Genomic imprinting: Male mice with uniparentally derived sex chromosomes

1991 ◽  
Vol 28 (4) ◽  
pp. 337-340 ◽  
Author(s):  
Mary Ann Handel ◽  
Patricia A. Hunt
Keyword(s):  
Genomic Imprinting ◽  
Sex Chromosomes ◽  
Male Mice

scholarly journals Genomic imprinting mediates dosage compensation in a young plant XY system

2017 ◽  
Author(s):  
Aline Muyle ◽  
Niklaus Zemp ◽  
Cécile Fruchard ◽  
Radim Cegan ◽  
Jan Vrana ◽  
...  
Keyword(s):  
Gene Expression ◽  
Genomic Imprinting ◽  
Dosage Compensation ◽  
Sex Chromosomes ◽  
Evolutionary Biology ◽  
Early Stage ◽  
Silene Latifolia ◽  
Negative Effects ◽  
Y Chromosomes ◽  
Sex Determination System

This preprint has been reviewed and recommended by Peer Community In Evolutionary Biology (http://dx.doi.org/10.24072/pci.evolbiol.100044).Sex chromosomes have repeatedly evolved from a pair of autosomes1. Consequently, X and Y chromosomes initially have similar gene content, but ongoing Y degeneration leads to reduced Y gene expression and eventual Y gene loss. The resulting imbalance in gene expression between Y genes and the rest of the genome is expected to reduce male fitness, especially when protein networks have components from both autosomes and sex chromosomes. A diverse set of dosage compensating mechanisms that alleviates these negative effects has been described in animals2–4. However, the early steps in the evolution of dosage compensation remain unknown and dosage compensation is poorly understood in plants5. Here we show a novel dosage compensation mechanism in the evolutionarily young XY sex determination system of the plant Silene latifolia. Genomic imprinting results in higher expression from the maternal X chromosome in both males and females. This compensates for reduced Y expression in males but results in X overexpression in females and may be detrimental. It could represent a transient early stage in the evolution of dosage compensation. Our finding has striking resemblance to the first stage proposed by Ohno for the evolution of X inactivation in mammals.

scholarly journals Mode of inheritance of the higher degree of megakaryocyte polyploidization in C3H mice. I. Evidence for a role of genomic imprinting in megakaryocyte polyploidy determination

Blood ◽  
1994 ◽  
Vol 83 (6) ◽  
pp. 1493-1498 ◽  
Author(s):  
TP McDonald ◽  
CW Jackson
Keyword(s):  
Genomic Imprinting ◽  
Dna Content ◽  
Female Offspring ◽  
Male Parent ◽  
Male Mice ◽  
Male And Female ◽  
Female Mice ◽  
C3h Mice ◽  
High Ploidy ◽  
Mode Of Inheritance

Abstract C3H mice have higher average ploidy megakaryocytes than all other mouse strains tested, but the mode of inheritance of this anomaly is unknown. Therefore, to clarify the genetics of high ploidy megakaryocytes in C3H mice, we measured megakaryocyte DNA content from both male and female offspring from F1, as well as backcross matings. In all, offspring from seven different matings of mice were studied: (1) C57BL X C57BL (the first strain listed is the male parent in each case), (2) B6C3F1 (offspring from C57BL X C3H mating) X C57BL, (3) C57BL X B6C3F1, (4) C57BL X C3H, (5) C3H X B6C3F1, (6) B6C3F1 X C3H, and (7) C3H X C3H. The polyploid megakaryocyte DNA content distributions of the offspring from these matings show that C3H mice have higher percentages of high ploidy megakaryocytes than did all other mice. Also, male mice had significantly higher percentages of high ploidy (32N and 64N) megakaryocytes than did female mice for all matings, except backcross mating no. 6. The megakaryocyte DNA content for individual offspring of a given backcross appeared to form a single, continuous distribution, rather than segregate into two distinct groups, suggesting that the higher megakaryocyte DNA content of C3H mice is caused by involvement of multiple allelles. This conclusion is further supported by our finding that the frequency of high ploidy megakaryocytes among offspring of the various matings was related to the proportion of C3H genotype contributed by the parents, ie, average megakaryocyte DNA content increased linearly (r2 = .88 for male mice and .84 for female mice. P < .0001) with increasing C3H gene dosage; the correlations for both male and female mice were essentially parallel (slope = 0.08 and 0.09, respectively). In addition, we found an effect of genomic imprinting on megakaryocyte DNA content in backcross offspring. The genetic imprinting was characterized by the female parent having a greater influence on the offspring's megakaryocyte DNA content than the male parent, ie, although the overall genetic makeup was the same, female offspring from backcross no. 6 (in which the female was C3H) had higher average megakaryocyte ploidy values than those from backcross no. 5 (in which the female was B6C3F1

scholarly journals Genomic imprinting mediates sexual experience-dependent olfactory learning in male mice

