Flow sorting of the mouse Cattanach X chromosome, T (X; 7) 1 Ct, in an active or inactive state

1981 ◽  
Vol 29 (4) ◽  
pp. 189-197 ◽  
Author(s):  
C.M. Disteche ◽  
A.V. Carrano ◽  
L.K. Ashworth ◽  
K. Burkhart-Schultz ◽  
S.A. Latt
Keyword(s):  
X Chromosome ◽  
Inactive State ◽  
Flow Sorting ◽  
Chromosome I

scholarly journals Synergism of Xist Rna, DNA Methylation, and Histone Hypoacetylation in Maintaining X Chromosome Inactivation

2001 ◽  
Vol 153 (4) ◽  
pp. 773-784 ◽  
Author(s):  
Györgyi Csankovszki ◽  
András Nagy ◽  
Rudolf Jaenisch
Keyword(s):  
X Chromosome ◽  
Trichostatin A ◽  
Cpg Islands ◽  
Hypoxanthine Phosphoribosyl Transferase ◽  
Histone H4 ◽  
Inactive State ◽  
Conditional Mutant ◽  
Xist Rna ◽  
Histone Hypoacetylation ◽  
Distinguishing Features

Xist RNA expression, methylation of CpG islands, and hypoacetylation of histone H4 are distinguishing features of inactive X chromatin. Here, we show that these silencing mechanisms act synergistically to maintain the inactive state. Xist RNA has been shown to be essential for initiation of X inactivation, but not required for maintenance. We have developed a system in which the reactivation frequency of individual X-linked genes can be assessed quantitatively. Using a conditional mutant Xist allele, we provide direct evidence for that loss of Xist RNA destabilizes the inactive state in somatic cells, leading to an increased reactivation frequency of an X-linked GFP transgene and of the endogenous hypoxanthine phosphoribosyl transferase (Hprt) gene in mouse embryonic fibroblasts. Demethylation of DNA, using 5-azadC or by introducing a mutation in Dnmt1, and inhibition of histone hypoacetylation using trichostatin A further increases reactivation in Xist mutant fibroblasts, indicating a synergistic interaction of X chromosome silencing mechanisms.

CpG methylation of an X-linked transgene is determined by somatic events postfertilization and not germline imprinting

Development ◽  
1988 ◽  
Vol 104 (2) ◽  
pp. 235-244
Author(s):  
A. Collick ◽  
W. Reik ◽  
S.C. Barton ◽  
A.H. Surani
Keyword(s):  
Dna Methylation ◽  
X Chromosome ◽  
De Novo ◽  
Cpg Methylation ◽  
Parental Origin ◽  
Cpg Dinucleotides ◽  
Inactive State ◽  
Methylation Of Dna ◽  
Methylation Patterns ◽  
Extraembryonic Tissues

The process of X-inactivation in mammals requires at least two events, the initiation of inactivation and the maintenance of the inactive state. One possible mechanism of control is by methylation of DNA at CpG dinucleotides to maintain the inactive state. Furthermore, the paternal X-chromosome is frequently inactivated in the extraembryonic membranes. The relationship between the parental origin of the chromosome, nonrandom inactivation and DNA methylation is not clear. In this paper, we report on the CpG methylation of an X-linked transgene, CAT-32. The levels of methylation in embryonic, extraembryonic and germline cells indicates that the modifications of the transgene are broadly similar to those reported for endogenous X-linked genes. Interestingly, the methylation of CAT-32 transgene in extraembryonic tissues displays patterns that could be linked to the germline origin of each allele. Hence, the maternally derived copy of CAT-32 was relatively undermethylated when compared to the paternal one. The changes in DNA methylation were attributed to de novo methylation occurring after fertilization, most probably during differentiation of extraembryonic tissues. In order to determine whether or not the patterns of DNA methylation reflected the germline origin of the X-chromosome, we constructed triploid embryos specifically to introduce two maternal X-chromosomes in the same embryo. In some of these triploid conceptuses, methylation patterns characteristic of the paternally derived transgene were observed. This observation indicates that the methylation patterns are not necessarily dependent on the parental origin of the X-chromosome, but could be changed by somatic events after fertilization. One of the more likely mechanisms is methylation of the transgene following inactivation of the X-chromosome in extraembryonic tissues.

scholarly journals Ectopic Splicing Disturbs the Function of Xist RNA to Establish the Stable Heterochromatin State

