The cosmid CSSM25 assigns syntenic group U2 to bovine Chromosome 9 and is localized to ovine Chromosome 8

1995 ◽  
Vol 6 (8) ◽  
pp. 529-531 ◽  
Author(s):  
S. E. Johnson ◽  
S. S. Moore ◽  
R. MacKinnon ◽  
D. J. S. Hetzel ◽  
W. Barendse
Keyword(s):  
Bovine Chromosome ◽  
Chromosome 8 ◽  
Chromosome 9 ◽  
Syntenic Group

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 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.

A t(8;21) Fusion Protein Disrupts the Spindle Checkpoint and Promotes Aneuploidy.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 1345-1345
Author(s):  
Anita Boyapati ◽  
Luke F. Peterson ◽  
Ming Yan ◽  
Michelle M. Le Beau ◽  
Dong-Er Zhang
Keyword(s):  
Fusion Protein ◽  
Sex Chromosome ◽  
Chromosomal Abnormalities ◽  
Spindle Checkpoint ◽  
Full Length ◽  
Chromosome 8 ◽  
Chromosome 9 ◽  
Chromosome 21 ◽  
Chromosome Loss ◽  
Truncated Form

Abstract The 8;21 translocation occurs in approximately 8% of patients with acute myeloid leukemia. This chromosomal lesion results in the fusion of the AML1 (RUNX1) gene on chromosome 21 to the ETO (MTG8) gene on chromosome 8 and generates the AML1-ETO fusion protein. We identified a truncated form of AML1-ETO which lacks approximately 200 amino acids at the C-terminus of full length AML1-ETO and strongly induces leukemia development (Yan et al, PNAS101(49): 17186–91, 2004). This protein is almost identical to a natural splice form of AML1-ETO designated AML1-ETO9a, which is expressed in t(8;21) patients. To study the leukemogenic properties of the truncated form of AML1-ETO (AEtr), we examined cell cycle profiles to compare it to full length AML1-ETO. In contrast to full length AML1-ETO which induced growth arrest of K562 cells, AEtr did not inhibit cell proliferation. Interestingly, AEtr expressing cells continued to proliferate in the presence of microtubule toxins that normally activate the spindle checkpoint and arrest cells in prometaphase of mitosis. Evaluation of critical components of the spindle checkpoint revealed a significant decrease in BubR1 protein in AEtr cells compared to vector control cells. BubR1 is a potent inhibitor of the anaphase promoting complex and reduction of BubR1 by either siRNA approaches or gene deletion in mice results in aneuploidy. Cytogenetic analyses of leukemic splenocytes from mice transplanted with AEtr cells identified multiple chromosomal abnormalities, including chromosome loss and gain as well as translocations. Observations of chromosomal alterations in t(8;21) patients have been well documented and include loss of either sex chromosome in 70% of patients, deletions of chromosome 9, and trisomy 8. These results indicate that inactivation of the spindle checkpoint through BubR1 reduction may be an important event in the development of t(8;21) leukemias.

Integrative Analysis of Genomic Aberration and Gene Expression Suggests That MPD with Loss of Heterozygosity or Gain of Chromosome 9 Represents a Distinct Entity

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 3735-3735
Author(s):  
Weijia Zhang ◽  
Benjamin L. Ebert ◽  
Windy Berkofsky-Fessler ◽  
Monica Buzzai ◽  
Yezhou Sun ◽  
...  
Keyword(s):  
Gene Expression ◽  
Genomic Instability ◽  
Loss Of Heterozygosity ◽  
Copy Number ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Chromosome 8 ◽  
Chromosome 9 ◽  
Chromosomal Anomalies ◽  
Multiple Testing Correction

