191-1204 ◽  
Author(s):  
Jeffrey B Virgin ◽  
Jeffrey P Bailey
Keyword(s):  
Homologous Recombination ◽  
Schizosaccharomyces Pombe ◽  
Dna Sequences ◽  
Chromosomal Rearrangements ◽  
Low Frequency ◽  
Repeated Sequences ◽  
Crossing Over ◽  
Ectopic Recombination ◽  
Recombination Hotspots ◽  
Integration Sites

Abstract Homologous recombination is increased during meiosis between DNA sequences at the same chromosomal position (allelic recombination) and at different chromosomal positions (ectopic recombination). Recombination hotspots are important elements in controlling meiotic allelic recombination. We have used artificially dispersed copies of the ade6 gene in Schizosaccharomyces pombe to study hotspot activity in meiotic ectopic recombination. Ectopic recombination was reduced 10–1000-fold relative to allelic recombination, and was similar to the low frequency of ectopic recombination between naturally repeated sequences in S. pombe. The M26 hotspot was active in ectopic recombination in some, but not all, integration sites, with the same pattern of activity and inactivity in ectopic and allelic recombination. Crossing over in ectopic recombination, resulting in chromosomal rearrangements, was associated with 35–60% of recombination events and was stimulated 12-fold by M26. These results suggest overlap in the mechanisms of ectopic and allelic recombination and indicate that hotspots can stimulate chromosomal rearrangements.

scholarly journals Genome-wide analysis of over 106 000 individuals identifies 9 neuroticism-associated loci

2016 ◽  
Vol 21 (6) ◽  
pp. 749-757 ◽  
Author(s):  
D J Smith ◽  
V Escott-Price ◽  
G Davies ◽  
M E S Bailey ◽  
L Colodro-Conde ◽  
...  
Keyword(s):  
Medical Research ◽  
Genetic Correlation ◽  
Meta Analysis ◽  
Small Sample ◽  
Chromosome 8 ◽  
Chromosome 17 ◽  
Chromosome 1 ◽  
Eysenck Personality Questionnaire ◽  
Uk Biobank ◽  
Genome Wide

Abstract Neuroticism is a personality trait of fundamental importance for psychological well-being and public health. It is strongly associated with major depressive disorder (MDD) and several other psychiatric conditions. Although neuroticism is heritable, attempts to identify the alleles involved in previous studies have been limited by relatively small sample sizes. Here we report a combined meta-analysis of genome-wide association study (GWAS) of neuroticism that includes 91 370 participants from the UK Biobank cohort, 6659 participants from the Generation Scotland: Scottish Family Health Study (GS:SFHS) and 8687 participants from a QIMR (Queensland Institute of Medical Research) Berghofer Medical Research Institute (QIMR) cohort. All participants were assessed using the same neuroticism instrument, the Eysenck Personality Questionnaire-Revised (EPQ-R-S) Short Form’s Neuroticism scale. We found a single-nucleotide polymorphism-based heritability estimate for neuroticism of ∼15% (s.e.=0.7%). Meta-analysis identified nine novel loci associated with neuroticism. The strongest evidence for association was at a locus on chromosome 8 (P=1.5 × 10−15) spanning 4 Mb and containing at least 36 genes. Other associated loci included interesting candidate genes on chromosome 1 (GRIK3 (glutamate receptor ionotropic kainate 3)), chromosome 4 (KLHL2 (Kelch-like protein 2)), chromosome 17 (CRHR1 (corticotropin-releasing hormone receptor 1) and MAPT (microtubule-associated protein Tau)) and on chromosome 18 (CELF4 (CUGBP elav-like family member 4)). We found no evidence for genetic differences in the common allelic architecture of neuroticism by sex. By comparing our findings with those of the Psychiatric Genetics Consortia, we identified a strong genetic correlation between neuroticism and MDD and a less strong but significant genetic correlation with schizophrenia, although not with bipolar disorder. Polygenic risk scores derived from the primary UK Biobank sample captured ∼1% of the variance in neuroticism in the GS:SFHS and QIMR samples, although most of the genome-wide significant alleles identified within a UK Biobank-only GWAS of neuroticism were not independently replicated within these cohorts. The identification of nine novel neuroticism-associated loci will drive forward future work on the neurobiology of neuroticism and related phenotypes.