2007 ◽  
Vol 104 (14) ◽  
pp. 6084-6089 ◽  
Author(s):  
W. T. Swaney ◽  
J. P. Curley ◽  
F. A. Champagne ◽  
E. B. Keverne
Keyword(s):  
Genomic Imprinting ◽  
Sexual Experience ◽  
Olfactory Learning ◽  
Male Mice

scholarly journals Male mice with large inversions or deletions of X-palindrome arms are fertile and express their associated genes post-meiosis

2018 ◽  
Author(s):  
Alyssa N. Kruger ◽  
Quinn Ellison ◽  
Michele A. Brogley ◽  
Emma R. Gerlinger ◽  
Jacob L. Mueller
Keyword(s):  
Gene Expression ◽  
Sex Chromosomes ◽  
Transcriptional Repression ◽  
Sex Chromosome ◽  
Gene Families ◽  
Single Copy ◽  
Male Mice ◽  
Expression Levels ◽  
Gene Copies ◽  
Palindromic Structure

AbstractLarge (>10 kb) palindromic sequences are enriched on mammalian sex chromosomes. In mice, these palindromes harbor gene families (≥2 gene copies) expressed exclusively in post-meiotic testicular germ cells, at a time when most single-copy sex-linked genes are transcriptionally repressed. This distinct expression pattern led to the hypothesis that containment within palindrome structures or having ≥2 gene enables post-meiotic gene expression. We tested these two hypotheses by using CRISPR to precisely engineer large (10’s of kb) inversions and deletions of X chromosome palindrome arms for two regions carrying the mouse 4930567H17Rik and Mageb5 gene families. We found that 4930567H17Rik and Mageb5 gene expression is unaffected in mice carrying palindrome arm inversions, suggesting that palindromic structure is not important for mediating palindrome-associated gene expression. We also found that 4930567H17Rik and Mageb5 gene expression is reduced by half in mice carrying palindrome arm deletions, allowing us to test whether palindrome-associated genes are sensitive to reduced expression levels resulting in spermatogenic defects. Male mice carrying palindrome arm deletions of 4930567H17Rik or Mageb5, however, are fertile, have normal testis histology, and show no aberrations in spermatogenic cell population frequencies via FACS quantification. Together, these findings suggest that large palindromic structures on the sex chromosomes are not necessary for their associated genes to evade post-meiotic transcriptional repression and that these genes are not sensitive to reduced expression levels. Large sex chromosome palindromes may thus be important for other reasons, such as the long-term evolutionary stability of their associated gene families.

Spermatogenic failure in male mice with four sex chromosomes

Chromosoma ◽  
2001 ◽  
Vol 110 (2) ◽  
pp. 124-129 ◽  
Author(s):  
Tristan A. Rodriguez ◽  
Paul S. Burgoyne
Keyword(s):  
Sex Chromosomes ◽  
Male Mice ◽  
Spermatogenic Failure

scholarly journals Mode of inheritance of the higher degree of megakaryocyte polyploidization in C3H mice. I. Evidence for a role of genomic imprinting in megakaryocyte polyploidy determination

Blood ◽  
1994 ◽  
Vol 83 (6) ◽  
pp. 1493-1498
Author(s):  
TP McDonald ◽  
CW Jackson
Keyword(s):  
Genomic Imprinting ◽  
Dna Content ◽  
Female Offspring ◽  
Male Parent ◽  
Male Mice ◽  
Male And Female ◽  
Female Mice ◽  
C3h Mice ◽  
High Ploidy ◽  
Mode Of Inheritance

