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  • 1
    Electronic Resource
    Electronic Resource
    Dual evolutionary modes in the bovine globin locus (1986)
    s.l. : American Chemical Society
    Biochemistry 25 (1986), S. 5028-5035 
    Details
    ISSN: 1520-4995
    Source: ACS Legacy Archives
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/bi00366a009
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  • 2
    Electronic Resource
    Electronic Resource
    DelBank: a mouse ES-cell resource for generating deletions (2001)
    [s.l.] : Nature Publishing Group
    Nature genetics 28 (2001), S. 310-311 
    Details
    ISSN: 1546-1718
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] Chromosomal deletions are valuable reagents for identifying and mapping genetic function. To simplify the creation of deletions in mice, we developed a collection of embryonic stem (ES) cell clones called DelBank. DelBank is based upon a technology in which radiation-induced deletions of herpes ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/91064
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  • 3
    Electronic Resource
    Electronic Resource
    Mouse mutants from chemically mutagenized embryonic stem cells (2000)
    [s.l.] : Nature America Inc.
    Nature genetics 24 (2000), S. 318-321 
    Details
    ISSN: 1546-1718
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] The drive to characterize functions of human genes on a global scale has stimulated interest in large-scale generation of mouse mutants. Conventional germ-cell mutagenesis with N-ethyl-N-nitrosourea (ENU) is compromised by an inability to monitor mutation efficiency, strain and interlocus ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/73563
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  • 4
    Electronic Resource
    Electronic Resource
    A viable allele of Mcm4 causes chromosome instability and mammary adenocarcinomas in mice (2007)
    [s.l.] : Nature Publishing Group
    Nature genetics 39 (2007), S. 93-98 
    Details
    ISSN: 1546-1718
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] Mcm4 (minichromosome maintenance–deficient 4 homolog) encodes a subunit of the MCM2-7 complex (also known as MCM2–MCM7), the replication licensing factor and presumptive replicative helicase. Here, we report that the mouse chromosome instability mutation Chaos3 (chromosome aberrations ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/ng1936
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  • 5
    Electronic Resource
    Electronic Resource
    Sodium butyrate causes reexpression of three membrane proteins on glycolipid-anchoring mutants (1991)
    Springer
    Somatic cell and molecular genetics 17 (1991), S. 349-357 
    Details
    ISSN: 1572-9931
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Murine Thy-1-negative lymphoma mutants synthesize membrane proteins that normally bear glycolipid anchors but do not express these proteins on the cell surface. This phenotype may reflect altered regulation of gene(s) required for anchor biosynthesis. Since tissue culture cells treated with sodium butyrate transcribe new DNA sequences and since these transcripts are translated, it was of interest to determine whether butyrate treatment could restore surface expression of lipid-anchored proteins. When Thy-1-negative lymphoma mutants (complementation groups A–C, E, F, and H) were cultured for three days in 1.5 mM butyrate, a small percentage of the class H cells acquired phosphatidylinositol-specific phospholipase C-releasable surface Thy-1 and J11d. Membrane-associated Thy-1 was not observed before 24 h of treatment. Induction was reversible. Cell fusion studies have shown that murine LM (TK−) fibroblasts can be assigned to the class H lymphoma complementation group. Although these cells synthesize Ly-6, this normally lipid-anchored protein is absent from the cell surface. When LM (TK−) cells were cultured for three days in butyrate, 10% of the cells reversibly expressed Ly-6. In addition, LM (TK−) cells transfected with a plasmid encoding Thy-1 do not express Thy-1, but could be induced to express both Ly-6 and Thy-1 by butyrate treatment. Northern analysis of total RNA from Ly-6/Thy-1-expressing cells indicates that increased steady-state transcript levels cannot account for surface expression of these proteins. We conclude that the lack of expression of three proteins at the surface of class H mutant and the LM (TK−) cells is not due to gross structural lesions in genes along the anchor biosynthetic pathway.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01233060
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  • 6
    Electronic Resource
    Electronic Resource
    Factors affecting ectopic gene conversion in mice (1998)
    Springer
    Mammalian genome 9 (1998), S. 355-360 