Cytology of triploid and pentaploid hybrids of Elymus trachycaulus × Pseudoroegneria spicata and P. spicata ssp. inermis

Genome ◽  
1987 ◽  
Vol 29 (3) ◽  
pp. 470-480 ◽  
Author(s):  
Taing Aung ◽  
P. D. Walton
Keyword(s):  
Low Frequency ◽  
Plant Size ◽  
Double Dose ◽  
Homoeologous Pairing ◽  
Pseudoroegneria Spicata ◽  
Elymus Trachycaulus ◽  
Chromosome Associations ◽  
Size Variability ◽  
High Degree ◽  
Very High

Emasculated clones of tetraploid and octaploid Elymus trachycaulus crossed with Pseudoroegneria spicata yielded 69 triploids and 13 pentaploid hybrids. The triploid hybrids were morphologically intermediate between the parental species but the pentaploid hybrids resembled E. trachycaulus more closely than P. spicata. A very high degree of plant size variability (very weak to very vigorous) was observed among the 50 triploids that survived to maturity. The variability among the pentaploids, though apparent, was not high. Mean chromosome associations among the selected eight triploids varied from low multivalent formation at meiosis (7.60 I + 6.18 II + 0.24 III + 0.08 IV) to high multivalent-forming meiosis (7.28 I + 5.66 II + 0.32 III + 0.36 IV). The bivalent configurations in these triploids were attributed to homoeologous pairing between the S1 genome of P. spicata and S genomes of E. trachycaulus and the multivalents indicated intergenomal and intragenomal pairings. Mean chromosome associations of 5.22 I + 11.94 II + 1.97 III in 78.7% and 7 I + 14 II in 21.3% of the 150 cells were distributed among the three pentaploid hybrids. The low frequency of trivalents and the absence of multivalents higher than trivalent configurations suggest that homoeologous pairing was substantially reduced and there was no intergenomal and intragenomal pairing in these 2n = 35 x hybrids. Fourteen triploids and three pentaploid hybrids were produced from 4x and 8x forms of E. trachycaulus and P. spicata spp. inermis crosses. The triploids were intermediate between the parents but the pentaploids were more similar to E. trachycaulus. Mean chromosome associations in the triploids (6.020 I + 5.315 II + 0.554 III + 0.235 IV + 0.250 V + 0.048 VI + 0.03 VII) and in the pentaploids (3.50 I + 10.18 II + 3.54 III + 0.13 IV) indicated a very high degree of intergenomal and intragenomal pairing in the triploids; nevertheless, it was greatly reduced in the pentaploids. The Pseudoroegneria spicata ssp. inermis genome may have gene(s) that affect a high degree of intergenomal and intragenomal pairing in triploid hybrids with E. trachycaulus. However, in pentaploid hybrids (SS HH S2) the S and H genomes of E. trachycaulus in double dose seem to have restored its regular meiotic bahaviour, at least partially, and reduced homoeologous pairing as well as intergenomal and intragenomal pairing. Key words: Elymus trachycaulus, Pseudoroegneria spicata, regular meiotic behaviour, double dose, intergenomal pairing, intragenomal pairing.

scholarly journals An Induced Mutation in HvRECQL4 Increases the Overall Recombination and Restores Fertility in a Barley HvMLH3 Mutant Background

2021 ◽  
Vol 12 ◽  
Author(s):  
Mikel Arrieta ◽  
Malcolm Macaulay ◽  
Isabelle Colas ◽  
Miriam Schreiber ◽  
Paul D. Shaw ◽  
...  
Keyword(s):  
Crop Improvement ◽  
Low Frequency ◽  
Crossing Over ◽  
Target Sequence ◽  
Helicase Domain ◽  
Dna Mismatch ◽  
Complete Restoration ◽  
Dna Mismatch Repair Genes ◽  
Restoration Of Fertility

