scholarly journals Comparison of Eco-Mse and Pst-Mse Primer Combinations in Generating AFLP Map of Tomato

2005 ◽  
Vol 26 ◽  
pp. 27-35 ◽  
Author(s):  
BR Ojha
Keyword(s):  
Chromosome Number ◽  
The Netherlands ◽  
Chromosome 8 ◽  
Chromosome 9 ◽  
Aflp Markers ◽  
Chromosome 1 ◽  
Research Centre ◽  
Back Cross ◽  
Lycopersicon Pennellii ◽  
Key Words Tomato

An experiment was conducted at Wageningen University and Research Centre (WUR), Unifarm, Haarweg, Wageningen, The Netherlands in 2000 to compare Eco-Mse and Pst-Mse primer combinations to generate AFLP markers of tomato. Back cross first (BC1) population ofLycopersicon esculentum cv money maker and Lycopersicon pennellii LA716 was used. Six primer combinations (three of Eco-Mse and three of Pst-Mse) were used. A total of 122 AFLP markers were found generating 76 markers by Eco-Mse primer combination and 46 markers by Pst-Mse primer combination. The average number of informative markers per primer combination was 20.33 ranging from 11 (P11M50) to 36 (E35M48). Similarly the average number of informative markers per chromosome was 10.16 ranging from 4 (chromosome number 8) to 16 (chromosome number 1). Within Eco-Mse primer combinations, E32M50 generated the least (18) and E35M48 generated the highest (36) AFLP markers. Similarly, within Pst-Mse primer combination, P14M50 generated the highest (20) and P11M50 generated the least (11) AFLP markers. The Eco-Mse primer combination generated the highest number of marker (12) in chromosome 9 and the lowest (2) in chromosome number 8. Similarly, the Pst-Mse primer combination generated the highest number of markers (9) in chromosome number 1 and the lowest (2) in chromosome number 3, 8, 11 and 12. The AFLP map spanned 843 cM. The longest AFLP map was found in chromosome 1 and spanned 98 cM and the shortest in chromosome 8 and spanned 46 cM. Key words: Tomato, Back cross, Primer combination, AFLP map J. Inst. Agric. Anim. Sci. 26:27-35 (2005)

scholarly journals Two large reciprocal translocations characterized in the disease resistance-rich burmannica genetic group of Musa acuminata

2019 ◽  
Vol 124 (2) ◽  
pp. 319-329 ◽  
Author(s):  
Marion Dupouy ◽  
Franc-Christophe Baurens ◽  
Paco Derouault ◽  
Catherine Hervouet ◽  
Céline Cardi ◽  
...  
Keyword(s):  
Disease Resistance ◽  
Distal Region ◽  
Musa Acuminata ◽  
Genetic Group ◽  
Chromosome 8 ◽  
Chromosome 9 ◽  
Chromosome 1 ◽  
Reference Sequence ◽  
Whole Genome Sequencing Data ◽  
Reciprocal Translocations

Abstract Background and Aims Banana cultivars are derived from hybridizations involving Musa acuminata subspecies. The latter diverged following geographical isolation in distinct South-east Asian continental regions and islands. Observation of chromosome pairing irregularities in meiosis of hybrids between these subspecies suggested the presence of large chromosomal structural variations. The aim of this study was to characterize such rearrangements. Methods Marker (single nucleotide polymorphism) segregation in a self-progeny of the ‘Calcutta 4’ accession and mate-pair sequencing were used to search for chromosomal rearrangements in comparison with the M. acuminata ssp. malaccensis genome reference sequence. Signature segment junctions of the revealed chromosome structures were identified and searched in whole-genome sequencing data from 123 wild and cultivated Musa accessions. Key Results Two large reciprocal translocations were characterized in the seedy banana M. acuminata ssp. burmannicoides ‘Calcutta 4’ accession. One consisted of an exchange of a 240 kb distal region of chromosome 2 with a 7.2 Mb distal region of chromosome 8. The other involved an exchange of a 20.8 Mb distal region of chromosome 1 with a 11.6 Mb distal region of chromosome 9. Both translocations were found only in wild accessions belonging to the burmannicoides/burmannica/siamea subspecies. Only two of the 87 cultivars analysed displayed the 2/8 translocation, while none displayed the 1/9 translocation. Conclusion Two large reciprocal translocations were identified that probably originated in the burmannica genetic group. Accurate characterization of these translocations should enhance the use of this disease resistance-rich burmannica group in breeding programmes.

