Development of interspecific hybrids of Mus

Development ◽  
1977 ◽  
Vol 41 (1) ◽  
pp. 233-243
Author(s):  
John D. West ◽  
William I. Frels ◽  
Virginia E. Papaioannou ◽  
James P. Karr ◽  
Verne M. Chapman
Keyword(s):  
Early Development ◽  
X Chromosome ◽  
Mus Musculus ◽  
Artificial Insemination ◽  
Interspecific Hybrids ◽  
Genetic System ◽  
X Chromosome Inactivation ◽  
Chromosome Inactivation ◽  
Foetal Development ◽  
Further Development

Artificial insemination has been used to produce interspecific mouse hybrids. Mus musculus × Mus cervicolor cervicolor hybrids failed to complete more than a few cleavage divisions but both M. musculus × M. dunni and M. musculus × M. caroli hybrids completed preimplantation development. These hybrid embryos are heterozygous for various X-linked enzymes and may provide a useful genetic system for studying X-chromosome inactivation during early development. Further development of M. musculus × M. caroli hybrids was studied: several completed foetal development; a few survived to maturity but none has yet reproduced.

Preferential X-chromosome inactivation, DNA methylation and imprinting

Development ◽  
1990 ◽  
Vol 108 (Supplement) ◽  
pp. 55-62
Author(s):  
Marilyn Monk ◽  
Mark Grant
Keyword(s):  
Dna Methylation ◽  
Early Development ◽  
X Chromosome ◽  
Expression Patterns ◽  
Genetic Material ◽  
X Chromosome Inactivation ◽  
Differential Methylation ◽  
X Inactivation ◽  
Chromosome Inactivation ◽  
Embryonic Tissues

Non-random X-chromosome inactivation in mammals was one of the first observed examples of differential expression dependent on the gamete of origin of the genetic material. The paternally-inherited X chromosome is preferentially inactive in all cells of female marsupials and in the extra-embryonic tissues of developing female rodents. Some form of parental imprinting during male and female gametogenesis must provide a recognition signal that determines the nonrandomness of X-inactivation but its nature is thus far unknown. In the mouse, the imprint distinguishing the X chromosomes in the extra-embryonic tissues must be erased early in development since X-inactivation is random in the embryonic cells. Random X-chromosome inactivation leads to cellular mosaicism in expression and differential methylation of active and inactive X-linked genes. Transgene imprinting shares many features with X-inactivation, including differential DNA methylation. In this paper we consider when methylation differences in early development affecting X-chromosome activity and imprinting are established. There are processes of methylation and demethylation occurring in early development, as well as changes in the activity of the DNA methylase itself. Methylation of a specific CpG site associated with activity of the X-linked PGK-1 gene has been studied. This site is already methylated on the inactive X chromosome by 6.5 days' gestation, close to the time of X-inactivation. However, differential methylation of this site is not the primary imprint marking the paternal X chromosome for preferential inactivation in the extra-embryonic membranes. A consideration of factors influencing both X-chromosome inactivation and imprinting suggests that a process of communication and comparison between nonidentical alleles might by the basis for the differential modification and expression patterns observed.

X-linked CNV and skewed X-chromosome inactivation

2020 ◽  
pp. 19-21
Author(s):  
Е.А. Фонова ◽  
Е.Н. Толмачева ◽  
А.А. Кашеварова ◽  
М.Е. Лопаткина ◽  
К.А. Павлова ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Intellectual Disability ◽  
X Chromosome ◽  
Copy Number ◽  
Copy Number Variations ◽  
X Chromosome Inactivation ◽  
Chromosome Inactivation ◽  
Chromosome X ◽  
Skewed X Chromosome Inactivation

Смещение инактивации Х-хромосомы может быть следствием и маркером нарушения клеточной пролиферации при вариациях числа копий ДНК на Х-хромосоме. Х-сцепленные CNV выявляются как у женщин с невынашиванием беременности и смещением инактивации Х-хромосомы (с частотой 33,3%), так и у пациентов с умственной отсталостью и смещением инактивацией у их матерей (с частотой 40%). A skewed X-chromosome inactivation can be a consequence and a marker of impaired cell proliferation in the presence of copy number variations (CNV) on the X chromosome. X-linked CNVs are detected in women with miscarriages and a skewed X-chromosome inactivation (with a frequency of 33.3%), as well as in patients with intellectual disability and skewed X-chromosome inactivation in their mothers (with a frequency of 40%).

scholarly journals X-Linked Emery–Dreifuss Muscular Dystrophy: Study Of X-Chromosome Inactivation and Its Relation with Clinical Phenotypes in Female Carriers