Plant breeding relies on the meiotic recombination or crossing over to generate the new combinations of the alleles along and among the chromosomes. However, crossing over is constrained in the crops such as barley by a combination of the low frequency and biased distribution. In this study, we attempted to identify the genes that limit the recombination by performing a suppressor screen for the restoration of fertility to the semi-fertile barley mutant desynaptic10 (des10), carrying a mutation in the barley ortholog of MutL-Homolog 3 (HvMLH3), a member of the MutL-homolog (MLH) family of DNA mismatch repair genes. des10 mutants exhibit reduced recombination and fewer chiasmata, resulting in the loss of obligate crossovers (COs) leading to chromosome mis-segregation. We identified several candidate suppressor lines and confirmed their restored fertility in an Hvmlh3 background in the subsequent generations. We focus on one of the candidate suppressor lines, SuppLine2099, which showed the most complete restoration of fertility. We characterized this line by using a target-sequence enrichment and sequencing (TENSEQ) capture array representing barley orthologs of 46 meiotic genes. We found that SuppLine2099 contained a C/T change in the anti-CO gene RecQ-like helicase 4 (RECQL4) resulting in the substitution of a non-polar glycine to a polar aspartic acid (G700D) amino acid in the conserved helicase domain. Single nucleotide polymorphism (SNP) genotyping of F3 populations revealed a significant increase in the recombination frequency in lines with Hvrecql4 in the Hvmlh3 background that was associated with the restoration of fertility. The genotyping also indicated that there was nearly double the recombination levels in homozygous Hvrecql4 lines compared to the wild type (WT). However, we did not observe any significant change in the distribution of CO events. Our results confirm the anti-CO role of RECQL4 in a large genome cereal and establish the possibility of testing the utility of increasing recombination in the context of traditional crop improvement.

scholarly journals A gene regulatory network for tiller development mediated by Tin8 in maize

2021 ◽  
Author(s):  
Zhelong Lin ◽  
Leina Zhou ◽  
Shuyang Zhong ◽  
Xiaojian Fang ◽  
Hangqin Liu ◽  
...  
Keyword(s):  
Gene Regulatory Network ◽  
Strong Interaction ◽  
Regulatory Network ◽  
Tiller Number ◽  
Chromosome 8 ◽  
Chromosome 1 ◽  
Rna Seq ◽  
Hormonal Responses ◽  
Gene Regulatory ◽  
Tiller Bud

Abstract The complex gene regulatory network underlying maize tiller development remains largely unknown. Here we identified two major quantitative trait loci (QTLs) for tiller number, Tin8 on chromosome 8 and the previously known Tb1 on chromosome 1, in a population derived from a teosinte–maize cross. Map-based cloning and association mapping revealed that Tin8 corresponding to Zcn8 encoding a PEBP-related kinase, is down-regulated in transcription and thus results in decreased tiller number. Strong interaction between Tin8 and the key gen Tb1 was detected for tiller number. Further RNA-seq analysis showed that the expressions of 13 genes related to tiller development were controlled by Tin8. Our results support the existence of a complex gene regulatory network for the outgrowth of maize tiller bud, in which Zcn8 controls 13 tiller-related genes including four genes for hormonal responses. Especially, Zcn8 represses Gt1, D14 and Tru1, through the interaction of Tb1.

Recurrent Additional Genetic Aberrations and a Novel Mechanism of CBFB-MYH11-Rearrangement in AML M4eo Are Detected Using High-Resolution Genome-Wide Single Nucleotide Polymorphisms (SNPs) Microarrays

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 3115-3115
Author(s):  
Alexander Kohlmann ◽  
Sonja Rauhut ◽  
Frank Dicker ◽  
Susanne Schnittger ◽  
Wolfgang Kern ◽  
...  
Keyword(s):  
Copy Number ◽  
Chromosome Banding ◽  
Fusion Gene ◽  
Physical Map ◽  
Snp Array ◽  
Chromosome 8 ◽  
Chromosome 1 ◽  
Banding Analysis ◽  
Chromosome Banding Analysis ◽  
7Q Deletion

