Two new mouse chromosome 11 balancers

Kłysik, Jan; Dinh, Chris; Bradley, Allan

doi:10.1016/j.ygeno.2003.08.011

Cited by 18 publications

(11 citation statements)

References 30 publications

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“…Following electroporation of the linear pEGFP-C1(AscI)Egfr into the AB2.2 ES cells, multiple G418-resistant cell lines were identified by Southern analysis at a frequency of 26%. This frequency of G418-resistant colony formation was consistent with prior studies in which the same locus has been targeted (Klysik et al, 2004). Southern blot analysis confirmed the expected size change of the restriction fragment resulting from the homologous recombination events (Fig.…”

Section: Generation Of the Egfp Knock-in Es Cell Linessupporting

confidence: 90%

“…Large segmental inversions, or balancers (Frank et al, 2003;Justice et al, 1999;Kile et al, 2003;Klysik et al, 2003Klysik et al, , 2004Rinchik, 2000), constitute effective tools that allow one to address ∼2% of the genome in a single mutagenesis experiment. Balancers were first observed in Drosophila melanogaster stocks causing self-perpetuating maintenance of lethal mutations located on homologous chromosomes (Muller, 1918).…”

Section: Introductionmentioning

confidence: 99%

“…1), which are not viable (Zheng et al, 1999b). Typically, engineering the mouse inversion chromosome involves the disruption of a known recessive lethal function to produce a balancer (Klysik et al, 2004;Zheng et al, 1999b). In addition, a coat color marker is usually introduced into the inverted allele, and this feature allows for recognizing inversion carriers in the stock without the necessity for molecular genotyping.…”

Section: Introductionmentioning

confidence: 99%

“…2) and two strains of mice, one should carry the recombination suppressive element (inversion) tagged by the first coat marker, while the second strain should carry the second coat color tag within the chromosomal region that is inverted in the first strain. Recently, we generated two new inversions on mouse chromosome 11 (Klysik et al, 2004). A dominant K14-agouti minigene was used to tag both inversions and to make these mice visibly distinguishable from their wild-type littermates (yellowing ears and tails).…”

Section: Introductionmentioning

confidence: 99%

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Mice with the Enhanced Green Fluorescent Protein Gene Knocked in to Chromosome 11 Exhibit Normal Transmission Ratios

Kłysik

Singer

2005

Biochem Genet

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Meiotic recombination between homologous chromosomes can be suppressed within a chosen segment by a regional inversion. In mice, this feature can be engineered and conveniently used in genetic screens to maintain chemically induced mutations within the homologous chromosome. The efficiency of an inversion-based mutagenesis screen can be substantially enhanced provided that the inversion chromosome and its wild-type (WT) homologue are both visibly tagged by two different coat color markers. Dual tagging eliminates labor associated with molecular genotyping. Previously, we reported the generation of the In(11)10Brd strain of mice carrying K14-agouti tagging a 30-cM inversion between the Trp53 and Egfr loci on mouse chromosome 11. Since K14-agouti causes yellowing of ears and tails, the In(11)10Brd mice are easily distinguishable from their WT littermates. In this paper, we describe the construction of a second strain of mice that carry the enhanced green fluorescent protein (EGFP) transgene at the Egfr locus. The EGFP carriers are visually recognizable by emitting green fluorescent light upon UV illumination. We found that the EGFP function was transmitted from one generation to another with expected Mendelian frequencies, and no detrimental effects of EGFP expression were detected in hemizygous or homozygous animals. The EGFP mice together with the previously generated In(11)10Brd inversion carriers constitute a complete set of reagents required for initiation of a regional ENU mutagenesis screen to address functionally more than one-third of mouse chromosome 11.