Reconsidering Early Detection in Countering Violent Extremism (CVE) by Local Frontline Professionals

Proceedings ◽  
2021 ◽  
Vol 77 (1) ◽  
pp. 12
Author(s):  
Annemarie van de Weert
Keyword(s):  
Early Detection ◽  
The Netherlands ◽  
Political Violence ◽  
Social Innovation ◽  
Early Stage ◽  
Violent Behavior ◽  
Research Centre ◽  
Access To Justice ◽  
Local Approach ◽  
Performative Power

In recent years, the fight against terrorism and political violence has focused more on anticipating the threats that they pose. Therefore, early detection of ideas by local professionals has become an important part of the preventive approach in countering radicalization. Frontline workers who operate in the arteries of society are encouraged to identify processes towards violent behavior at an early stage. To date, however, little is known about how these professionals take on this screening task at their own discretion. Research from the Netherlands suggests that subjective assessment appears to exist. This is due to the absence of a clear norm for preliminary judgments. However, such an approach affects prejudice or administrative arbitrariness, which may cause side effects due to unjustified profiling. The publications about the Dutch case are inspired by the concept of “performativity”, (de Graaf, B., & de Graaff, B. G. J. (2010). Bringing politics back in: The introduction of the ‘performative power’ of counterterrorism. Critical Studies on Terrorism, 3(2), pp. 261–275.) which points to a distinct relationship between the performative power of counterterrorism instruments and the effectiveness of the local approach. Performativity contends that the overall effect of the policy in question is not necessarily determined by the policy measures and their intended results, as such, but more by the way in which they are presented and perceived. This means that, in order to create an equitable approach, governments, whether local or national, should focus more on the actual practice performed by frontline practitioners. The focus on practices is part of a larger project, entitled ‘Gatekeepers of Justice’ (See: https://www.internationalhu.com/research/access-to-justice), by the Research Group Access2Justice (Research Centre of Social Innovation at Utrecht University of Applied Science), led by professor Quirine Eijkman, Deputy President of the Netherlands Institute for Human Rights.

scholarly journals Cloning and Mapping of a Putative Barley NADPH-Dependent HC-Toxin Reductase

1997 ◽  
Vol 10 (2) ◽  
pp. 234-239 ◽  
Author(s):  
F. Han ◽  
A. Kleinhofs ◽  
A. Kilian ◽  
S. E. Ullrich
Keyword(s):  
Plant Species ◽  
Chromosome 9 ◽  
Immature Embryos ◽  
Chromosome 1 ◽  
Grass Species ◽  
Cochliobolus Carbonum ◽  
Wide Range ◽  
Young Leaves ◽  
High Conservation ◽  
Hc Toxin

The NADPH-dependent HC-toxin reductase (HCTR), encoded by Hm1 in maize, inactivates HC-toxin produced by the fungus Cochliobolus carbonum, and thus confers resistance to the pathogen. The fact that C. carbonum only infects maize (Zea mays) and is the only species known to produce HC-toxin raises the question: What are the biological functions of HCTR in other plant species? An HCTR-like enzyme may function to detoxify toxins produced by pathogens which infect other plant species (R. B. Meeley, G. S. Johal, S. E. Briggs, and J. D. Walton, Plant Cell, 4:71–77, 1992). Hm1 homolog in rice (Y. Hihara, M. Umeda, C. Hara, Q. Liu, S. Aotsuka, K. Toriyama, and H. Uchimiya, unpublished) and HCTR activity in barley, wheat, oats and sorghum have been reported (R. B. Meeley and J. D. Walton, Plant Physiol. 97:1080–1086, 1993). To investigate the sequence conservation of Hm1 and HCTR in barley and the possible relationship of barley Hm1 homolog to the known disease resistance genes, we cloned and mapped a barley (Hordeum vulgare) Hm1-like gene. A putative full-length cDNA clone, Bhm1-18, was isolated from a cDNA library consisting of mRNA from young leaves, inflorescences, and immature embryos. This 1,297-bp clone encodes 363 amino acids which show great similarity (81.6%) with the amino acid sequence of HM1 in maize. Two loci were mapped to barley molecular marker linkage maps with Bhm1-18 as the probe; locus A (Bhm1A) on the long arm of chromosome 1, and locus B (Bhm1B) on the short arm of chromosome 1 which is syntenic to maize chromosome 9 containing the Hm2 locus. The Bhm1-18 probe hybridized strongly to a Southern blot of a wide range of grass species, indicating high conservation of HCTR at the DNA sequence level among grasses. The HCTR mRNA was detected in barley roots, leaves, inflorescences, and immature embryos. The conservation of the HCTR sequence, together with its expression in other plant species (R. B. Meeley and J. D. Walton, Plant Physiol. 97:1080–1086, 1993), suggests HCTR plays an important functional role in other plant species.