Abstract Leukemia specific fusion genes such as CBFB-MYH11 play a major role in the pathogenesis of distinct AML entities. However, additional genetic aberrations seem necessary for the development of full blown leukemia. This study was performed to decipher CBFB-MYH11 rearrangements and their accompanying genetic lesions at the molecular level. Therefore, Affymetrix SNP Array 6.0 analyses, featuring >1.8 million markers for genetic variation (>906,600 SNPs and >946,000 probes for the detection of copy number variations), were performed in 35 newly diagnosed AML with inv(16) (p13q22) or t(16;16)(p13;q22) and CBFB-MYH11-rearrangement. First, as a proof of principle, additional gains and losses of chromosomal material as observed by cytogenetics were also detected by the SNP technology. This included gains of whole chromosome 8 (n=7) and 22 (n=8). In addition, a partial trisomy 13 and a partial trisomy 6 resulting from an unbalanced translocation were confirmed. In two cases a 7q deletion was observed by chromosome banding analysis. One of these was missed by SNP array as the 7q deletion occurred in a subclone only (11% of cells with 7q deletion as determined by interphase FISH). However, SNP array analyses detected loss of 7q in two additional cases which was missed by cytogenetics. Based on SNP array data the commonly deleted region was identified to range from 7q36.1 to 7q36.3 (size: 8.5 MB; physical map position 147,549,804–156,038,680). In addition to a gain of the whole chromosome 8, frequently observed as an additional aberration, in one case SNP array analyses revealed only a partial gain on 8q ranging from 8q24.13 to 8q24.3 (size: 25.3 MB; physical map position 120,986,982–146,268,936). Furthermore, a recurrent deletion (n=2) on chromosome 18 was detected by SNP array but not detected by cytogenetics. The commonly deleted region was localized in 18q23 (size: 3.1 MB; physical map position 72,481,657–75,604,994). In two cases the CBFB-MYH11 rearrangement was cryptic and could not be detected by chromosome banding analysis or FISH using two probes flanking the breakpoints within the CBFB gene, however, a CBFB-MYH11 transcript was amplified by RT-PCR. In one of these cases SNP array data revealed a small gain on 16p13 including 3′ part of the MYH11 gene (size: 71 kb; physical map position 15,654,558–15,725,636) suggesting the insertion of additional 3′ MYH11 sequences into the CBFB rearrangement leading to a CBFB-MYH11 fusion gene. Interestingly, four cases showed a deletion on 16p13 (sizes: 176 kb, 461 kb, 464 kb, 468 kb; physical map positions 15,729,932–15,906,308, 15,726,920–16,188,116, 15,725,663–16,189,984, 15,721,133–16,189,807). All included the 5′ part of the MYH11 gene, and in 3 cases, the ABCC1 gene (multidrug resistance-associated protein 1) was included in the deleted region, which could have an impact on prognosis. The patient with the smallest deletion in 16p13 also showed a deletion on 16q22 including the ′ part of CBFB (size: 35 kb, physical map position 65,672,864–65,707,954). This would be in line with findings in chronic myeloid leukemia where comparable small deletions in the breakpoint region of BCR and ABL have been described. Furthermore, large regions of copy-neutral loss of heterozygosity were observed for the whole short arm of chromosome 1 in two cases, for 17q12 to 17qter and 19q in one case each. In conclusion, a novel mechanism leading to a CBFB-MYH11 fusion gene was identified: A cytogenetically cryptic insertion of additional MYH11 sequences into the CBFB locus. A distinct pattern of additional aberrations was confirmed showing gains of whole chromosomes 8 and 22. Small copy number changes not observable in chromosome banding analysis were detected on 7q, 8q and 18q. A recurrent region of loss of heterozygosity without copy number change was found for the whole short arm of chromosome 1 suggesting that candidate genes in this region are mutated and potentially play a pathogenetic role in AML with CBFB-MYH11-rearrangement.

scholarly journals Hitchhiking and Selective Sweeps of Plasmodium falciparum Sulfadoxine and Pyrimethamine Resistance Alleles in a Population from Central Africa