    Details
    ISSN: 1432-1777
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract. Duplicated genes and repetitive sequences are distributed throughout the genomes of complex organisms. The homology between related sequences can promote nonallelic (ectopic) recombination, including gene conversion and reciprocal exchange. Resolution of these events can result in translocations, deletions, or other harmful rearrangements. In yeast, ectopic recombination between sequences on nonhomologous chromosomes occurs at high frequency. Because the mammalian genome is replete with duplicated sequences and repetitive elements, high levels of ectopic exchange would cause aneuploidy and genome instability. To understand the factors regulating ectopic recombination in mice, we evaluated the effects of homology length on gene conversion between unlinked sequences in the male germline. Previously, we found high levels of gene conversion between lacZ transgenes containing 2557 bp of homology. We report here that genetic background can play a major role in ectopic recombination; frequency of gene conversion was reduced by more than an order of magnitude by transferring the transgenes from a CF1 strain background to C57BL/6J. Additionally, conversion rates decreased as the homology length decreased. Sequences sharing 1214 bp of sequence identity underwent ectopic conversion less frequently than a pair sharing 2557 bp of identity, while 624 bp was insufficient to catalyze gene conversion at significant levels. These results suggest that the germline recombination machinery in mammals has evolved in a way that prevents high levels of ectopic recombination between smaller classes of repetitive sequences, such as the Alu family. Additionally, genomic location appeared to influence the availability of sequences for ectopic recombination.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s003359900769
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  • 7
    Electronic Resource
    Electronic Resource
    Functional analysis of a t complex responder locus transgene in mice (1992)
    Springer
    Mammalian genome 3 (1992), S. 579-587 
    Details
    ISSN: 1432-1777
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Transmission ratio distortion (TRD) of mouse t haplotypes occurs through the interaction of multiple distorter loci with the t complex responder (Tcr) locus. Males heterozygous for a t haplotype will transmit the t-bearing chromosome to nearly all of their offspring. This process is mediated by the production of functionally inequivalent gametes: wildtype meiotic partners of t spermatozoa are rendered functionally inactive. The Tcr locus, which is required for TRD to occur, is thought to somehow protect its host spermatid from the sperm-inactivating effects of linked distorter genes (Lyon 1984). In previous work, Tcr was mapped to a small genetic interval in t haplotypes, and a candidate gene from this region was isolated (Tcp-10b t). In this work, we further localize Tcr to a 40-kb region that contains the 21-kb Tcp-10b t gene. A cloned genomic copy of Tcp-10b t was used to generate transgenic mice. The transgene was bred into a variety of genetic backgrounds to test for non-Mendelian segregation. Abberrant segregation was observed in some mice carrying either a complete t haplotype or a combination of certain partial t haplotypes. These observations, coupled with those of Snyder and colleagues (in this issue), provide genetic and functional evidence that the Tcp-10b t gene is Tcr. However, other genotypes that were predicted to produce distortion did not. The unexpected data from a variety of crosses in this work and those of our colleagues suggest that elements to the TRD system and the Tcr locus remain to be identified.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00350625
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  • 8
    Electronic Resource
    Electronic Resource
    Molecular structure of Tcp-10 genes from the t complex responder locus (1991)
    Springer
    Mammalian genome 1 (1991), S. 228-234 
    Details
    ISSN: 1432-1777
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Male transmission ratio distortion (TRD) is a property of mouse t haplotypes which requires the t complex responder locus (Tcr). Tcr has been localized to a 70–160 kb region in t haplotypes. A candidate gene for the responder, called Tcp-10b t, has been cloned and is one member of a highly related gene family called Tcp-10 (formerly T66). Molecular evidence suggests that unique alternative splicing of the Tcp-10b t gene may be responsible for the mutant responder activity. Here we present the intron/exon structure of a representative Tcp-10 gene, and the charaterization of alternative polyadenylation sites. The Tcp-10 genes contain 12 exons which span approximately 21 kb of DNA. At least six different polyadenylation sites are used, and none have a perfect consensus signal. This appears to be a common feature associated with testes-expressed transcripts. Since the gene we have analyzed is absent from many t haplotypes without apparent consequence, and no corresponding cDNAs have been isolated, it was speculated to be a pseudogene. However, no major sequence differences were found within the coding sequence to conclude that Tcp-10ps t is a pseudogene.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00352329
