scholarly journals LINKAGE RELATIONSHIPS OF 19 ENZYME LOCI IN MAIZE

Genetics ◽  
1980 ◽  
Vol 96 (3) ◽  
pp. 697-710 ◽  
Author(s):  
M M Goodman ◽  
C W Stuber ◽  
K Newton ◽  
H H Weissinger
Keyword(s):  
Chromosome 8 ◽  
Chromosome 1 ◽  
Chromosome 6 ◽  
Linkage Studies ◽  
Chromosome 5 ◽  
Chromosome Marker ◽  
Enzyme Loci ◽  
First Time ◽  
Linkage Relationships

ABSTRACT Linkage relationships of 19 enzyme loci have been examined. The chromosomal locations of eight of these loci are formally reported for the first time in this paper. These localizations should assist in the construction of additional useful chromosome marker stocks, especially since several of these enzyme loci lie in regions that were previously poorly mapped. Six loci are on the long arm of chromosome 1. The arrangement is (centromere)—Mdh4-mmm-Pgm1-Adh1-Phi-Gdh1, with about 46% recombination between Mdh4 and Gdh1.—Linkage studies with a2 and pr have resulted in the localization of four enzyme genes to chromosome 5 with arrangement Pgm2-Mdh5-Got3-a2-(centromere)-pr-Got2. Pgm2 lies approximately 35 map units distal to a2 in a previously unmapped region of the short arm of 5, beyond ameiotic.—Approximately 23% recombination was observed between Mdh4 and Pgm1 on chromosome 1, while 17% recombination occurred between Mdh5 and Pgm2 on chromosome 5. Similarly, linkages between Idh1 and Mdh1, about 22 map units apart on chromosome 8, and between Mdh2 and Idh2, less than 5 map units apart on chromosome 6, were observed. Thus, segments of chromosomes 1 and 5 and segments of 6 and 8 may represent duplications on nonhomologous chromosomes.

scholarly journals GENETIC BASIS OF THE MAJOR MALATE DEHYDROGENASE ISOZYMES IN MAIZE

Genetics ◽  
1980 ◽  
Vol 95 (2) ◽  
pp. 425-442
Author(s):  
Kathleen J Newton ◽  
Drew Schwartz
Keyword(s):  
Genetic Basis ◽  
Polyacrylamide Gel Electrophoresis ◽  
Distal Region ◽  
Chromosome 8 ◽  
Chromosome 1 ◽  
Duplicate Genes ◽  
Chromosome 6 ◽  
Gene Products ◽  
Subcellular Compartment ◽  
Malate Dehydrogenase Isozymes

ABSTRACT The mitochondrial MDH isozymes in the scutellum of the mature maize (Zen mays L.) kernel are encoded by three independently inherited nuclear genes. Mdhl is located on chromosome 8, close to the breakpoint (8L.35) of a waxy-marked reciprocal translocation between chromosomes 8 and 9. Mdh2 is located in the distal region of the long arm of chromosome 6. Mdh3 is on the long arm of chromosome 3, approximately 2.6 map units from sh2. A modifier of the mitochondrial MDH isozymes (Mmm) maps approximately 27.5 units proximal to Adh1 in the central portion of the long arm of chromosome 1. Independently assorting duplicate genes code for the soluble MDH isozymes. Mdh4 is located in the same region of chromosome 1 as Mmm, approximately 29 map units proximal to Adh1. Mdh5 maps approximately 20 units distal to a2 in the short arm of chromosome 5.——Intergenic and interallelic heterodimer formation occurs among gene products that occupy the same subcellular compartment. MDH isozymes were purified and analyzed by native-SDS two-dimensional polyacrylamide gel electrophoresis. The proposed mitochondrial MDH intergenic heterodimer bands were found to be composed of two subunits, which differ in their migrations on SDS gels; whereas, genetically defined homodimers contained only one type of subunit.——This evidence is discussed in terms Of two genetic models proposed for the maize mitochondrial MDH isozymes.

scholarly journals QTL Mapping for Gummy Stem Blight Resistance in Watermelon (Citrullus spp.)

Plants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 500
Author(s):  
Eun Su Lee ◽  
Do-Sun Kim ◽  
Sang Gyu Kim ◽  
Yun-Chan Huh ◽  
Chang-Gi Back ◽  
...  
Keyword(s):  
Chromosome 8 ◽  
Chromosome 6 ◽  
Potential Candidate ◽  
Stem Blight ◽  
Gummy Stem Blight ◽  
F2 Population ◽  
Leaf Lesion ◽  
Phenotypic Variations ◽  
A Minor ◽  
Selection Of

