Sex difference in neural tube defects in <i>p53</i>‐null mice is caused by differences in the complement of X not Y genes

Chen, Xuqi; Watkins, Rebecca; Délot, Emmanuèle C.; Reliene, Ramune; Schiestl, Robert H.; Burgoyne, Paul S.; Arnold, Arthur P.

doi:10.1002/dneu.20581

Cited by 85 publications

(97 citation statements)

References 50 publications

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“…The impact of TP53 loss of function has previously been described as sex dependent. Deletion of Tp53 in mice results in disproportionate loss of female embryos from neural tube defects, subsequently ascribed to differences in X chromosome dosage and Lyar function (65,66). The presence of sexual dimorphism in response to loss of Tp53 activity has also been reported in neurofibromatosis 1-null (Nf1-null) mouse astrocytes.…”

Section: Discussionmentioning

confidence: 88%

Sexual dimorphism in glioma glycolysis underlies sex differences in survival

Ippolito¹,

Yim²,

Luo

et al. 2017

JCI Insight

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Section: Discussionmentioning

confidence: 88%

Sexual dimorphism in glioma glycolysis underlies sex differences in survival

Ippolito¹,

Yim²,

Luo

et al. 2017

JCI Insight

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“…The Y* chromosome includes a complex rearrangement of the PAR and produces mice with unusual complements of sex chromosomes genetically similar to XX, XY, XXY, XO, and XOϩPAR (11)(12)(13). Comparisons include mice with 1 vs 2 copies of most regions of the X chromosome (groups 1 and 2 vs groups 3 and 5; Table 1), or mice with (groups 4 and 5) vs without (groups 1, 2, and 3) most regions of the Y chromosome.…”

Section: Micementioning

confidence: 99%

“…The X Y* chromosome in group 5 of cross C is the fusion of NPY and NPX with an aberrant intervening PAR. The Y Ϫ chromosome is from strain 129 (11). In cross B, genotypes 4 and 5 are rare.…”

Section: Micementioning

confidence: 99%

“…Cross B (Table 1) This cross, designed by Paul Burgoyne, allows the detection of effects of 2 vs 1 sex chromosome, independent of gonadal sex, keeping the number of pseudoautosomal regions (PAR) equal to 2 as in WT XX and XY mice. XX females were mated with XY Ϫ Y* X (Sryϩ) gonadal males that possess the Y Ϫ chromosome from FCG mice (cross A), plus the small Y* X chromosome that is nearly equivalent to a PAR (11), plus the autosomal Sry transgene. The cross produces progeny with 14 different genotypes, 7 different combinations of sex chromosomes each with or without Sry.…”

Section: Micementioning

confidence: 99%

“…Schematic diagrams of the component regions of the sex chromosomes of mice used in the present study, expanded from(11). See…”

mentioning

confidence: 99%

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X and Y Chromosome Complement Influence Adiposity and Metabolism in Mice

et al. 2013

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Three different models of MF1 strain mice were studied to measure the effects of gonadal secretions and sex chromosome type and number on body weight and composition, and on related metabolic variables such as glucose homeostasis, feeding, and activity. The 3 genetic models varied sex chromosome complement in different ways, as follows: 1) "four core genotypes" mice, comprising XX and XY gonadal males, and XX and XY gonadal females; 2) the XY* model comprising groups similar to XO, XX, XY, and XXY; and 3) a novel model comprising 6 groups having XO, XX, and XY chromosomes with either testes or ovaries. In gonadally intact mice, gonadal males were heavier than gonadal females, but sex chromosome complement also influenced weight. The male/female difference was abolished by adult gonadectomy, after which mice with 2 sex chromosomes (XX or XY) had greater body weight and percentage of body fat than mice with 1 X chromosome. A second sex chromosome of either type, X or Y, had similar effects, indicating that the 2 sex chromosomes each possess factors that influence body weight and composition in the MF1 genetic background. Sex chromosome complement also influenced metabolic variables such as food intake and glucose tolerance. The results reveal a role for the Y chromosome in metabolism independent of testes and gonadal hormones and point to a small number of X-Y gene pairs with similar coding sequences as candidates for causing these effects.

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The mouse as a model of fundamental concepts related to Turner syndrome

Arnold

2019

American J of Med Genetics Pt C

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Although XO mice do not show many of the overt phenotypic features of Turner syndrome (TS; 45,X or XO), mice and humans share different classes of genes on the X chromosome that are more or less likely to cause TS phenotypes. Based on the evolutionary history of the sex chromosomes, and the pattern of dosage balancing among sex chromosomal and autosomal genes in functional gene networks, it is possible to prioritize types of X genes for study as potential causes of features of TS. For example, X‐Y gene pairs are among the most interesting because of the convergent effects of X and Y genes that both are likely to prevent the effects of TS in XX and XY individuals. Many of the high‐priority genes are shared by mouse and human X chromosomes, but are easier to study in genetically tractable mouse models. Several mouse models, used primarily for the study of sex differences in physiology and disease, also produce XO mice that can be investigated to understand the effects of X monosomy. Using these models will lead to the identification of specific X genes that make a difference when present in one or two copies. These studies will help to achieve a better appreciation of the contribution of these specific X genes to the syndromic features of TS.

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Sex difference in neural tube defects in p53‐null mice is caused by differences in the complement of X not Y genes

Cited by 85 publications

References 50 publications

Sexual dimorphism in glioma glycolysis underlies sex differences in survival

Sexual dimorphism in glioma glycolysis underlies sex differences in survival

X and Y Chromosome Complement Influence Adiposity and Metabolism in Mice

The mouse as a model of fundamental concepts related to Turner syndrome

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