Genetic control over the inactivation of autosomal genes attached to the X-chromosome

Cattanach, B.M.; Isaacson, J. H.

doi:10.1007/bf00895048

Cited by 44 publications

(45 citation statements)

References 27 publications

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“…This observation may be explained by instability of the limited inactivation of autosomal material. Consistent with this, Cattanach reported that as Is1Ct mice age, the albino gene on the inserted chromosome 7 material reactivated, producing a coat-colour change [54,55]. Reactivation with age, however, has also been reported for true X-linked genes [56,57].…”

Section: Propagation and Maintenancesupporting

confidence: 50%

X chromosome inactivation and the Xist gene

Brockdorff¹,

Duthie²

1998

Cellular and Molecular Life Sciences (CMLS)

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Recent years have seen rapid progress towards understanding the molecular mechanisms involved in X chromosome inactivation (X inactivation). This progress has largely revolved around the discovery of the X inactive specific transcript (Xist) gene, which is known now to represent the master switch locus regulating X inactivation. In adult cells Xist is transcribed exclusively from the inactive X chromosome. The transcript has no apparent protein-coding potential and is retained in the nucleus in close association with the domain occupied by the inactive X chromosome. It is thus thought to represent a functional RNA molecule which acts as the primary signal responsible for the propagation of X inactivation. Developmental regulation of Xist correlates with the developmental timing of X inactivation. Recent results have demonstrated that Xist is both necessary and sufficient for X inactivation. Goals for the future are to understand the mechanism of Xist regulation which underlies the establishment of appropriate X inactivation patterns and to determine how Xist RNA participates in the process of propagating inactivation in cis.

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Section: Propagation and Maintenancesupporting

confidence: 50%

X chromosome inactivation and the Xist gene

Brockdorff¹,

Duthie²

1998

Cellular and Molecular Life Sciences (CMLS)

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“…The 'state' designated high permits a near-50 % level of c-variegation, that designated low, a near-30 % level. The difference is attributed to the frequency of X T -inactive cells in which the rearranged c + gene is inactivated (Cattanach & Isaacson, 1965.…”

Section: Methodsmentioning

confidence: 99%

“…When the reciprocal cross difference was first observed it was thought that selection might be operating differentially on the viabilities of the Dp females produced in the two types of cross. The rationale was as follows, (a) It is known that the viability of the hemizygous Dp male is very low and that that of the heterozygous Dp female is somewhat reduced (Cattanach, 1961a;Cattanach & Isaacson, 1965), (6) it is reasonable to suppose (in the absence of evidence) that the degree of reduction in Dp female viability will be proportional to the number of cells with the autosomal duplication (or X T ) genetically active, (c) it is then likely that any factor which enhances viability will allow the survival of those Dp females possessing greater number of cells with the duplication genetically active. It should be noted that the argument rests on the assumption that the proportion of cells with the duplication active will tend to be the same in all cell types.…”

Section: Methodsmentioning

confidence: 99%

“…Although JT-inactivation appears to be a random process, the mechanism causing the Drosophila-type position effect variegation is under genetic control (Cattanach & Isaacson, 1965. Located in the X chromosome is a controlling element which is closely linked to the T(l; X)Ct break point and alternative ' states' of the element have been found which permit different levels of T(l; X)Ct position effect variegation.…”

Section: Introductionmentioning

confidence: 99%

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Parental influence onX-autosome translocation-induced variegation in the mouse

Cattanach

Pérez

1970

Genet. Res.

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Females heterozygous for the T(l; X)Ct X-autosome translocation tend to have lower levels of c-variegation when their rearranged X is inherited from the father rather than from the mother. The difference is not due to a maternal effect. It is postulated that a paternal or parentalsource effect, such as that found to modify position effect variegation in Drosophila, is operating but the possibility that a bias in the inactivation of the maternal and paternal X chromosomes is responsible cannot be ruled out.

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“…The locus of scurfy lies near the centromere of the mouse X chromosome, close to the locus of sparse-fur, spf (5), which involves a mutation of the ornithine transcarbamylase gene, Otc (Fig. 1).…”

mentioning

confidence: 99%

The scurfy mouse mutant has previously unrecognized hematological abnormalities and resembles Wiskott-Aldrich syndrome.

Lyon

Peters

Glenister

et al. 1990

Proc. Natl. Acad. Sci. U.S.A.

159

109

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The X chromosome-linked scurfy (sf) mutant of the mouse is recognized by the scaliness of the skin from which the name is derived and results in death of affected males at about 3-4 weeks ofage. Consideration ofknown man-mouse homologies of the X chromosome prompted hematological studies, which have shown that the blood is highly abnormal. The platelet and erythrocyte counts are both reduced and become progressively lower relative to normal as the disease progresses. There is gastrointestinal bleeding, and most animals appear to die of severe anemia. By contrast, the leukocyte count is consistently raised. Some animals showed signs of infection but it is not yet clear whether there is immunodeficiency. Other features include the scaly skin and apparently reduced lateral growth of the skin, conjunctivitis, and diarrhea in some animals. The mutant resembles Wiskott-Aldrich syndrome in man, which is characterized by thrombocytopenia, eczema, diarrhea, and immunodeficiency. The loci of the human and mouse genes lie in homologous segments of the X chromosome, although apparently in somewhat different positions relative to other gene loci. Scurfy differs from WiskottAldrich syndrome in that scurfy males are consistently hypogonadal.

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Genetic control over the inactivation of autosomal genes attached to the X-chromosome

Cited by 44 publications

References 27 publications

X chromosome inactivation and the Xist gene

X chromosome inactivation and the Xist gene

Parental influence onX-autosome translocation-induced variegation in the mouse

The scurfy mouse mutant has previously unrecognized hematological abnormalities and resembles Wiskott-Aldrich syndrome.

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