The proximal end of mouse chromosome 17: new molecular markers identify a deletion associated with quakingviable.

Abstract Five randomly identified cosmids have been mapped proximal to the Leh66D locus on mouse chromosome 17. Two of these cosmids, Au10 and Au119, map near the neurological mutation quaking. Au119 is deleted in qkviable/qkviable DNA, whereas Au10 is not. Au76 maps to a gene-rich region near the Time locus. The Au76 locus encodes a member of a low copy gene family expressed in embryos, the adult central nervous system and testis. A second member of this family has been mapped to chromosome 15 near c-sis (PDGF-B). At the centromeric end of chromosome 17, Au116 maps near the Tu1 locus, and along with Au217rs identifies a region of unusually high recombinational activity between t-haplotypes and wild-type chromosomes. Au217I and II map to the large inverted repeats found at the proximal end of the wild-type chromosome. In addition, the Au217I and/or II loci encode testis transcripts not expressed from t-haplotypes.

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Two Chimeric Chromosomes of Streptomyces coelicolor A3(2) Generated by Single Crossover of the Wild-Type Chromosome and Linear Plasmid SCP1

Journal of Bacteriology ◽

10.1128/jb.186.19.6553-6559.2004 ◽

2004 ◽

Vol 186 (19) ◽

pp. 6553-6559 ◽

Cited By ~ 23

Author(s):

Masayuki Yamasaki ◽

Haruyasu Kinashi

Keyword(s):

Genome Evolution ◽

Streptomyces Coelicolor ◽

Linear Plasmid ◽

Nucleotide Sequencing ◽

Inverted Repeats ◽

Wild Type ◽

Linear Chromosome ◽

Terminal Inverted Repeats ◽

Type Chromosome ◽

Chromosomal Duplication

ABSTRACT Streptomyces coelicolor A3(2) strain 2106 carries a 1.85-Mb linear plasmid, SCP1′-cysD, in addition to a 7.2-Mb linear chromosome. Macrorestriction analysis indicated that both linear DNAs are hybrids of the wild-type chromosome and the linear plasmid SCP1 on each side. Nucleotide sequencing of the fusion junctions revealed no homology between the recombination regions. SCP1′-cysD contains an SCP1 telomere and a chromosomal telomere at each end and therefore does not have terminal inverted repeats. In addition, SCP1′-cysD could not be eliminated from strain 2106 by various mutagenic treatments. Thus, we concluded that both the 7.2-Mb chromosome and SCP1′-cysD are chimeric chromosomes generated by a single crossover of the wild-type chromosome and SCP1. This may be regarded as a model of chromosomal duplication in genome evolution.

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Three ENU-induced alleles of the murine quaking locus are recessive embryonic lethal mutations

Genetics Research ◽

10.1017/s0016672300024101 ◽

1988 ◽

Vol 51 (2) ◽

pp. 95-102 ◽

Cited By ~ 52

Author(s):

Monica J. Justice ◽

Vernon C. Bode

Keyword(s):

Mouse Chromosome ◽

Lethal Mutation ◽

Chromosome 17 ◽

Wild Type ◽

Embryonic Survival ◽

Lethal Mutations ◽

Embryonic Lethal ◽

Embryonic Lethal Mutations ◽

Precise Time ◽

New Alleles

SummaryThe quaking (qk) locus on mouse chromosome 17 has been defined by a single viable quaking allele. Three new alleles of quaking were selected after ENU mutagenesis by their failure to complement the quaking phenotype. The qkk2 allele was induced on wild-type chromatin and the qkkt1 and qkkt4 alleles were induced on t-chromatin. Each is a recessive embryonic lethal mutation. They fail to complement each other and are not complemented by the deletion, TtOrl. Homozygotes and hemizygotes die at 8–9·5 days gestation, but not at a single precise time. Because the classical quaking mutation complements the lethality of these new alleles, but they fail to complement its quaking phenotype (myelination defect), we conclude that the quaking+ function is required for embryonic survival as well as for myelination.

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Genetic Modifiers of Oral Nicotine Consumption in Chrna5 Null Mutant Mice

Frontiers in Psychiatry ◽

10.3389/fpsyt.2021.773400 ◽

2021 ◽

Vol 12 ◽

Author(s):

Erin Meyers ◽

Zachary Werner ◽

David Wichman ◽

Hunter L. Mathews ◽

Richard A. Radcliffe ◽

...