2008 ◽  
Vol 52 (11) ◽  
pp. 4089-4097 ◽  
Author(s):  
Andrea M. McCollum ◽  
Leonardo K. Basco ◽  
Rachida Tahar ◽  
Venkatachalam Udhayakumar ◽  
Ananias A. Escalante
Keyword(s):  
Plasmodium Falciparum ◽  
Selective Sweep ◽  
Point Mutations ◽  
Central Africa ◽  
Low Frequency ◽  
Population Based ◽  
Chromosome 8 ◽  
Drug Selection ◽  
Triple Mutant ◽  
Parasite Populations

ABSTRACT Sulfadoxine-pyrimethamine (SP) resistance in Plasmodium falciparum is encoded by a number of mutations in the dihydrofolate reductase (dhfr) and dihydropteroate synthetase (dhps) genes. Here, we have characterized point mutations in dhfr and dhps and microsatellite loci around dhfr on chromosome 4 and dhps on chromosome 8 as well as neutral markers on chromosomes 2 and 3 in 332 samples from Yaoundé, Cameroon. The triple mutant dhfr haplotype that originated in Southeast Asia is the most predominant in this sample set, but we also find additional independent haplotypes at low frequency and an incipient process of genetic differentiation among alleles of Southeast Asian origin. As reported for other African populations, we find evidence of a selective sweep for resistant dhfr mutants in this Cameroonian population due to drug selection. Although we find evidence for a selective sweep in dhps mutants associated with SP resistance, the dynamics of dhps mutants appear different than those observed for dhfr mutants. Overall, our results yield support for the use of microsatellite markers to track resistant parasites; however, the detection of resistant dhfr alleles in low frequency, the evidence of divergence among dhfr alleles that share a common evolutionary origin, and the distinct dynamics of resistant dhps alleles emphasize the importance of comprehensive, population-based investigations to evaluate the effects of drug selection on parasite populations.

scholarly journals Genetic Analysis of the Hypothalamic Corticotropin-Releasing Factor System

Endocrinology ◽  
2005 ◽  
Vol 146 (5) ◽  
pp. 2362-2368 ◽  
Author(s):  
Steven J. Garlow ◽  
Ericka Boone ◽  
Wei Li ◽  
Michael J. Owens ◽  
Charles B. Nemeroff
Keyword(s):  
Binding Protein ◽  
Transcript Abundance ◽  
Interval Mapping ◽  
Chromosome 8 ◽  
Chromosome 7 ◽  
Chromosome 1 ◽  
Chromosome 12 ◽  
Potential Candidate ◽  
Chromosome 13 ◽  
Crf System

Abstract The goal of this study was to use BxD recombinant inbred mice to search for genes that control the hypothalamic corticotrophin-releasing factor (CRF) system. The specific phenotype that was measured was abundance of transcripts that encode CRF, CRF receptor (Crf-R1), CRF binding protein, and arginine vasopressin (AVP) in total hypothalamic RNA. The strain distribution patterns for the transcript abundances for each target were continuously distributed, consistent with these being quantitative traits. Marker regression and interval mapping revealed associations with quantitative trait loci (QTL) for CRF transcript abundance on chromosome 1 (at 89.2 cM), chromosome 12 (between 54–58 cM), and chromosome 13 (between 26–30 cM); for Crf-R1 transcript abundance on chromosome 7 (at 1.5 cM), chromosome 12 (at 37 cM), and chromosome X (at 30 cM); for CRF binding protein transcript abundance on chromosome 7 (at 48.5 cM), chromosome 8 (at 65 cM), and chromosome 12 (at 19 cM); and for AVP transcript abundance on chromosome 7 (at 1 cM), chromosome 12 (at 13 cM), and chromosome 13 (at 45 cM). The transcript abundance QTL were not linked to their respective structural genes. Interval mapping on chromosome 7 reveals substantial overlap between QTL that control AVP and Crf-R1 transcript abundance and on chromosome 12 for QTL that control CRF and Crf-R1, which may indicate loci that coordinate regulation of the CRF system. There are QTL for all four targets on chromosome 12. There are a number of neurodevelopmental genes in very close proximity to the transcript abundance QTL that are potential candidate genes.

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