Watermelon (Citrulluslanatus) is an economically important fruit crop worldwide. Gummy stem blight (GSB) is one of the most damaging diseases encountered during watermelon cultivation. In the present study, we identified quantitative trait loci (QTLs) associated with GSB resistance in an F2 population derived from a cross between maternal-susceptible line ‘920533’ (C. lanatus) and the paternal-resistant line ‘PI 189225’ (C. amarus). The resistance of 178 F2 plants was assessed by two different evaluation methods, including leaf lesion (LL) and stem blight (SB). To analyze the QTLs associated with GSB resistance, a linkage map was constructed covering a total genetic distance of 1070.2 cM. QTL analysis detected three QTLs associated with GSB resistance on chromosome 8 and 6. Among them, two QTLs, qLL8.1 and qSB8.1 on chromosome 8 identified as major QTLs, explaining 10.5 and 10.0% of the phenotypic variations localizing at same area and sharing the same top markers for both LL and SB traits, respectively. A minor QTL, qSB6.1, explains 9.7% of phenotypic variations detected on chromosome 6 only for the SB trait. High-throughput markers were developed and validated for the selection of resistant QTLs using watermelon accessions, and commercial cultivars. Four potential candidate genes were predicted associated with GSB resistance based on the physical location of flanking markers on chromosome 8. These findings will be helpful for the development of watermelon cultivars resistant to GSB.

Recovery of a telomere-truncated chromosome via a compensating translocation in maize

Genome ◽  
2011 ◽  
Vol 54 (3) ◽  
pp. 184-195 ◽  
Author(s):  
Robert T. Gaeta ◽  
Tatiana V. Danilova ◽  
Changzeng Zhao ◽  
Rick E. Masonbrink ◽  
Morgan E. McCaw ◽  
...  
Keyword(s):  
In Situ Hybridization ◽  
Fluorescent In Situ Hybridization ◽  
Transgene Expression ◽  
De Novo ◽  
Extra Chromosome ◽  
Single Gene ◽  
B Chromosomes ◽  
Chromosome 1 ◽  
Chromosome 6

Maize-engineered minichromosomes are easily recovered from telomere-truncated B chromosomes but are rarely recovered from A chromosomes. B chromosomes lack known genes, and their truncation products are tolerated and transmitted during meiosis. In contrast, deficiency gametes resulting from truncated A chromosomes prevent their transmission. We report here a de novo compensating translocation that permitted recovery of a large truncation of chromosome 1 in maize. The truncation (trunc-1) and translocation with chromosome 6 (super-6) occurred during telomere-mediated truncation experiments and were characterized using single-gene fluorescent in situ hybridization (FISH) probes. The truncation contained a transgene signal near the end of the broken chromosome and transmitted together with the compensating translocation as a heterozygote to approximately 41%–55% of progeny. Transmission as an addition chromosome occurred in ~15% of progeny. Neither chromosome transmitted through pollen. Transgene expression (Bar) cosegregated with trunc-1 transcriptionally and phenotypically. Meiosis in T1 plants revealed eight bivalents and one tetravalent chain composed of chromosome 1, trunc-1, chromosome 6, and super-6 in diplotene and diakinesis. Our data suggest that de novo compensating translocations allow recovery of truncated A chromosomes by compensating deficiency in female gametes and by affecting chromosome pairing and segregation. The truncated chromosome can be maintained as an extra chromosome or together with the super-6 as a heterozygote.

scholarly journals Methylome-wide analysis reveals epigenetic marks associated with resistance to tuberculosis in HIV-infected individuals from East Africa

2020 ◽  
Author(s):  
Catherine Stein ◽  
Penelope Bencheck ◽  
Jacquelaine Bartlett ◽  
Robert P Igo ◽  
Rafal S Sobota ◽  
...  
Keyword(s):  
Genome Wide Association Study ◽  
Sub Saharan Africa ◽  
Chromosome 1 ◽  
Chromosome 2 ◽  
Chromosome 5 ◽  
Epigenetic Marks ◽  
Genome Wide ◽  
A Genome ◽  
Immunodeficiency Virus ◽  
Sub Saharan

Background: Tuberculosis (TB) is the most deadly infectious disease globally and highly prevalent in the developing world, especially sub-Saharan Africa. Even though a third of humans are exposed to Myocbacterium tuberculosis (Mtb), most infected immunocompetent individuals do not develop active TB. In contrast, for individuals infected with both TB and the human immunodeficiency virus (HIV), the risk of active disease is 10% or more per year. Previously, we identified in a genome-wide association study a region on chromosome 5 that was associated with resistance to TB. This region included epigenetic marks that could influence gene regulation so we hypothesized that HIV-infected individuals exposed to Mtb, who remain disease free, carry epigenetic changes that strongly protect them from active TB. To test this hypothesis, we conducted a methylome-wide study in HIV-infected, TB-exposed cohorts from Uganda and Tanzania. Results: In 221 HIV-infected adults from Uganda and Tanzania, we identified 3 regions of interest that included markers that were differentially methylated between TB cases and LTBI controls, that also included methylation QTLs and associated SNPs: chromosome 1 (RNF220, p=4x10-5), chromosome 2 (between COPS8 and COL6A3 genes, p=2.7x10-5), and chromosome 5 (CEP72, p=1.3x10-5). These methylation results colocalized with associated SNPs, methylation QTLs, and methylation x SNP interaction effects. These markers were in regions with regulatory markers for cells involved in TB immunity and/or lung. Conclusion: Epigenetic regulation is a potential biologic factor underlying resistance to TB in immunocompromised individuals that can act in conjunction with genetic variants.

