Molecular identification of t(w5): Vps52 promotes pluripotential cell differentiation through cell-cell interactions.

After implantation, pluripotent epiblasts are converted to embryonic ectoderm through cell-cell interactions that significantly change the transcriptional and epigenetic networks. An entrée to understanding this vital developmental transition is the t(w5) mutation of the mouse t complex. This mutation produces highly specific defects in the embryonic ectoderm before gastrulation, leading to death of the embryonic ectoderm.

Disruption of genetic interaction between two autosomal regions and the X chromosome causes reproductive isolation between mouse strains derived from different subspecies.

Reproductive isolation that initiates speciation is likely caused by incompatibility among multiple loci in organisms belonging to genetically diverging populations. Laboratory C57BL/6J mice, which predominantly originated from Mus musculus domesticus, and a MSM/Ms strain derived from Japanese wild mice (M. m.

Attenuated spread of X-inactivation in an X;autosome translocation.

X inactivation in female mammals involves transcriptional silencing of an entire chromosome in response to a cis-acting noncoding RNA, the X inactive-specific transcript (Xist). Xist can also inactivate autosomal sequences, for example, in X;autosome translocations; but here, silencing appears to be relatively inefficient. This variation has been attributed to either attenuated spreading of Xist RNA at the onset of X inactivation or inefficient maintenance of autosomal silencing.

X-chromosome inactivation in differentiating mouse embryonic stem cells carrying X-linked GFP and lacZ transgenes.

Three new female ES cell lines (GLM1, GLP1 and GLP2) were established from mouse embryos carrying GFP (green fluorescent protein) and HMG-lacZ transgenes on one of two X chromosomes in cis. Using these cell lines, we studied the temporal relationships among three events relevant to X-chromosome inactivation: replication asynchrony of the X chromosome, and quenching of GFP fluorescence and beta-galactosidase (beta-gal) activity, during cell differentiation induced by embryoid body (EB) formation and retinoic acid (RA) treatment. In embryoid bodies adhering to the bottom of culture dishes, GFP-negative cells appeared first in the peripheral outgrowths 4 days after the initiation of EB formation, followed about 24 hours later by the appearance of cells negative for beta-gal and those having a single allocyclic X chromosome.

Analysis of promoter region of X-linked pgk-1 gene polymorphisms: evidence for polyclonality of adult mouse gastric glands.

The clonality of gastric glands remains a controversial topic. Chimeric mouse studies suggested that all gastric glands were monoclonal. However, using the X-linked transgenic mouse model, we have suggested that most glands are polyclonal during development and that the fraction of monoclonal glands increases after birth.

Hybrid breakdown caused by substitution of the X chromosome between two mouse subspecies.

Hybrid breakdown is a type of reproductive failure that appears after the F2 generation of crosses between different species or subspecies. It is caused by incompatibility between interacting genes. Genetic analysis of hybrid breakdown, particularly in higher animals, has been hampered by its complex nature (i.

Imprinted X-chromosome inactivation: enlightenment from embryos in vivo.

There are two forms of X chromosome inactivation (XCI) in the laboratory mouse, random XCI in the fetus and imprinted paternal XCI limited to the extraembryonic tissues supporting the fetal life in utero. Imprinted XCI has been studied extensively because it takes place first in embryogenesis and it may hold clues to the mechanism of control of XCI in general and to the evolution of random' XCI. Classical microscopic and biochemical studies of embryos in vivo provide a basis for interpreting the multifaceted information yielded by various inventive approaches and for planning further experiments.

Tetraploid embryos rescue the early defects of tw5/tw5 mouse embryos.

tclw5 is a t-complex recessive lethal mutation of the tw5-haplotype. Since tw5/tw5 embryos die soon after implantation, the tclw5 gene is thought to play an important role in early embryogenesis. Previous histological studies have demonstrated that tw5 homozygotes do not survive past the gastrulation stage due to extensive death of the embryonic ectoderm, whereas the extraembryonic tissues were less affected.

Developmental abnormalities in mouse embryos tetrasomic for chromosome 11: apparent similarity to embryos functionally disomic for the x chromosome.

Adopting a mating system involving two different Robertsonian translocations with monobrachial homology, we studied the early development of mouse embryos trisomic or tetrasomic for chromosome 11. A developmental delay of 12-24 hours was evident in trisomic embryos at embryonic day (E)7.5, whereas tetrasomic embryos apparently had stopped growth by E6.

