Timing of Sex Chromosome Replication in Somatic and Germ-Line Cells of the Mouse and the Rat

1967 ◽  
Vol 6 (1) ◽  
pp. 51-66 ◽  
Author(s):  
L. Tiepolo ◽  
M. Fraccaro ◽  
Maj Hultén ◽  
J. Lindsten ◽  
Anna Mannini ◽  
...  
Keyword(s):  
Sex Chromosome ◽  
Germ Line ◽  
Chromosome Replication

Sex chromosome replication and sex chromatin inAkodon azarae (Rodentia Cricetidae)

1968 ◽  
Vol 38 (8) ◽  
pp. 343-347 ◽  
Author(s):  
N. O. Bianchi ◽  
F. N. Dulout ◽  
J. Contreras
Keyword(s):  
Sex Chromosome ◽  
Chromosome Replication ◽  
Sex Chromatin

scholarly journals DNA damage response protein TOPBP1 regulates X chromosome silencing in the mammalian germ line

2017 ◽  
Vol 114 (47) ◽  
pp. 12536-12541 ◽  
Author(s):  
Elias ElInati ◽  
Helen R. Russell ◽  
Obah A. Ojarikre ◽  
Mahesh Sangrithi ◽  
Takayuki Hirota ◽  
...  
Keyword(s):  
Dna Damage ◽  
X Chromosome ◽  
Sex Chromosome ◽  
Germ Line ◽  
Direct Interaction ◽  
Critical Factor ◽  
Dna Double Strand Breaks ◽  
Meiotic Silencing ◽  
Meiotic Sex Chromosome Inactivation ◽  
Meiotic Synapsis

Meiotic synapsis and recombination between homologs permits the formation of cross-overs that are essential for generating chromosomally balanced sperm and eggs. In mammals, surveillance mechanisms eliminate meiotic cells with defective synapsis, thereby minimizing transmission of aneuploidy. One such surveillance mechanism is meiotic silencing, the inactivation of genes located on asynapsed chromosomes, via ATR-dependent serine-139 phosphorylation of histone H2AFX (γH2AFX). Stimulation of ATR activity requires direct interaction with an ATR activation domain (AAD)-containing partner. However, which partner facilitates the meiotic silencing properties of ATR is unknown. Focusing on the best-characterized example of meiotic silencing, meiotic sex chromosome inactivation, we reveal this AAD-containing partner to be the DNA damage and checkpoint protein TOPBP1. Conditional TOPBP1 deletion during pachynema causes germ cell elimination associated with defective X chromosome gene silencing and sex chromosome condensation. TOPBP1 is essential for localization to the X chromosome of silencing “sensors,” including BRCA1, and effectors, including ATR, γH2AFX, and canonical repressive histone marks. We present evidence that persistent DNA double-strand breaks act as silencing initiation sites. Our study identifies TOPBP1 as a critical factor in meiotic sex chromosome silencing.

scholarly journals Sex chromosome silencing in the marsupial male germ line

2007 ◽  
Vol 104 (23) ◽  
pp. 9730-9735 ◽  
Author(s):  
S. H. Namekawa ◽  
J. L. VandeBerg ◽  
J. R. McCarrey ◽  
J. T. Lee
Keyword(s):  
Sex Chromosome ◽  
Germ Line ◽  
Male Germ Line

scholarly journals C57BL/6J-Aw-J/J (B6 agouti) mouse embryonic stem cell lines

2018 ◽  
Author(s):  
Jeff Mann
Keyword(s):  
Cell Lines ◽  
Sex Chromosome ◽  
Coat Color ◽  
Germ Line ◽  
Embryonic Stem ◽  
Mouse Embryonic Stem Cell ◽  
Es Cell ◽  
Genome Modification ◽  
Stem Cell Lines ◽  
Cell Genome

Several embryonic stem (ES) cell lines were derived from an agouti coisogenic C57BL/6J mouse strain, C57BL/6J-Aw-J/J. Standard C57BL/6J mice are non-agouti, or black. Because agouti is dominant to black, transmission of the ES cell genome through the germ line can be visualized by coat color while working within a coiosgenic system. One line of XY sex chromosome constitution, called B6AW1, resulted in high frequency extreme chimerism when injected into blastocysts. It therefore has potential for genome modification experiments in mice.