Insertion of part of chromosome 5 into chromosome 1 in a case of sideroblastic anemia with an excess of blasts

1985 ◽  
Vol 16 (4) ◽  
pp. 353-355
Author(s):  
M.F. Turchini ◽  
P. Travade ◽  
A. Geneix ◽  
A. De Laroque ◽  
M.J. Bezou ◽  
...  
Keyword(s):  
Chromosome 1 ◽  
Chromosome 5 ◽  
Sideroblastic Anemia

Karyotypic characterization of Apatemon gracilis

1999 ◽  
Vol 73 (1) ◽  
pp. 73-77 ◽  
Author(s):  
R. Petkevičiūtė ◽  
G. Stanevičiūtė
Keyword(s):  
B Chromosome ◽  
Chromosome Morphology ◽  
Chromosome 1 ◽  
Size Groups ◽  
First Time

The cytotaxonomical characteristics of parthenitae of Apatemon gracilis (Rudolphi, 1819) Szidat, 1928 were studied using karyometric analysis to extend our knowledge of chromosome morphology and karyosystematics among trematodes. The karyotype, reported here for the first time, consists of ten pairs (2n = 20) of chromosomes divided into two size groups: five pairs of comparatively large and five pairs of small chromosomes. Biarmed chromosomes prevail in the chromosome set. According to centromere index values, chromosome 1 is submetacentric to metacentric, 2 is subtelocentric, 3 and 5 are acrocentric, 4, 9 and 10 are metacentric, 6 is submetacentric and 7 and 8 are submeta-subtelocentric. The small uniarmed B-chromosome was found in the chromosome set of parthenitae of A. gracilis from one snail. Data are discussed with reference to the karyotypes previously described within the Strigeidae.

scholarly journals Linkage studies between chromosome inversions and enzyme loci in the mosquito Anopheles stephensi

Heredity ◽  
1978 ◽  
Vol 40 (3) ◽  
pp. 457-458 ◽  
Author(s):  
M Di Deco ◽  
G Cancrini ◽  
M Coluzzi ◽  
A P Bianchi Bullini ◽  
R Cianchi ◽  
...  
Keyword(s):  
Anopheles Stephensi ◽  
Linkage Studies ◽  
Chromosome Inversions ◽  
Enzyme Loci

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.

Array CGH Discovers Novel Genomic Signatures in De Novo Acute Myeloid Leukemia (AML): Results of Children’s Oncology Group (COG) Study POG #9421.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 2771-2771
Author(s):  
Dennis J. Kuo ◽  
Norman J. Lacayo ◽  
Don Hoang ◽  
Dejan Juric ◽  
Susana C. Raimondi ◽  
...  
Keyword(s):  
Copy Number ◽  
Myeloid Leukemia ◽  
Array Cgh ◽  
De Novo ◽  
Gene Copy Number ◽  
Chromosome 8 ◽  
Gene Copy ◽  
Chromosome 6 ◽  
De Novo Aml ◽  
Acute Myeloid

Abstract Acute myeloid leukemia (AML) is a heterogeneous disease. Risk factors such as karyotype, FAB subtype, FLT3 status and response to induction therapy are determinants of outcome with current therapies. We hypothesize that array comparative genomic hybridization (CGH) will identify gene copy number changes that are determinants of outcome. Array CGH was performed on diagnostic bone marrow samples from patients on the COG study POG #9421. In order to determine regions of altered gene copy number, labeled genomic DNA samples were hybridized together with sex-matching normal human reference DNA to cDNA microarrays with 41,751 features (corresponding to 24,473 unique Unigene cluster IDs), arrays were obtained from the Stanford University Microarray Core Facility. Control hybridizations were performed to assess intra- and inter-experimental variability. We studied 70 samples with adequate high-quality DNA. Circular binary segmentation was used to distinguish discrete gene copy number transition points from chance noise events and to transform primary clone-by-clone data into genomic regions of equal copy number. Using gain/loss threshold, based on two-standard deviation range of control self-to-self distribution, novel gene amplifications and deletions were found in profiled samples. The highest alteration recurrence was observed for gains of chromosome 8 (21%) and losses of chromosome 6 (29%). The area of chromosome 8 which was found to be gained is notable for the presence of potential oncogenes such as ERK8. The deleted area of chromosome 6 is notable for the presence of potential regulators of oncogenesis: MDC1, DDR1, NFKBIL1, TNF, and BRD2. In summary, array CGH has identified novel areas of gene copy number gain and loss in this population of pediatric de novo AML patients. Further studies are needed to assess whether these genes are associated with outcome, known risk factors and whether they will provide insight into the heterogeneity of de novo AML.

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