Developmental potential of mouse tetraploid cells in diploid <--> tetraploid chimeric embryos.

Mouse 2n (lacZ-) <--> 4n (lacZ+) aggregation chimeras were examined 5 or 10 days after uterine transfer to test the potential of 4n cells to contribute to embryonic tissues. Recovered embryos corresponded to embryonic day 7.5 approximately 8.

Genomic imprinting contributes to thyroid hormone metabolism in the mouse embryo.

Many genes subject to genomic imprinting function in a number of endocrine/paracrine pathways that are important for normal mammalian development. Here, we show that an endocrine/paracrine pathway involving thyroid hormone metabolism is also regulated by imprinting. Thyroid hormone action depends on thyroid hormone receptors and their predominant ligand, 3,5,3'-triiodothyronine (T3).

A Novel Mesoderm-Specific cDNA Isolated from a Mouse Embryonal Carcinoma Cell Line: (embryonal carcinoma cell/cDNA/in situ hybridization/mesoderm/mouse embryo).

A novel mesoderm-specific cDNA clone has been isolated by differential screening of cDNA library from an embryonal carcinoma (EC) cell line MC12. The cDNA clone 121a is about 2.5 kb in length and apparently encodes a putative polypeptide of 335 amino acids which may be secreted or membrane anchored glycoprotein since it has a possible signal sequence and a potential N-linked glycosylation site.

Abnormal X-Chromosome Dosage Compensation as a Possible Cause of Early Developmental Failure in Mice: (X-chromosome inactivation/trophectoderm/imprinting/embryonic development).

An extra maternally derived X chromosome (X ) but not a paternally derived one (X ) is detrimental in early mouse embryogenesis resulting in failure to form the ectoplacental cone and extra-embryonic ectoderm. Cytogenetic studies suggested that two X chromosomes remain active in the trophectoderm and possibly also the primitive endoderm, in which X is preferentially inactivated in normal female embyos. Two copies of an active X chromosome due to maternal imprinting seem to prevent further differentiation of the trophectoderm.

A New Monoclonal Antibody that Recognizes 180 kDa Polypeptide Expressed on Early Mouse Embryos and Mouse Embryonal Carcinoma Cells: (embryonal carcinoma/monoclonal antibody/intrasplenic primary immunization/180 kDa polypeptide).

A hybridoma clone 1F7 producing a monoclonal antibody against OTF9-63 mouse embryonal carcinoma cell line was isolated with the aid of the intrasplenic primary immunization technique. This antibody was capable of recognizing embryonal carcinoma cell lines originated from certain mouse strains, including 129/Sv, but not those which were established from other strains as well as human and other murine cell lines except FM3A, a mouse mammary carcinoma cell line. Indirect immunofluorescence study revealed that 1F7 antigen was expressed on early mouse embryos in a stage specific manner.

Construction of a DNA Library Enriched with Mouse 4 Chromosome of T(X;4)37H Translocation: (flow cytometry/mouse DNA library/hybrid cell/chromosome translocation/X-inactivation).

Normal mouse chromosomes are routinely separated into only 5 peaks by the current flow cytometry. Since this limited resolution hindered isolation of the normal mouse X chromosome with an appropriate purity, we attempted to sort the mouse 4 chromosome, a larger translocation chromosome of T(X;4)37H, consisting of nearly the entire chromosome 4 and chromosome X by flow cytometry. To obtain a large number of cells having 4 chromosome for flow sorting, we isolated a somatic hybrid cell line MHH-1 formed between S194 myelome cell line and normal splenocytes from a male mouse carrying T(X;4)37H.

Presence of an Allocyclic Early Replicating X Chromosome in Female Embryos of the Rat, Chinese Hamster and Rabbit: (X chromosome inactivation/allocyclic X chromosome/rat/Chinese hamster/rabbit).

Previous studies on early female mouse embryos revealed the presence of two kinds of inactive X chromosomes, one replicating late and the other early in the DNA synthetic period. The X chromosome that replicates early is of special interest because of its paternal origin, preferential occurrence in trophectoderm and primitive endoderm derivatives, and programmed shift to the late replicator. This study by BrdU labeling and acridine orange fluorescence staining was undertaken to examine whether the inactive X chromosome behaves in a similar manner in other laboratory mammals.