scholarly journals t-Specific DNA polymorphisms among wild mice from Israel and Spain.

Genetics ◽  
1988 ◽  
Vol 119 (1) ◽  
pp. 157-160
Author(s):  
F Figueroa ◽  
E Neufeld ◽  
U Ritte ◽  
J Klein
Keyword(s):  
Laboratory Mouse ◽  
The Other ◽  
Dna Polymorphisms ◽  
Chromosome 17 ◽  
Mouse Strains ◽  
Laboratory Mice ◽  
Wild Type ◽  
Wild Mice ◽  
T Complex ◽  
Length Polymorphisms

Abstract Lehrach and his coworkers have isolated a series of DNA probes that specifically hybridize with different regions of mouse chromosome 17 within the t complex. The probes display restriction fragment length polymorphisms, RFLPs, which are specific for the t haplotypes in all laboratory mouse strains tested thus far. Some of these probes have been used to test wild mice populations for these t-associated DNA forms. It is demonstrated that populations from Germany, Switzerland, Italy, Greece, Yugoslavia, Australia, Costa Rica, and Venezuela contain chromosomes in which all the tested DNA loci display the t-specific polymorphisms. The frequency of mice carrying these chromosomes is as high as 31%. Wild mice from Israel and Spain, on the other hand, carry chromosomes displaying t-specific DNA forms only at one or two of the probed loci, while the other loci carry the wild-type (+) forms. These chromosomes thus resemble the partial t haplotypes known from the study of laboratory mice. One possible interpretation of these findings is that these DNA polymorphisms contributed to the assembly of the complete t haplotypes and that these haplotypes may have originated in the Middle East.

scholarly journals Polymorphism of Unique Noncoding DNA Sequences in Wild and Laboratory Mice

Genetics ◽  
1987 ◽  
Vol 117 (1) ◽  
pp. 101-108
Author(s):  
Felipe Figueroa ◽  
Masanori Kasahara ◽  
Herbert Tichy ◽  
Esther Neufeld ◽  
Uzi Ritte ◽  
...  
Keyword(s):  
Dna Sequences ◽  
Inbred Mouse ◽  
Inbred Strains ◽  
Chromosome 17 ◽  
Mouse Strains ◽  
Laboratory Mice ◽  
Noncoding Dna ◽  
Wild Mice ◽  
Dna Library ◽  
T Complex

ABSTRACT Two DNA probes, D17Tul and D17Tu2, were isolated from a genomic DNA library containing only two mouse chromosomes, one of which is chromosome 17, carrying the major histocompatibility complex (H-2), as well as the t complex genes. The D17Tul probe was mapped to the centromeric region of chromosome 17 and the D17Tu2 probe to the S region of the H-2 complex. Neither of the two probes appeared to detect any genes, but both contained unique, nonrepetitive sequences. Typing of DNA obtained from a large panel of mice revealed the presence of four D17Tul patterns in inbred mouse strains, one very common, one less common, and two present in one strain each. The two common patterns could not be detected in appreciable frequencies in the European wild mice tested (one of the two patterns was, however, found in Australian wild mice). Conversely, the patterns found frequently in European wild mice are absent in the laboratory mice. We therefore conclude that wild mice from the sampled regions of Europe could not have provided the ancestral stocks from which inbred strains were derived. Only one D17Tul pattern was found in all the populations of Mus musculus tested, while eight patterns were found in Mus domesticus, with virtually all the populations being polymorphic. We suggest that this difference reflects different modes in which the two species colonized Europe. The distribution of the D17Tu2 patterns in inbred strains correlates with the distribution of H-2 haplotypes.

scholarly journals GENETIC ANALYSIS OF A MOUSE t COMPLEX LOCUS THAT IS HOMOLOGOUS TO A KIDNEY cDNA CLONE