scholarly journals Specific chromosomal aberrations in polycythemia vera

Blood ◽  
1976 ◽  
Vol 48 (5) ◽  
pp. 687-696 ◽  
Author(s):  
L Zech ◽  
C Gahrton ◽  
D Killander ◽  
S Franzen ◽  
U Haglund
Keyword(s):  
Polycythemia Vera ◽  
Chromosomal Aberrations ◽  
Bone Marrow Cells ◽  
Chromosome Abnormality ◽  
Extra Chromosome ◽  
Acute Myeloblastic Leukemia ◽  
Chromosome 8 ◽  
Chromosome 9 ◽  
The Other ◽  
Chromosome 20

Abstract The chromosomes of bone marrow cells from ten patients with polycythemia vera (PV) were identified by Q-, G-, and C-banding techniques. Four of the patients had received no treatment with cytotoxic drugs, while three had received 32P only and the other three, in addition, had received busulfan or busulfan and procarbazine. One 73- yr-old male patient treated with venesection only for 4 yr lacked the Y chromosome and had a deletion of the long arm of chromosome 20 (20q-) in all cells investigated. One of the other three patients who had received no drugs had a chromosome abnormality, but only in 1 of 19 identifiable metaphases. However, the abnormality was the same (+9) as the most common one in treated patients. In the group of treated patients, an extra chromosome 9 (+9) was found in three patients, an extra chromosome 8 (+8) in one, and a deletion of the long arm of one chromosome 20 (20q-) in one patient. Multiple aberrations in addition to the extra chromosome 9 were found in one patient in whom the disease had transformed into acute myeloblastic leukemia. The finding of identical chromosomal aberrations (20q- and +9, respectively) in two patients who had received no drugs and in four patients who had received 32P and busulfan or procarbazine favors the view that these aberrations are specifically associated with the disease and not induced by the drugs. With the exception of the patient with acute myeloblastic leukemia, all other patients are alive 1–11 mo after chromosome analyses and 1–229 mo after diagnosis.

scholarly journals Genetic dissection of canine hip dysplasia phenotypes and osteoarthritis reveals three novel loci

BMC Genomics ◽  
2019 ◽  
Vol 20 (1) ◽  
Author(s):  
Lea Mikkola ◽  
Saila Holopainen ◽  
Tiina Pessa-Morikawa ◽  
Anu K. Lappalainen ◽  
Marjo K. Hytönen ◽  
...  
Keyword(s):  
Hip Dysplasia ◽  
Cartilage Degradation ◽  
Chromosome 9 ◽  
Chromosome 1 ◽  
Severe Dysplasia ◽  
Genetic Dissection ◽  
Genes Encoding ◽  
Joint Incongruity ◽  
Canine Hip Dysplasia ◽  
Norberg Angle