Genes ◽  
2019 ◽  
Vol 10 (11) ◽  
pp. 919 ◽  
Author(s):  
Viggiano ◽  
Madej-Pilarczyk ◽  
Carboni ◽  
Picillo ◽  
Ergoli ◽  
...  
Keyword(s):  
Muscular Dystrophy ◽  
X Chromosome ◽  
Clinical Symptoms ◽  
Fibrous Tissue ◽  
X Chromosome Inactivation ◽  
Chromosome Inactivation ◽  
Cardiac Conduction ◽  
Asymptomatic Carriers ◽  
Cardiac Symptoms ◽  
Female Carriers

X-linked Emery–Dreifuss muscular dystrophy (EDMD1) affects approximately 1:100,000 male births. Female carriers are usually asymptomatic but, in some cases, they may present clinical symptoms after age 50 at cardiac level, especially in the form of conduction tissue anomalies. The aim of this study was to evaluate the relation between heart involvement in symptomatic EDMD1 carriers and the X-chromosome inactivation (XCI) pattern. The XCI pattern was determined on the lymphocytes of 30 symptomatic and asymptomatic EDMD1 female carriers—25 familial and 5 sporadic cases—seeking genetic advice using the androgen receptor (AR) methylation-based assay. Carriers were subdivided according to whether they were above or below 50 years of age. A variance analysis was performed to compare the XCI pattern between symptomatic and asymptomatic carriers. The results show that 20% of EDMD1 carriers had cardiac symptoms, and that 50% of these were ≥50 years of age. The XCI pattern was similar in both symptomatic and asymptomatic carriers. Conclusions: Arrhythmias in EDMD1 carriers poorly correlate on lymphocytes to a skewed XCI, probably due to (a) the different embryological origin of cardiac conduction tissue compared to lymphocytes or (b) the preferential loss of atrial cells replaced by fibrous tissue.

scholarly journals Loss of p53 Causes Stochastic Aberrant X-Chromosome Inactivation and Female-Specific Neural Tube Defects

Cell Reports ◽  
2019 ◽  
Vol 27 (2) ◽  
pp. 442-454.e5 ◽  
Author(s):  
Alex R.D. Delbridge ◽  
Andrew J. Kueh ◽  
Francine Ke ◽  
Natasha M. Zamudio ◽  
Farrah El-Saafin ◽  
...  
Keyword(s):  
X Chromosome ◽  
Neural Tube ◽  
Neural Tube Defects ◽  
X Chromosome Inactivation ◽  
Chromosome Inactivation ◽  
Female Specific

Spread of X‐chromosome inactivation into autosomal regions in patients with unbalanced X‐autosome translocations and its phenotypic effects

2021 ◽  
Author(s):  
Bianca Pereira Favilla ◽  
Vera Ayres Meloni ◽  
Ana Beatriz Perez ◽  
Danilo Moretti‐Ferreira ◽  
Deise Helena Souza ◽  
...  
Keyword(s):  
X Chromosome ◽  
X Chromosome Inactivation ◽  
Chromosome Inactivation

scholarly journals XChromosome Effect on Maternal Recombination and Meiotic Drive in the Mouse

Genetics ◽  
2002 ◽  
Vol 161 (4) ◽  
pp. 1651-1659 ◽  
Author(s):  
Elena de la Casa-Esperón ◽  
J Concepción Loredo-Osti ◽  
Fernando Pardo-Manuel de Villena ◽  
Tammi L Briscoe ◽  
Jan Michel Malette ◽  
...  
Keyword(s):  
Mouse Chromosome ◽  
X Chromosome ◽  
Meiotic Recombination ◽  
Meiotic Drive ◽  
X Chromosome Inactivation ◽  
Chromosome Inactivation ◽  
Chromosome 11 ◽  
Genome Wide ◽  
Mouse Chromosome 11 ◽  
Segregation Of Chromosomes

AbstractWe observed that maternal meiotic drive favoring the inheritance of DDK alleles at the Om locus on mouse chromosome 11 was correlated with the X chromosome inactivation phenotype of (C57BL/ 6-Pgk1a × DDK)F1 mothers. The basis for this unexpected observation appears to lie in the well-documented effect of recombination on meiotic drive that results from nonrandom segregation of chromosomes. Our analysis of genome-wide levels of meiotic recombination in females that vary in their X-inactivation phenotype indicates that an allelic difference at an X-linked locus is responsible for modulating levels of recombination in oocytes.

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