Genetics ◽  
1986 ◽  
Vol 114 (3) ◽  
pp. 993-1006
Author(s):  
Elizabeth A Mann ◽  
Lee M Silver ◽  
Rosemary W Elliott
Keyword(s):  
Cdna Clone ◽  
Chinese Hamster ◽  
Chromosome 17 ◽  
Chromosome 4 ◽  
Wild Type ◽  
Hybrid Analysis ◽  
T Complex ◽  
Proximal Half ◽  
Length Polymorphisms ◽  
Complex Locus

ABSTRACT A mouse kidney cDNA clone, pMK174, identifies restriction fragment length polymorphisms (RFLPs) that map to two unlinked loci. One, designated D17Rp17, has been mapped near quaking, (qk), on chromosome 17 using three sets of recombinant inbred (RI) strains. A study of several t haplotypes resulted in the identification of t-specific alleles of D17Rp17 that map to the proximal half of the t complex. Neither t-specific nor wild-type D17Rp17 alleles are present in chromosomes carrying either the T Orleans (TtOrl) or the T hairpin tail (Thp) deletions. Comparison with other molecular markers indicates that pMK174 identifies a new proximal t complex locus, Rp17. The second locus identified by pMK174, termed D4Rp18, is tentatively assigned to chromosome 4 by mouse-Chinese hamster somatic cell hybrid analysis.

Homology of p53 intronic sequences between four laboratory mouse strains and Japanese wild mouse (Mus musculus molossinus Mishima)

Genome ◽  
1994 ◽  
Vol 37 (6) ◽  
pp. 1022-1026 ◽  
Author(s):  
Masayuki Tokumitsu ◽  
Katsuhiro Ogawa
Keyword(s):  
Loss Of Heterozygosity ◽  
Mus Musculus ◽  
Laboratory Mouse ◽  
Wild Mouse ◽  
P53 Gene ◽  
Inbred Strains ◽  
Mouse Strains ◽  
Restriction Enzyme Digestion ◽  
Laboratory Mice ◽  
Wild Mice

Strain variation in the mouse p53 gene sequences was investigated in various regions of the gene in 14 inbred strains of laboratory mice and one Japanese wild mouse strain (Mus musculus molossinus Mishima, M. MOL-MSM). Nucleotides within p53 introns 1 and 7, found to be identical in 10 of the laboratory strains (129/J, A/J, AKR/J, BALB/cJ, C3H/HeJ, C57BL/6J, CBA/J, CE/J, NZB, and SWR/J), were substituted for other nucleotide sequences in common with M. MOL-MSM and the four other strains (DBA/1J, DBA/2J, I/LnJ, and P/J). The latter were documented to have originated from a common ancestor. These observations thus suggested the possibility that the p53 gene may have become substituted by outcrossing of this ancestral strain with Asian mice; this is presumably related to the documentation that Japanese mice brought to western countries were used as laboratory mice early in this century. To establish p53 gene heterozygosity, female C3H/HeJ and male DBA/2J mice were mated to produce F1, hybrids (C3D2F1,). Electrophoresis of PCR fragments including polymorphic regions with or without restriction enzyme digestion, allowed clear distinction of paternal and maternal p53 alleles. These markers, therefore, should be useful for studying the loss of heterozygosity of the p53 gene during the carcinogenic process.Key words: p53 gene, polymorphism, Japanese wild mice, laboratory mice, loss of heterozygosity.

Haplotypes that are mosaic for wild-type and t complex-specific alleles in wild mice.