Abstract Polycythemia vera (PV), essential thrombocythemia (ET) and idiopathic myelofibrosis (IMF) can all be associated with the JAK2V617F gain of function mutation. MPDs are also associated with gross cytogenetic anomalies including genomic gain/loss or loss of heterozygosity (LOH) due to mitotic homologous recombination. To determine whether genomic anomalies may be associated with JAK mutation status/disease phenotype we subjected genomic DNA from the granulocytes of 87 patients with PV, ET or IMF to analysis using high resolution Affymetrix 250K Nsp SNP arrays with an average probe spacing of 12Kb. Firstly this analysis precisely mapped previously identified anomalies in MPD patients such as gain of chromosome 1q chromosome 9 (Chr9), chromosome 8, and deletion of 20q and 13q indicating the robustness of the technique. By removing genomic Copy Number Polymorphisms (CNPs) ascertained from 90 normal individuals from the HapMap dataset, we further detected a number of novel alterations such as frequent gain of Chr9p33–34 harboring among other genes, Notch1. MPD patients heterozygous for the JAK V617F mutation exhibited higher genomic instability than JAK2 V617 homozygous or wild type patients. IMF patients had overall more aberrations than PV or ET patients but unsupervised hierarchical clustering of chromosomal anomalies could not distinguish patients with PV, ET or IMF. Whole chromosomal gain or loss was equally frequent among the three diseases, however IMF patients had more frequent alteration of 10Mb or greater when compared to ET or PV (p<0.01) and ET and IMF patients both more frequently exhibited changes ranging from 1–10Mb in size than PV patients (p<0.01). Correlation of gene expression profiles from the granulocytes of 38 MPD patients with copy number profiles from DNA of the patients indicated that gene expression in regions of copy number gain or loss correlated with gene dosages in general. From 2493 genes residing in regions of copy number change region, 259 genes exhibited a positive correlation between copy number and gene expression. By calculating the t–statistics of expression values between samples with and without chromosomal aberrations we further identified 28 genes that showed a change of at least 1.5 fold (p<0.05), 27 of which were located on chromosome 9. Among these were Smarca2, NOTCH1 JAK2 itself. JAK2V617F expression was highly elevated by gain of Chr9 or Chr9p LOH. LOH on chr9p was detected in 16 patients, the majority of whom were confirmed as homozygous for JAK2V617F. To investigate how the over-expression of JAK2V617F might affect the expression of other genes and pathways, gene expression profiles of patients with Chr9 abnormality including Chr9 gain or Chr9p LOH were compared to samples with a normal copy number for Chr9. We identified 493 genes including 210 up-regulated and 283 down-regulated genes by at least 1.5 fold at a p value of 0.05 after multiple-testing correction. As a control gene expression patterns in JAK2-wildtype MPD granulocytes were compared to expression in normal granulocytes. This analysis identified an almost completely different set of genes; 441/493 (89%) of genes differentially expressed in Chr9 abnormal cases versus Chr9 normal cases were not found in the Chr9 normal versus normal control dataset. Up-regulated genes in Chr9 abnormal cases included CD177, CDK5RAP2, BIRC1, STAT5, TLR4 and down-regulated genes include KLRB1, Myc, RUNX3, P53CSV, Pathway analysis of dysregulated genes in Chr9 gain/LOH cases showed that genes involved in p38/MAP kinase, Toll-like receptor and Fc epsilon RI signaling were up-regulated and the genes involved in pathways of protein synthesis/translation and T cell receptor signaling were down-regulated. Collectively these findings suggest that MPD associated with Chr9 gain or 9pLOH and increased expression of JAK2V617F represents a distinct subset of MPD, characterized by less genomic instability than other cases. Furthermore, increased JAK2 and STAT5 expression and activity in these cases may induce distinct downstream pathways and alterations in gene expression.

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.

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 Comparative mapping of bovine chromosome 27 with human chromosome 8 near a dairy form QTL in cattle

2005 ◽  
Vol 112 (1-2) ◽  
pp. 98-102 ◽  
Author(s):  
E.E. Connor ◽  
M.S. Ashwell ◽  
R. Schnabel ◽  
J.L. Williams
Keyword(s):  
Human Chromosome ◽  
Comparative Mapping ◽  
Bovine Chromosome ◽  
Chromosome 8
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