2021 ◽  
Vol 9 ◽  
Author(s):  
Ruka Matsuura ◽  
Tatsuro Nakajima ◽  
Saya Ichihara ◽  
Takashi Sado
Keyword(s):  
Gene Silencing ◽  
X Chromosome ◽  
Molecular Basis ◽  
Essential Role ◽  
X Chromosome Inactivation ◽  
Chromosome Inactivation ◽  
Inactive State ◽  
Xist Rna ◽  
In Cis ◽  
Insight Into

Non-coding Xist RNA plays an essential role in X chromosome inactivation (XCI) in female mammals. It coats the X chromosome in cis and mediates the recruitment of many proteins involved in gene silencing and heterochromatinization. The molecular basis of how Xist RNA initiates chromosomal silencing and what proteins participate in this process has been extensively studied and elucidated. Its involvement in the establishment and maintenance of the X-inactivated state is, however, less understood. The XistIVS allele we previously reported is peculiar in that it can initiate XCI but fails to establish the inactive state that is stably maintained and, therefore, may provide an opportunity to explore how Xist RNA contributes to establish a robust heterochromatin state. Here we demonstrate that ectopic splicing taking place to produce XistIVS RNA disturbs its function to properly establish stable XCI state. This finding warrants the potential of XistIVS RNA to provide further insight into our understanding of how Xist RNA contributes to establish sustainable heterochromatin.

scholarly journals Controlling elements in the mouse X-chromosome: I. Interaction with the X-linked genes

1969 ◽  
Vol 14 (3) ◽  
pp. 223-235 ◽  
Author(s):  
B. M. Cattanach ◽  
C. E. Pollard ◽  
J. N. Perez
Keyword(s):  
X Chromosome ◽  
Position Effect ◽  
The State ◽  
Position Effect Variegation ◽  
Autosome Translocation ◽  
Effect Variegation ◽  
Controlling Elements ◽  
Controlling Element ◽  
Chromosome I ◽  
Partial Reversal

The mouse X-chromosome controlling elements, detected by their influence on the position effect variegation caused by the X-autosome translocation T (1; X) Ct, have been found to modify the heterozygous phenotypes of two X-linked genes. It is proposed that X-inactivation can be incomplete, the level of inactivation or the frequency of cells in which inactivation is incomplete being dependent upon the ‘state’ of the controlling element located in the X. The data suggest that this is a consequence of a reversal, or partial reversal, of inactivation of the X as a whole in some cells rather than a vairable spread of inactivation along the length of the X.

Spontaneous duplication loss and breakage in Caenorhabditis elegans

Genome ◽  
1994 ◽  
Vol 37 (4) ◽  
pp. 595-606
Author(s):  
Kim S. McKim ◽  
Ann M. Rose
Keyword(s):  
Caenorhabditis Elegans ◽  
X Chromosome ◽  
Fragile Site ◽  
Ring Chromosome ◽  
Chromosome Breakage ◽  
Chromosome Loss ◽  
Spontaneous Breakage ◽  
Ring Chromosomes ◽  
Ring Structures ◽  
Chromosome I

Duplications in Caenorhabditis elegans spontaneously delete at frequencies ranging from 10−4 to 10−5. We have analyzed the structure and mitotic stability of 33 deleted duplications resulting from spontaneous breakage events. (i) Breakage usually occurred at a variety of sites; that is, there were no hot spots for breakage. An exception was the spontaneous breakage of the X chromosome into which hDp14 was inserted. These breaks were close to or at the site of the chromosome I insertion; therefore, the insertion created a type of fragile site. (ii) Spontaneous duplications often had complex structures. In some cases, their structures were most simply resolved by proposing that the progenitor duplication was a ring chromosome with a superimposed inversion. Most of the proposed ring chromosomes were mitotically unstable, suggesting that ring structures increase the frequency of chromosome loss, (iii) Clusters of spontaneous deletion events were rarely observed, suggesting that the majority of spontaneous breakage events probably occurred during meiosis. (iv) A minority of the spontaneous breakage events were associated with linkage to an autosome. Like free duplications of chromosome I, these linked duplications tended to segregate from the X chromosome in males. (v) Three meiotic mutants, him-3, him-6, and him-8, had no effect on somatic loss of the duplications but did reduce the frequency of breakage events. Given the conclusion that chromosome breakage is a meiotic event, these data are consistent with the function of the three meiotic genes being restricted to meiosis.Key words: chromosome structure, duplication, mitosis, meiosis, Caenorhabditis species.

Sign in / Sign up

Export Citation Format

Share Document