scholarly journals Imprinting of the Y Chromosome Influences Dosage Compensation in roX1 roX2 Drosophila melanogaster

Genetics ◽  
2009 ◽  
Vol 183 (3) ◽  
pp. 811-820 ◽  
Author(s):  
Debashish U. Menon ◽  
Victoria H. Meller
Keyword(s):  
Drosophila Melanogaster ◽  
Y Chromosome ◽  
Dosage Compensation ◽  
Sex Chromosome ◽  
Germ Line ◽  
Chromatin Modification ◽  
Regulatory System ◽  
The Body ◽  
Autosomal Gene ◽  
Y Chromosomes

Drosophila melanogaster males have a well-characterized regulatory system that increases X-linked gene expression. This essential process restores the balance between X-linked and autosomal gene products in males. A complex composed of the male-specific lethal (MSL) proteins and RNA is recruited to the body of transcribed X-linked genes where it modifies chromatin to increase expression. The RNA components of this complex, roX1 and roX2 (RNA on the X1, RNA on the X2), are functionally redundant. Males mutated for both roX genes have dramatically reduced survival. We show that reversal of sex chromosome inheritance suppresses lethality in roX1 roX2 males. Genetic tests indicate that the effect on male survival depends upon the presence and source of the Y chromosome, revealing a germ line imprint that influences dosage compensation. Conventional paternal transmission of the Y chromosome enhances roX1 roX2 lethality, while maternal transmission of the Y chromosome suppresses lethality. roX1 roX2 males with both maternal and paternal Y chromosomes have very low survival, indicating dominance of the paternal imprint. In an otherwise wild-type male, the Y chromosome does not appreciably affect dosage compensation. The influence of the Y chromosome, clearly apparent in roX1 roX2 mutants, thus requires a sensitized genetic background. We believe that the Y chromosome is likely to act through modulation of a process that is defective in roX1 roX2 mutants: X chromosome recognition or chromatin modification by the MSL complex.

Genetic activity of sex chromosomes in germinal cells

1970 ◽  
Vol 259 (828) ◽  
pp. 53-58 ◽  
Keyword(s):  
Germ Cells ◽  
Sex Chromosomes ◽  
Sex Chromosome ◽  
Germ Line ◽  
Sampling Error ◽  
Primordial Germ Cells ◽  
Coat Colour ◽  
Chromosome Constitution ◽  
Y Chromosomes ◽  
Genetic Activity

If I adhere strictly to the title proposed for me and speak only of the genetic activity of the sex chromosomes in germ cells, there is very little to say. The evidence is necessarily indirect and includes, first, examples of differential behaviour of germ cells of different sex chromosome constitution in situations where competitive proliferation is a possibility, as in some mosaics and chimaeras; and secondly, exceptional species in which the sex chromosome constitution is normally different in germ cells and soma. The species concerned are all mammals. An instance of the first kind is provided by observations made on a 39,X /41,XYY mosaic mouse discovered by chance in the course of an irradiation experiment (Evans, Ford & Searle 1969). All the spermatogonia and spermatocytes examined contained 41 chromosomes, including two Y chromosomes, whereas bone marrow (the only other tissue examined) was mosaic, the probability of difference being due to sampling error being very low. The question, then, was whether the failure to detect mosaicism among the germ cells was a consequence of chance exclusion of the 39, X cell type from the germ line during development, or of differential proliferation and/or survival of 41,XYY germ cells in the testicular environment. The latter interpretation was favoured on the grounds: (1) A 39,X /41,XYY mosaic is likely to have originated by non-disjunction of the Y chromosome at the first cleavage division of a 40,XY zygote, since other theoretically possible modes of origin would require the combination of rare events or other implausible assumptions. (2) Primordial germ cells of the constitution 39, X are capable of reaching the developing gonad and subsequently forming functional oocytes as evidenced by the fertility of 39, X female mice (Russell, Russell & Gower 1959). (3) Nearly all half-and-half coat colour mosaic mutants are also germ cell mosaics (Russell 1964), implying that when two distinct cell lines are present very early in development both lines are likely to be represented among the germ cells

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