Genetics ◽  
1989 ◽  
Vol 123 (2) ◽  
pp. 405-415 ◽  
Author(s):  
M A Erhart ◽  
S J Phillips ◽  
F Bonhomme ◽  
P Boursot ◽  
E K Wakeland ◽  
...  
Keyword(s):  
Restriction Fragment ◽  
Mus Musculus ◽  
Genetic Recombination ◽  
Chromosome 17 ◽  
Mus Musculus Domesticus ◽  
Wild Type ◽  
Wild Mice ◽  
T Complex ◽  
Mus Musculus Musculus ◽  
In The Wild

Abstract Two outstanding problems pertaining to the population dynamics and evolution of the t complex in mice concern the frequency of t haplotypes in the wild and the degree to which these haplotypes recombine with their wild-type homologs. To address these problems, the frequency and distribution of several t complex-associated restriction fragment variants in wild mice were estimated. Sixty-four versions of chromosome 17 from wild-derived Mus musculus musculus and Mus musculus domesticus were examined with DNA probes for six loci within the t complex that exhibit restriction fragment variation. All six probes detect variants that have heretofore been found exclusively associated with the t complex. Haplotype analysis of wild-derived chromosomes revealed a high frequency (45.3%) of "mosaic" haplotypes with a mixture of t-specific and wild-type variants and only one haplotype with t-specific variants at all six loci. When 12 well-characterized t haplotypes isolated from diverse geographic regions were analyzed, only three had a complete set of t-specific restriction fragments for the six loci examined. The preponderance of mosaic haplotypes in both groups of mice can be explained by any one of the following hypotheses: genetic recombination between t haplotypes and their wild-type homologs, the persistence in wild populations of haplotypes that have descended from ancestral partial t haplotypes, or that the restriction fragment variants fixed in the ancestral t haplotype were also fixed in some wild-type haplotypes. There is evidence to support all three of these hypotheses in our data. The allelic composition of some mosaic haplotypes indicates that they may have been formed by segmental recombination, either double crossing over or gene conversion, rather than by simple single crossovers. The occurrence of indistinguishable mosaic haplotypes in both M. m. musculus and M. m. domesticus suggests that these haplotypes are ancestral rather than recently derived.

scholarly journals Functional analysis of mutations of murine chromosome 17 with the use of tertiary trisomy.

Genetics ◽  
1991 ◽  
Vol 127 (4) ◽  
pp. 781-788
Author(s):  
A Ruvinsky ◽  
A Agulnik ◽  
S Agulnik ◽  
M Rogachova
Keyword(s):  
Functional Analysis ◽  
Gene Dosage ◽  
Tail Length ◽  
Proximal Region ◽  
The Other ◽  
Chromosome 17 ◽  
Recessive Mutations ◽  
T Complex ◽  
Functional Nature ◽  
Morphogenetic Effects

Abstract Analysis of the functional nature of mutations can be based on comparisons of their manifestation in organisms with a deletion or duplication of a particular chromosome segment. With the use of reciprocal translocation T(16;17)43H, it is feasible to produce mice with tertiary trisomy of the proximal region of chromosome 17. The mutations on chromosome 17 we tested included brachyury (T), hairpin tail (Thp), kinky (Fuki), quaking (qk), tufted (tf), as well as tct (t complex tail interaction), and tcl (t complex lethal) that are specific to t haplotypes. The set of dominant and recessive mutations was assigned to two groups: one obligatory, manifesting itself in the phenotype independently of the number of normal alleles in di- and trisomics, and the other facultative, phenotypically manifesting itself depending upon the dosage of mutant alleles. A model was derived from analysis of the interaction of the T and Thp mutations with t haplotypes. It seeks to explain the morphogenetic effects of the mutations observed in mice of different genotypes. The tir gene is postulated to reside on chromosome 17 within its framework. It is suggested that the gene dosage ratio at the tir and tct loci determines tail length.

scholarly journals Genetic and molecular analysis of the proximal region of the mouse t-complex using new molecular probes and partial t-haplotypes.