Keyword(s):

Chromosome 17 ◽

Chromosome 1 ◽

Chromosome 15 ◽

Genetic Modifiers ◽

Loss Of Function ◽

Wild Type ◽

Nicotine Intake ◽

Nicotine Consumption ◽

Null Mutant Mice ◽

Oral Nicotine

The gene CHRNA5 is strongly associated with the level of nicotine consumption in humans and manipulation of the expression or function of Chrna5 similarly alters nicotine consumption in rodents. In both humans and rodents, reduced or complete loss of function of Chrna5 leads to increased nicotine consumption. However, the mechanism through which decreased function of Chrna5 increases nicotine intake is not well-understood. Toward a better understanding of how loss of function of Chrna5 increases nicotine consumption, we have initiated efforts to identify genetic modifiers of Chrna5 deletion-dependent oral nicotine consumption in mice. For this, we introgressed the Chrna5 knockout (KO) mutation onto a panel of C57BL/6J-Chr#A/J/NAJ chromosome substitution strains (CSS) and measured oral nicotine consumption in 18 CSS and C57BL/6 (B6) mice homozygous for the Chrna5 KO allele as well as their Chrna5 wild type littermates. As expected, nicotine consumption was significantly increased in Chrna5 KO mice relative to Chrna5 wildtype mice on a B6 background. Among the CSS homozygous for the Chrna5 KO allele, several exhibited altered nicotine consumption relative to B6 Chrna5 KO mice. Sex-independent modifiers were detected in CSS possessing A/J chromosomes 5 and 11 and a male-specific modifier was found on chromosome 15. In all cases nicotine consumption was reduced in the CSS Chrna5 KO mice relative to B6 Chrna5 KO mice and consumption in the CSS KO mice was indistinguishable from their wild type littermates. Nicotine consumption was also reduced in both Chrna5 KO and wildtype CSS mice possessing A/J chromosome 1 and increased in both KO and wild type chromosome 17 CSS relative to KO and wild type B6 mice. These results demonstrate the presence of several genetic modifiers of nicotine consumption in Chrna5 KO mice as well as identify loci that may affect nicotine consumption independent of Chrna5 genotype. Identification of the genes that underlie the altered nicotine consumption may provide novel insight into the mechanism through which Chrna5 deletion increases nicotine consumption and, more generally, a better appreciation of the neurobiology of nicotine intake.

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ETHYLNITROSOUREA MUTAGENESIS AND THE ISOLATION OF MUTANT ALLELES FOR SPECIFIC GENES LOCATED IN THE t REGION OF MOUSE CHROMOSOME 17

Genetics ◽

10.1093/genetics/108.2.457 ◽

1984 ◽

Vol 108 (2) ◽

pp. 457-470 ◽

Cited By ~ 2

Author(s):

Vernon C Bode

Keyword(s):

Mouse Chromosome ◽

Chromosome 17 ◽

Male Mice ◽

Wild Type ◽

Chromosome 5 ◽

Dominant Mutation ◽

New Mutations

ABSTRACT Ethylnitrosourea mutagenesis of spermatogonia in male mice is very efficient and makes it practical to isolate new desired mutant alleles by subsequent progeny screening. This is demonstrated for three genes in the t region of chromosome 17. The first, a mutation designated t-int, interacts with the dominant mutation, T (Brachyury), to produce a tailless mouse. Previously, mutant alleles of the t-int gene were available only in t haplotypes, where they are part of a t chromatin block within which recombination with wild-type chromosomes is inhibited. In addition to t-int, new mutations at the quaking and tufted loci were obtained, as well as at several loci not on chromosome 17, e.g., an X-linked lethal that causes a mottled phenotype in the heterozygote and four new mutant W alleles on chromosome 5. In the experiment, an average of one fertilizing spermatozoan in 1500 was mutant at a given locus and an average of one male in five was able to sire mutants at that locus.

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Genome imprinting phenomena on mouse chromosome 7

Genetics Research ◽

10.1017/s0016672300035333 ◽

1990 ◽

Vol 56 (2-3) ◽

pp. 237-244 ◽

Cited By ~ 75

Author(s):

Antony G. Searle ◽

Colin V. Beechey

Keyword(s):