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  • 9
    Electronic Resource
    Electronic Resource
    ORFless, intronless, and mutant transcription units in the mouse t complex responder (Tcr) locus (1999)
    Springer
    Mammalian genome 10 (1999), S. 969-976 
    Details
    ISSN: 1432-1777
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract. Mouse t haplotypes exhibit transmission ratio distortion (TRD), whereby heterozygous males (+/t) transmit the t chromosome to nearly all offspring. TRD is mediated by the t complex responder locus (Tcr), whose transmission is elevated above Mendelian levels by additive contribution of several t haplotype-encoded quantitative trait loci (QTLs) called t complex distorters (Tcd1–Tcd5). The entire genetically defined Tcr interval has been cloned and consists of under 200 kb. This interval is one of three large duplication units in t haplotypes that retain high levels of similarity. The cis-active nature of Tcr raises the possibility that it is not a protein-encoding gene, but another anomaly such as a structural anomaly of chromatin. To further investigate the Tcr-critical interval, a 30-kb region upstream of the Tcp10b t gene (a testis-expressed former candidate for Tcr) was sequenced, along with the duplicated paralogous region associated with Tcp10c t , which lies immediately adjacent but outside the Tcr interval. Several genes or transcriptional units were identified, including the 3′ end of ribosomal s6 kinase (Rsk3); two apparently intronless and ORF-less genes; and Gpr31, an intronless, putative G-protein coupled receptor. While the 30-kb regions were 98% identical, the Gpr31 paralog from the Tcr-critical region (Gpr31b t ) contained an in-frame 210-bp deletion that disrupted two of the seven predicted transmembrane domains. Furthermore, an intronless and ORFless gene from this interval, Trex1b t , contained a 4-bp deletion that distinguished it from all other homologs in t haplotypes and wild-type chromosomes. Although it is unknown whether any of these genes are involved in TRD, their discovery raises new possibilities regarding the nature of Tcr, including a model whereby it might function as an RNA rather than a protein or chromatin anomaly.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s003359901142
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  • 10
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    Testis formation in XX individuals resulting from novel pathogenic variants in Wilms’ tumor 1 (WT1) gene (2020)
    National Academy of Sciences
    Details
    Publication Date: 2020-06-03
    Description: Sex determination in mammals is governed by antagonistic interactions of two genetic pathways, imbalance in which may lead to disorders/differences of sex development (DSD) in human. Among 46,XX individuals with testicular DSD (TDSD) or ovotesticular DSD (OTDSD), testicular tissue is present in the gonad. Although the testis-determining geneSRYis present in many cases, the etiology is unknown in mostSRY-negative patients. We performed exome sequencing on 78 individuals with 46,XX TDSD/OTDSD of unknown genetic etiology and identified seven (8.97%) with heterozygous variants affecting the fourth zinc finger (ZF4) of Wilms’ tumor 1 (WT1) (p.Ser478Thrfs*17, p.Pro481Leufs*15, p.Lys491Glu, p.Arg495Gln [x3], p.Arg495Gly). The variants were de novo in six families (P= 4.4 × 10−6), and the incidence of WT1 variants in 46,XX DSD is enriched compared to control populations (P〈 1.8 × 10−4). The introduction of ZF4 mutants into a human granulosa cell line resulted in up-regulation of endogenous Sertoli cell transcripts andWt1Arg495Gly/Arg495GlyXX mice display masculinization of the fetal gonads. The phenotype could be explained by the ability of the mutated proteins to physically interact with and sequester a key pro-ovary factor β-CATENIN, which may lead to up-regulation of testis-specific pathway. Our data show that unlike previous association of WT1 and 46,XY DSD, ZF4 variants of WT1 are a relatively common cause of 46,XX TDSD/OTDSD. This expands the spectrum of phenotypes associated with WT1 variants and shows that the WT1 protein affecting ZF4 can function as a protestis factor in an XX chromosomal context.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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