Abstract Background Hip dysplasia and osteoarthritis continue to be prevalent problems in veterinary and human medicine. Canine hip dysplasia is particularly problematic as it massively affects several large-sized breeds and can cause a severe impairment of the quality of life. In Finland, the complex condition is categorized to five classes from normal to severe dysplasia, but the categorization includes several sub-traits: congruity of the joint, Norberg angle, subluxation degree of the joint, shape and depth of the acetabulum, and osteoarthritis. Hip dysplasia and osteoarthritis have been proposed to have separate genetic etiologies. Results Using Fédération Cynologique Internationale -standardized ventrodorsal radiographs, German shepherds were rigorously phenotyped for osteoarthritis, and for joint incongruity by Norberg angle and femoral head center position in relation to dorsal acetabular edge. The affected dogs were categorized into mild, moderate and severe dysplastic phenotypes using official hip scores. Three different genome-wide significant loci were uncovered. The strongest candidate genes for hip joint incongruity were noggin (NOG), a bone and joint developmental gene on chromosome 9, and nanos C2HC-type zinc finger 1 (NANOS1), a regulator of matrix metalloproteinase 14 (MMP14) on chromosome 28. Osteoarthritis mapped to a long intergenic region on chromosome 1, between genes encoding for NADPH oxidase 3 (NOX3), an intriguing candidate for articular cartilage degradation, and AT-rich interactive domain 1B (ARID1B) that has been previously linked to joint laxity. Conclusions Our findings highlight the complexity of canine hip dysplasia phenotypes. In particular, the results of this study point to the potential involvement of specific and partially distinct loci and genes or pathways in the development of incongruity, mild dysplasia, moderate-to-severe dysplasia and osteoarthritis of canine hip joints. Further studies should unravel the unique and common mechanisms for the various sub-traits.

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.

Combined aCGH and Mutational Analysis of CLL Patients with 17p Deletion.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 2091-2091
Author(s):  
Hannah C. Rudenko ◽  
Vasantha Brito-Babapulle ◽  
David Gonzalez ◽  
Pilar Martinez ◽  
Paola E. Leone ◽  
...  
Keyword(s):  
Clinical Outcome ◽  
Mutational Analysis ◽  
Survival Curve ◽  
Progression Free Survival ◽  
Tp53 Gene ◽  
Chromosome 9 ◽  
Research Centre ◽  
Genomic Changes ◽  
Mutational Status ◽  
Trisomy 12

Abstract We have utilised aCGH (Breakthrough Breast Cancer Research Centre 5.8K array) and mutational analysis of the TP53 gene (exons 4–10) on 74 cases of CLL to define the extent of deletion at 17p, TP53 mutational status, additional genomic changes, and how this affects clinical outcome. 17p- cases were selected by FISH (n=37, Vysis LSI P53 probe) and 37 cases were selected as being representative of the survival curve of CLL patients without 17p-. FISH identified 22 cases with TP53- in ≥ 50% of cells, 4 cases with TP53- 20–50% and 11 cases with TP53- ≤ 20%. aCGH can detect abnormalities present in >50% of cells and all of the TP53- cases greater than 50% by FISH were detected with deletion ranging between 6-20Mb in length, the majority encompassing the entire p-arm. In addition aCGH detected deletion of 17p in 5/15 cases with TP53- <50%, and 2/37 with no detectable TP53- by FISH, these deletions clustered at 17p13.3 and 17p11.2, and did not involve the TP53 gene. Cases with 17p- >20% have a poor clinical outcome (median survival 11 months, median progression free survival 3 months), the majority of these (85%) also have a mutation of TP53 whereas in cases with ≤ 20% 17p- only 10% were mutated. The 17p- group was characterised by additional recurrent deletions involving 18p, 20p and 22q, which tended to occur as single additional events. Understanding the order in which these events occur is important, 18p- was found in 6 cases, 2 of which had <50% 17p- by FISH, suggesting that 18p- is present in a higher percentage of cells and by implication occurs prior to the 17p deletion, a similar finding was also present for the 20p- cases. 18p deletion varied in length between 5.9Mb and 12Mb, with the minimally deleted region (MDR) involving a 2.5Mb region spanning 18p11.23-p11.22. 20p- was found in 8 cases of which 3 covered almost the entire p-arm, and 5 formed 2 clusters at each end of the p-arm. 22q- was found in 8 cases, with only 1 outside of the 17p- group. Out of these 8 cases with deletion, 6 covered almost the complete q-arm but a MDR was difficult to define, however if the non-17p- case is excluded the MDR covers 1.4Mb at 22q12.3. Recurrent abnormalities were also found on other chromosomes, but did not differ between the two groups. These included regions with previously identified abnormalities; trisomy 12 (n=11), loss of 6q14.1–24.3 (n=11), loss of 11q12.1–25 (n=17) and loss of 13q12.1–21.1 (n=6) as well as detection of novel abnormalities; gain of 4p16.3–16.1 (n=23), gain of 11p15.5–15.3 (n=22), gain of 22q11.21–13.33 (n=22) and deletions on chromosome 9 (n=9). These results show that deletion of TP53 and mutation of the other allele are critical adverse prognostic factors. We have also defined a genetic background (18p-, 20p- and 22q-) on which these changes arise.