Mouse Chromosome ◽

Genetic Markers ◽

Reciprocal Translocation ◽

Neonatal Death ◽

Reciprocal Cross ◽

The Other ◽

Chromosome 7 ◽

Chromosome 15 ◽

Wild Type ◽

Parental Transmission

SummaryHeterozygotes for the reciprocal translocation T(7;15)9H were intercrossed, with albino (c) and underwhite (uw) as genetic markers, in order to study genetic complementation in mouse chromosome 7. Chromosome 15 is known to show normal complementation. Neither reciprocal cross in which one parent was c/c and the other wild type yielded albino progeny at birth although about 17% would be expected, but albino foetuses were recovered when the mother was c/c and father wild type. These products of maternal duplication/paternal deficiency for distal 7 were markedly retarded with small placentae. No albino foetuses were found when the father was c/c and mother wild type, which suggested earlier lethality. Equivalent crosses with uw (chromosome 15) as proximal marker gave normal underwhite progeny when the mother was uw/uw but small placentae, retardation and neonatal death of presumptive underwhites in the reciprocal cross. These abnormal newborn would have had a maternal duplication/paternal deficiency for proximal 7. These and other findings indicate that one region of defective complementation probably lies distal to the breakpoint of T(7;18)50H at 7E2-F2, while another is between the centromere and 7B3. Examination of man-mouse homologies suggests that the loci for three pathological human conditions (Beckwith-Weidemann syndrome, dystrophia myotonia and rhabdomyosarcoma) with differential parental transmission may be located in homologous regions to those affected by imprinting phenomena on mouse chromosome 7.

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Amplification and Rearrangement of DNA Sequences During the Evolutionary Divergence of t Haplotypes and Wild-Type Forms of Mouse Chromosome 17

The Wild Mouse in Immunology - Current Topics in Microbiology and Immunology ◽

10.1007/978-3-642-71304-0_28 ◽

1986 ◽

pp. 247-252

Author(s):

J. Schimenti ◽

L. M. Silver

Keyword(s):

Mouse Chromosome ◽

Dna Sequences ◽

Chromosome 17 ◽

Evolutionary Divergence ◽

Wild Type

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Genetic analysis of mouse t haplotypes using mutations induced by ethylnitrosourea mutagenesis: the order of T and qk is inverted in t mutants.

Genetics ◽

10.1093/genetics/120.2.533 ◽

1988 ◽

Vol 120 (2) ◽

pp. 533-543

Author(s):

M J Justice ◽

V C Bode

Keyword(s):

Genetic Analysis ◽

Mouse Chromosome ◽

Gene Rearrangement ◽

Recombination Frequency ◽

Chromosome 17 ◽

Genetic Dissection ◽

Wild Type ◽

Recombination Suppression ◽

Classical Genetic ◽

Simple Inversion

Abstract The t region of mouse chromosome 17 exhibits recombination suppression with wild-type chromatin. However, the region has resisted classical genetic dissection because of a lack of defined variants. Mutations induced by N-ethyl-N-nitrosourea (ENU) at the Brachyury (T), quaking (qk), and tufted (tf) loci of the mouse tw5 haplotype have now allowed the analysis of crossovers between two complete t haplotypes. A classical breeding analysis of the complete t haplotypes, tw5 and t12, utilizing the newly induced markers, reveals two inversions in t chromatin: one involving T and qk, and one involving tf and the H-2 complex. Moreover, the recombination frequency between the loci of T and qk is reduced compared to the frequency reported in normal chromatin. These two inversions are a sufficient explanation for the recombination inhibition with normal chromatin exhibited by t haplotypes isolated from the wild. Furthermore, the reduced recombination frequency between T and qk may indicate that the proximal gene rearrangement is not a simple inversion.

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Identification and Physical Localization of Useful Genes and Markers to a Major Gene-Rich Region on Wheat Group1SChromosomes

Genetics ◽

10.1093/genetics/157.4.1735 ◽

2001 ◽

Vol 157 (4) ◽

pp. 1735-1747 ◽

Cited By ~ 5

Author(s):

Devinder Sandhu ◽

Julie A Champoux ◽

Svetlana N Bondareva ◽

Kulvinder S Gill

Keyword(s):

Dna Analysis ◽

Major Gene ◽

Rflp Markers ◽

Rich Region ◽

Wheat Group ◽

Marker Loci ◽

Group 1 Chromosomes ◽

Gene Rich Region ◽

Homeologous Group ◽

Group 1

AbstractThe short arm of Triticeae homeologous group 1 chromosomes is known to contain many agronomically important genes. The objectives of this study were to physically localize gene-containing regions of the group 1 short arm, enrich these regions with markers, and study the distribution of genes and recombination. We focused on the major gene-rich region (“1S0.8 region”) and identified 75 useful genes along with 93 RFLP markers by comparing 35 different maps of Poaceae species. The RFLP markers were tested by gel blot DNA analysis of wheat group 1 nullisomic-tetrasomic lines, ditelosomic lines, and four single-break deletion lines for chromosome arm 1BS. Seventy-three of the 93 markers mapped to group 1 and detected 91 loci on chromosome 1B. Fifty-one of these markers mapped to two major gene-rich regions physically encompassing 14% of the short arm. Forty-one marker loci mapped to the 1S0.8 region and 10 to 1S0.5 region. Two cDNA markers mapped in the centromeric region and the remaining 24 loci were on the long arm. About 82% of short arm recombination was observed in the 1S0.8 region and 17% in the 1S0.5 region. Less than 1% recombination was observed for the remaining 85% of the physical arm length.

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