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Section: Generation Of the Egfp Knock-in Es Cell Linessupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Mice with the Enhanced Green Fluorescent Protein Gene Knocked in to Chromosome 11 Exhibit Normal Transmission Ratios

Kłysik

Singer

2005

Biochem Genet

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“…If this is indeed the case, the ''granular'' distribution of crossovers that we observed in the Xce region may not be unusual. Alternatively, the Xce locus may be marked by genomic rearrangements (such as inversions) between strains, as these have been shown to bias recombination rates (Singleton 1964), even in mice (Zheng et al 1999;Klysik et al 2004). Such genomic differences could either ablate binding sites for trans-acting factors entirely or bring these sites closer to (or farther from) other enhancer elements or the Tsix promoter.…”

Section: Discussionmentioning

confidence: 99%

Genetic Control of X Chromosome Inactivation in Mice: Definition of the Xce Candidate Interval

et al. 2006

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In early mammalian development, one of the two X chromosomes is silenced in each female cell as a result of X chromosome inactivation, the mammalian dosage compensation mechanism. In the mouse epiblast, the choice of which chromosome is inactivated is essentially random, but can be biased by alleles at the X-linked X controlling element (Xce). Although this locus was first described nearly four decades ago, the identity and precise genomic localization of Xce remains elusive. Within the X inactivation center region of the X chromosome, previous linkage disequilibrium studies comparing strains of known Xce genotypes have suggested that Xce is physically distinct from Xist, although this has not yet been established by genetic mapping or progeny testing. In this report, we used quantitative trait locus (QTL) mapping strategies to define the minimal Xce candidate interval. Subsequent analysis of recombinant chromosomes allowed for the establishment of a maximum 1.85-Mb candidate region for the Xce locus. Finally, we use QTL approaches in an effort to identify additional modifiers of the X chromosome choice, as we have previously demonstrated that choice in Xce heterozygous females is significantly influenced by genetic variation present on autosomes (Chadwick and Willard 2005). We did not identify any autosomal loci with significant associations and thus show conclusively that Xce is the only major locus to influence X inactivation patterns in the crosses analyzed. This study provides a foundation for future analyses into the genetic control of X chromosome inactivation and defines a 1.85-Mb interval encompassing all the major elements of the Xce locus.

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Genome engineering: Drosophila melanogaster and beyond

Sarrión-Perdigones¹,

Vandeventer²,

Abel

et al. 2015

WIREs Developmental Biology

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A central challenge to investigating biological phenomena is the development of techniques to modify genomic DNA with nucleotide precision that can be transmitted through the germ line. Recent years have brought a boon in these technologies, now collectively known as genome engineering. Defined genomic manipulations at the nucleotide level enable a variety of reverse engineering paradigms, providing new opportunities to interrogate diverse biological functions. These genetic modifications include controlled removal, insertion, and substitution of genetic fragments, both small and large. Small fragments up to a few kilobases (e.g., single nucleotide mutations, small deletions, or gene tagging at single or multiple gene loci) to large fragments up to megabase resolution can be manipulated at single loci to create deletions, duplications, inversions, or translocations of substantial sections of whole chromosome arms. A specialized substitution of chromosomal portions that presumably are functionally orthologous between different organisms through syntenic replacement, can provide proof of evolutionary conservation between regulatory sequences. Large transgenes containing endogenous or synthetic DNA can be integrated at defined genomic locations, permitting an alternative proof of evolutionary conservation, and sophisticated transgenes can be used to interrogate biological phenomena. Precision engineering can additionally be used to manipulate the genomes of organelles (e.g., mitochondria). Novel genome engineering paradigms are often accelerated in existing, easily genetically tractable model organisms, primarily because these paradigms can be integrated in a rigorous, existing technology foundation. The Drosophila melanogaster fly model is ideal for these types of studies. Due to its small genome size, having just four chromosomes, the vast amount of cutting-edge genetic technologies, and its short life-cycle and inexpensive maintenance requirements, the fly is exceptionally amenable to complex genetic analysis using advanced genome engineering. Thus, highly sophisticated methods developed in the fly model can be used in nearly any sequenced organism. Here, we summarize different ways to perform precise inheritable genome engineering using integrases, recombinases, and DNA nucleases in the D. melanogaster.

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Two new mouse chromosome 11 balancers

Cited by 18 publications

References 30 publications

Mice with the Enhanced Green Fluorescent Protein Gene Knocked in to Chromosome 11 Exhibit Normal Transmission Ratios

Mice with the Enhanced Green Fluorescent Protein Gene Knocked in to Chromosome 11 Exhibit Normal Transmission Ratios

Genetic Control of X Chromosome Inactivation in Mice: Definition of the Xce Candidate Interval

Genome engineering: Drosophila melanogaster and beyond

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