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 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 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 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.

scholarly journals Genetic variation between susceptible and non-susceptible snails to Schistosoma infection using random amplified polymorphic DNA analysis (RAPDs)

1999 ◽  
Vol 41 (5) ◽  
pp. 291-295 ◽  
Author(s):  
Abdel-Hamid Zaki ABDEL-HAMID ◽  
Jeanne Blanco de MOLFETTA ◽  
Vania FERNANDEZ ◽  
Vanderlei RODRIGUES
Keyword(s):  
Dna Analysis ◽  
Random Amplified Polymorphic Dna ◽  
Polyacrylamide Gel Electrophoresis ◽  
Genome Comparison ◽  
Gene Products ◽  
Chain Reaction ◽  
High Molecular Weight Dna ◽  
Polymerase Chain ◽  
Or Gene ◽  
Host Parasite

Susceptibility of snails to infection by certain trematodes and their suitability as hosts for continued development has been a bewildering problem in host-parasite relationships. The present work emphasizes our interest in snail genetics to determine what genes or gene products are specifically responsible for susceptibility of snails to infection. High molecular weight DNA was extracted from both susceptible and non-susceptible snails within the same species Biomphalaria tenagophila. RAPD was undertaken to distinguish between the two types of snails. Random primers (10 mers) were used to amplify the extracted DNA by the polymerase chain reaction (PCR) followed by polyacrylamide gel electrophoresis (PAGE) and silver staining. The results suggest that RAPD represents an efficient means of genome comparison, since many molecular markers were detected as genetic variations between susceptible and non-susceptible snails.

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.

Hoxa-13 and Hoxd-13 play a crucial role in the patterning of the limb autopod

Development ◽  
1996 ◽  
Vol 122 (10) ◽  
pp. 2997-3011 ◽  
Author(s):  
C. Fromental-Ramain ◽  
X. Warot ◽  
N. Messadecq ◽  
M. LeMeur ◽  
P. Dolle ◽  
...  
Keyword(s):  
Distal Region ◽  
Limb Bud ◽  
Gene Products ◽  
Loss Of Function ◽  
Paralogous Gene ◽  
Functional Specificity ◽  
Targeted Disruption ◽  
Group 13 ◽  
Hox Gene ◽  
Homology Groups

Members of the Abdominal-B-related Hox gene subfamily (belonging to homology groups 9 to 13) are coordinately expressed during limb bud development. Only two genes from homology group 13 (Hoxa-13 and Hoxd-13) are specifically expressed in the developing distal region (the autopod), which displays the most complex and evolutionarily flexible pattern among limb ‘segments’. We report here that targeted disruption of the Hoxa-13 gene leads to a specific forelimb and hindlimb autopodal phenotype, distinct from that of the Hoxd-13 paralogous gene inactivation. In both limbs, Hoxa-13 loss of function results in the lack of formation of the most anterior digit and to altered morphogenesis of some ‘preaxial’ carpal/tarsal elements. We have generated mice with all possible combinations of disrupted Hoxa-13 and/or Hoxd-13 alleles, which allowed us to investigate the degree of functional specificity versus redundancy of the corresponding gene products in the developing limb autopod. The phenotype of any double mutant was much more severe than the sum of the phenotypes seen in the corresponding single mutants, indicating that these genes act in a partially redundant manner. Our major findings were: (1) an abnormal autopodal phenotype in Hoxa-13+/−/Hoxd-13+/− double heterozygous mutants, which mostly consists of subsets of the alterations seen in each individual homozygous mutant, and therefore appears to result from quantitative, rather than qualitative, homeoprotein deficiency; (2) partly distinct alterations in mutants harboring a single non-disrupted allele of Hoxa-13 or Hoxd-13, indicating that the remaining reduced protein amounts are not functionally equivalent; (3) a polydactyly in the forelimbs of Hoxa-13+/−/Hoxd-13−/−double mutants, consisting of seven symmetrically arranged, truncated and mostly non-segmented digits; (4) an almost complete lack of chondrified condensations in the autopods of double homozygous mutants, showing that the activity of group 13 Hox gene products is essential for autopodal patterning in tetrapod limbs.

scholarly journals Mls is not a single gene, allelic system. Different stimulatory Mls determinants are the products of at least two nonallelic, unlinked genes.

1987 ◽  
Vol 166 (4) ◽  
pp. 1150-1155 ◽  
Author(s):  
R Abe ◽  
J J Ryan ◽  
R J Hodes
Keyword(s):  
T Cells ◽  
Single Gene ◽  
Surface Structures ◽  
Chromosome 1 ◽  
Gene Products ◽  
Spleen Cells ◽  
Gene Encoding ◽  
Cell Surface Structures ◽  
Genes Encoding ◽  
Polymorphic Cell