Albinistic common seals (Phoca vitulina) and melanistic grey seals (Halichoerus grypus) rehabilitated in the Netherlands

2010 ◽  
Vol 60 (3) ◽  
pp. 273-281 ◽  
Author(s):  
Nynke Osinga ◽  
Pieter 't Hart ◽  
Pieter van Voorst Vader
Keyword(s):  
The Netherlands ◽  
North Sea ◽  
Phoca Vitulina ◽  
Research Centre ◽  
Halichoerus Grypus ◽  
Normal Behaviour ◽  
Delta Area ◽  
The North ◽  
The North Sea ◽  
Photophobic Reaction

AbstractThe Seal Rehabilitation and Research Centre (SRRC) in Pieterburen, The Netherlands, rehabilitates seals from the waters of the Wadden Sea, North Sea and Southwest Delta area. Incidental observations of albinism and melanism in common and grey seals are known from countries surrounding the North Sea. However, observations on colour aberrations have not been systematically recorded. To obtain the frequency of occurrence of these colour aberrations, we analysed data of all seals admitted to our centre over the past 38 years. In the period 1971-2008, 3000 common seals (Phoca vitulina) were rehabilitated, as well as 1200 grey seals (Halichoerus grypus). A total of five albinistic common seals and four melanistic grey seals were identified. This results in an estimated incidence of albinism in common seals of approximately 1/600, and of melanism in grey seals of approximately 1/300. The seals displayed normal behaviour, although in the albinistic animals, a photophobic reaction was observed in daylight.

scholarly journals Specific chromosomal aberrations in polycythemia vera

Blood ◽  
1976 ◽  
Vol 48 (5) ◽  
pp. 687-696 ◽  
Author(s):  
L Zech ◽  
C Gahrton ◽  
D Killander ◽  
S Franzen ◽  
U Haglund
Keyword(s):  
Polycythemia Vera ◽  
Chromosomal Aberrations ◽  
Bone Marrow Cells ◽  
Chromosome Abnormality ◽  
Extra Chromosome ◽  
Acute Myeloblastic Leukemia ◽  
Chromosome 8 ◽  
Chromosome 9 ◽  
The Other ◽  
Chromosome 20

The chromosomes of bone marrow cells from ten patients with polycythemia vera (PV) were identified by Q-, G-, and C-banding techniques. Four of the patients had received no treatment with cytotoxic drugs, while three had received 32P only and the other three, in addition, had received busulfan or busulfan and procarbazine. One 73- yr-old male patient treated with venesection only for 4 yr lacked the Y chromosome and had a deletion of the long arm of chromosome 20 (20q-) in all cells investigated. One of the other three patients who had received no drugs had a chromosome abnormality, but only in 1 of 19 identifiable metaphases. However, the abnormality was the same (+9) as the most common one in treated patients. In the group of treated patients, an extra chromosome 9 (+9) was found in three patients, an extra chromosome 8 (+8) in one, and a deletion of the long arm of one chromosome 20 (20q-) in one patient. Multiple aberrations in addition to the extra chromosome 9 were found in one patient in whom the disease had transformed into acute myeloblastic leukemia. The finding of identical chromosomal aberrations (20q- and +9, respectively) in two patients who had received no drugs and in four patients who had received 32P and busulfan or procarbazine favors the view that these aberrations are specifically associated with the disease and not induced by the drugs. With the exception of the patient with acute myeloblastic leukemia, all other patients are alive 1–11 mo after chromosome analyses and 1–229 mo after diagnosis.

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