Genetics ◽  
1990 ◽  
Vol 126 (4) ◽  
pp. 1103-1114 ◽  
Author(s):  
C A Howard ◽  
G R Gummere ◽  
M F Lyon ◽  
D Bennett ◽  
K Artzt
Keyword(s):  
Wild Mouse ◽  
Molecular Probes ◽  
Proximal Region ◽  
Chromosome 17 ◽  
Lethal Gene ◽  
Strong Linkage Disequilibrium ◽  
Wild Type ◽  
T Complex ◽  
Naturally Occurring ◽  
Normal Transmission

Abstract The t-complex is located on the proximal third of chromosome 17 in the house mouse. Naturally occurring variant forms of the t-complex, known as complete t-haplotypes, are found in wild mouse populations. The t-haplotypes contain at least four nonoverlapping inversions that suppress recombination with the wild-type chromosome, and lock into strong linkage disequilibrium loci affecting normal transmission of the chromosome, male gametogenesis and embryonic development. Partial t-haplotypes derived through rare recombination between t-haplotypes and wild-type homologs have been critical in the analysis of these properties. Utilizing two new DNA probes. Au3 and Au9, and several previously described probes, we have analyzed the genetic structure of several partial t-haplotypes that have arisen in our laboratory, as well as several wild-type chromosomes deleted for loci in this region. With this approach we have been able to further our understanding of the structural and dynamic characteristics of the proximal region of the t-complex. Specifically, we have localized the D17Tul locus as most proximal known in t-haplotypes, achieved a better structural analysis of the partial t-haplotype t6, and defined the structure and lethal gene content of partial t-haplotypes derived from the lethal tw73 haplotype.

scholarly journals Distorter genes of the mouse t-complex impair male fertility when heterozygous

1987 ◽  
Vol 49 (1) ◽  
pp. 57-60 ◽  
Author(s):  
Mary F. Lyon
Keyword(s):  
Male Fertility ◽  
Genetic Background ◽  
Inbred Strains ◽  
Transmission Ratio Distortion ◽  
Chromosome 17 ◽  
Male Mice ◽  
Wild Type ◽  
T Complex ◽  
Ratio Distortion ◽  
Harmful Effects

SummaryMale mice heterozygous for two distorter genes, Tcd-1 and Tcd-2, of the mouse t-complex but homozygous wild type for the responder, were generated by crossing animals carrying the partial t-haplotypes th51 and th18 to inbred strains. The fertility of these males was then compared with that of their brothers carrying normal chromosome 17s. On three of the inbred backgrounds used, C3H/HeH, C57BL/6J and TFH/H, the th51th18 + / + + + males were significantly less fertile than their normal sibs. With the fourth inbred strain used, SM/JH, both types of male were nonnally fertile. This confirmed earlier preliminary findings that when both homologues of chromosome 17 carry wild-type alleles of the responder, heterozygosity for the distorter genes is sufficient to impair fertility, but the effect varies with genetic background. These results are consistent with the concept that both the transmission ratio distortion and the male sterility caused by the t-complex are due to harmful effects of the distorter genes on wild-type alleles of the responder.

scholarly journals Effect of Crossing C57BL/6 and FVB Mouse Strains on Basal Cytokine Expression

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Agata Szade ◽  
Witold N. Nowak ◽  
Krzysztof Szade ◽  
Anna Gese ◽  
Ryszard Czypicki ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Transgenic Mice ◽  
Mouse Strain ◽  
Laboratory Mouse ◽  
Cytokine Expression ◽  
The Other ◽  
Mouse Strains ◽  
Laboratory Mouse Strain ◽  
Common Strategy ◽  
Different Strains

C57BL/6 is the most often used laboratory mouse strain. However, sometimes it is beneficial to cross the transgenic mice on the C57BL/6 background to the other strain, such as FVB. Although this is a common strategy, the influence of crossing these different strains on homeostatic expression of cytokines is not known. Here we have investigated the differences in the expression of selected cytokines between C57BL/6J and C57BL/6JxFVB mice in serum and skeletal muscle. We have found that only few cytokines were altered by crossing of the strains. Concentrations of IL5, IL7, LIF, MIP-2, and IP-10 were higher in serum of C57BL/6J mice than in C57BL/6JxFVB mice, whereas concentration of G-CSF was lower in C57BL/6J. In the skeletal muscle only the concentration of VEGF was higher in C57BL/6J mice than in C57BL/6JxFVB mice. Concluding, the differences in cytokine expression upon crossing C57BL/6 and FVB strain in basal conditions are not profound.

scholarly journals Genetic evidence for two t complex tail interaction (tct) loci in t haplotypes.