Mls determinants share with MHC products the unique property of stimulating T cells at extraordinarily high precursor frequencies. The Mls system was originally described as a single locus on chromosome 1, with four alleles, Mlsa, Mlsb, Mlsc, and Mlsd, that encode polymorphic cell surface structures. However, the fundamental issues of polymorphism and allelism in the Mls system remain controversial. To clarify these questions, a formal segregation analysis of the genes encoding Mlsa and Mlsc determinants was carried out by testing the capacity of spleen cells from progeny of (Mlsa X Mlsc)F1 X Mlsb breedings to stimulate responses by unprimed T cells and by Mlsa- and Mlsc-specific cloned T cells. The results of this analysis indicated that the gene encoding Mlsa determinants is neither allelic to nor linked to the gene encoding Mlsc determinants. Together with previous findings, these results also suggest that another strongly stimulatory type, Mlsd, in fact results from the independent expression of unlinked Mlsa and Mlsc gene products. Based on these observations, it is concluded that, contrary to conventional concepts, the stimulatory phenotypes designated as Mlsa, Mlsc, and Mlsd can be accounted for by the independent expression of the products of at least two unlinked gene loci.

scholarly journals Cgnz1 allele confers kidney resistance to damage preventing progression of immune complex–mediated acute lupus glomerulonephritis

2013 ◽  
Vol 210 (11) ◽  
pp. 2387-2401 ◽  
Author(s):  
Yan Ge ◽  
Chao Jiang ◽  
Sun-Sang J. Sung ◽  
Harini Bagavant ◽  
Chao Dai ◽  
...  
Keyword(s):  
Immune Complex ◽  
Organ Damage ◽  
Distal Region ◽  
Chromosome 1 ◽  
Chronic Glomerulonephritis ◽  
Female Mice ◽  
Inflammatory Parameters ◽  
Stage Renal Disease ◽  
End Stage ◽  
Lupus Glomerulonephritis

Cgnz1 and Agnz1 on the distal region of mouse chromosome 1 are associated with chronic glomerulonephritis (cGN) and acute GN (aGN). NZM2328.Lc1R27 (R27) was generated by introgressing a C57L/J region where Cgnz1 is located to NZM2328. R27 female mice developed aGN mediated by immune complex (IC) deposition and complement activation without progression to cGN with severe proteinuria. End stage renal disease (ESRD) was not seen in R27 mice as old as 15 mo. Thus, aGN and cGN are under separate genetic control, and IC-mediated proliferative GN need not progress to cGN and ESRD. NZM2328 and R27 female mice have comparable immune and inflammatory parameters. In contrast to NZM2328, R27 mice were resistant to sheep anti–mouse GBM serum-induced nephritis, supporting the hypothesis that aGN is mediated by autoimmunity and resistance to the development of cGN is mediated by end organ resistance to damage. Thus, autoimmunity should be considered distinct from end organ damage. The Cgnz1 region has been mapped to a 1.34 MB region with 45 genes. Nine candidate genes were identified. Clinical relevance of these observations is supported by case studies. Clinical implications and the significance to human lupus and other diseases are presented.

scholarly journals Sexually Antagonistic Mitonuclear Coevolution in Duplicate Oxidative Phosphorylation Genes

2019 ◽  
Vol 59 (4) ◽  
pp. 864-874 ◽  
Author(s):  
Justin C Havird ◽  
Hunter J McConie
Keyword(s):  
Oxidative Phosphorylation ◽  
Structural Data ◽  
Mitochondrial Genomes ◽  
Duplicate Genes ◽  
Gene Products ◽  
Mitochondrial Mutations ◽  
Specific Expression ◽  
Chimeric Enzymes ◽  
Rates Of Evolution ◽  
Testis Specific Expression

Abstract Mitochondrial function is critical in eukaryotes. To maintain an adequate supply of energy, precise interactions must be maintained between nuclear- and mitochondrial-encoded gene products. Such interactions are paramount in chimeric enzymes such as the oxidative phosphorylation (OXPHOS) complexes. Mutualistic coevolution between the two genomes has therefore been suggested to be a critical, ubiquitous feature of eukaryotes that acts to maintain cellular function. However, mitochondrial genomes can also act selfishly and increase their own transmission at the expense of organismal function. For example, male-harming mutations are predisposed to accumulate in mitochondrial genomes due to their maternal inheritance (“mother’s curse”). Here, we investigate sexually antagonistic mitonuclear coevolution in nuclear-encoded OXPHOS paralogs from mammals and Drosophila. These duplicate genes are highly divergent but must interact with the same set of mitochondrial-encoded genes. Many such paralogs show testis-specific expression, prompting previous hypotheses suggesting they may have evolved under selection to counteract male-harming mitochondrial mutations. We found increased rates of evolution in OXPHOS paralogs with testis-specific expression in mammals and Drosophila, supporting this hypothesis. However, further analyses suggested such patterns may be due to relaxed, not positive selection, especially in Drosophila. Structural data also suggest that mitonuclear interactions do not play a major role in the evolution of many OXPHOS paralogs in a consistent way. In conclusion, no single OXPHOS paralog met all our criteria for being under selection to counteract male-harming mitochondrial mutations. We discuss alternative explanations for the drastic patterns of evolution in these genes, including mutualistic mitonuclear coevolution, adaptive subfunctionalization after gene duplication, and relaxed selection on OXPHOS in male tissues.

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.

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