Genetics ◽  
1989 ◽  
Vol 122 (4) ◽  
pp. 895-903
Author(s):  
J H Nadeau ◽  
D Varnum ◽  
D Burkart
Keyword(s):  
Genetic Analysis ◽  
Tail Length ◽  
Genetic Interactions ◽  
Chromosome 17 ◽  
Wild Type ◽  
T Complex ◽  
Inverted Duplication ◽  
Haplotype A ◽  
Recombination Breakpoints ◽  
T Haplotype

Abstract The t complex on chromosome 17 of the house mouse is an exceptional model for studying the genetic control of transmission ratio, gametogenesis, and embryogenesis. Partial haplotypes derived through rare recombination between a t haplotype and its wild-type homolog have been essential in the genetic analysis of these various properties of the t complex. A new partial t haplotype, which was derived from the complete tw71 haplotype and which is called tw71Jr1, was shown to have unexpected effects on tail length and unique recombination breakpoints. This haplotype, either when homozygous or when heterozygous with the progenitor tw71 haplotype, produced short-tailed rather than normal-tailed mice on certain genetic backgrounds. Genetic analysis of this exceptional haplotype showed that the recombination breakpoints were different from those leading to any other partial t haplotype. Based on this haplotype, a model is proposed that accounts for genetic interactions between the brachyury locus (T), the t complex tail interaction (tct) locus, and their wild-type homolog(s) that determine tail length. An important part of this model is the hypothesis that the tct locus, which enhances the tail-shortening effect of T mutations, is in fact at least two, genetically separable genes with different genetic activities. Genetic analysis of parental and recombinant haplotypes also suggests that intrachromosomal recombination involving an inverted duplicated segment can account for the variable orientation of loci within an inverted duplication on wild-type homologs of the t haplotype.

Identification of a germ-cell-specific transcriptional repressor in the promoter of Tctex-1

Development ◽  
1995 ◽  
Vol 121 (2) ◽  
pp. 561-568 ◽  
Author(s):  
M.J. O'Neill ◽  
K. Artzt
Keyword(s):  
Germ Cell ◽  
Gene Family ◽  
Binding Site ◽  
Transcriptional Repressor ◽  
Chromosome 17 ◽  
Wild Type ◽  
Aberrant Expression ◽  
T Complex ◽  
T Haplotype

The Tctex-1 gene family maps to the t complex of the mouse and consists of four copies on chromosome 17 in both wild-type and t-haplotypes. Tctex-1 mRNA is eightfold overexpressed in male and female germ cells in t-haplotype compound heterozygotes (tx/ty). In order to determine the cause of this aberrant expression and the role of this gene family in spermatogenesis and oogenesis it was subjected to extensive molecular analysis. We find that Tctex-1 protein is present in sperm tails and oocytes and that it is present at equal levels in wild-type and t-haplotype testis. Surprisingly, the excess message in t-haplotypes is not translated. Sequence analysis of the gene family reveals that one copy in t-haplotypes has a mutated start codon. This same copy is deleted for a protein-binding motif in its promoter. This motif, GIM (Germ cell Inhibitory Motif) has strong homology to the Xenopus AP-2-binding site but does not appear to be a binding site for mammalian AP-2. A factor(s) present in testis and ovary, but absent in other mouse tissues binds specifically to this site. Transfection assays using Tctex-1 promoter constructs suggest that GIM functions as a transcriptional repressor. The possible role of Tctex-1 in t complex transmission ratio distortion and sterility is discussed.

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