C3H mice have higher average ploidy megakaryocytes than all other mouse strains tested, but the mode of inheritance of this anomaly is unknown. Therefore, to clarify the genetics of high ploidy megakaryocytes in C3H mice, we measured megakaryocyte DNA content from both male and female offspring from F1, as well as backcross matings. In all, offspring from seven different matings of mice were studied: (1) C57BL X C57BL (the first strain listed is the male parent in each case), (2) B6C3F1 (offspring from C57BL X C3H mating) X C57BL, (3) C57BL X B6C3F1, (4) C57BL X C3H, (5) C3H X B6C3F1, (6) B6C3F1 X C3H, and (7) C3H X C3H. The polyploid megakaryocyte DNA content distributions of the offspring from these matings show that C3H mice have higher percentages of high ploidy megakaryocytes than did all other mice. Also, male mice had significantly higher percentages of high ploidy (32N and 64N) megakaryocytes than did female mice for all matings, except backcross mating no. 6. The megakaryocyte DNA content for individual offspring of a given backcross appeared to form a single, continuous distribution, rather than segregate into two distinct groups, suggesting that the higher megakaryocyte DNA content of C3H mice is caused by involvement of multiple allelles. This conclusion is further supported by our finding that the frequency of high ploidy megakaryocytes among offspring of the various matings was related to the proportion of C3H genotype contributed by the parents, ie, average megakaryocyte DNA content increased linearly (r2 = .88 for male mice and .84 for female mice. P < .0001) with increasing C3H gene dosage; the correlations for both male and female mice were essentially parallel (slope = 0.08 and 0.09, respectively). In addition, we found an effect of genomic imprinting on megakaryocyte DNA content in backcross offspring. The genetic imprinting was characterized by the female parent having a greater influence on the offspring's megakaryocyte DNA content than the male parent, ie, although the overall genetic makeup was the same, female offspring from backcross no. 6 (in which the female was C3H) had higher average megakaryocyte ploidy values than those from backcross no. 5 (in which the female was B6C3F1

Abstract 209: An XX Sex Chromosome Complement Promotes the Development of Obesity, Hypercholesterolemia and Atherosclerosis in Male and Female Ldlr -/- Mice Fed a Western Diet

2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Yasir Alsiraj ◽  
Sean Thatcher ◽  
Heba M. Ali ◽  
Ryan Temel ◽  
Alan Daugherty ◽  
...  
Keyword(s):  
Sexual Dimorphism ◽  
Cardiovascular Diseases ◽  
Surface Area ◽  
Y Chromosome ◽  
Sex Chromosomes ◽  
Sex Chromosome ◽  
Chromosome Complement ◽  
Atherosclerotic Lesion ◽  
Western Diet ◽  
Male Mice

Background: Underlying mechanisms contributing to sexual dimorphism of cardiovascular diseases are not well understood. Sex hormones are primary contributors to sexual dimorphism of cardiovascular diseases. By comparison, little is known regarding the contribution of genes on sex chromosomes (XX and XY) to sexual dimorphism of cardiovascular diseases, even though the X chromosome contains around 5% of the human genome. In this study, we hypothesized that genes on sex chromosomes influence the development of obesity, hypercholesterolemia and atherosclerosis. Methods and Results: Transgenic male mice with deletion of Sry from the Y-chromosome expressing Sry on autosomes (8-12 weeks of age) were bred to female Ldlr -/- mice to generate female and male mice with an XX or an XY sex chromosome complement (FXX, FXY, MXX, MXY). Mice were fed a Western diet (Teklad TD88137) for 3 months. XX mice exhibited increased body weight compared to mice with an XY sex chromosome complement, regardless of gonadal sex (FXX, 41.2 ± 2.4; FXY, 31.7 ± 2.5 g; P<0.05; MXX, 51.5 ± 1.2; MXY, 41.7 ± 1.8 g; P<0.05). Moreover, XX mice had increased serum cholesterol concentrations, regardless of gonadal sex (FXX, 2501 ± 192; FXY, 890 ± 141 mg/dl; P<0.05; MXX, 3814 ± 344; MXY, 1297 ± 385 mg/dl; P<0.05). Elevations in serum lipids were manifest as increased VLDL and LDL-cholesterol. The extent of atherosclerosis in aortic arch was significantly increased in XX compared to XY mice (XXF, 37 ± 2.1; XYF, 20 ± 3.2; XXM, 38 ± 3.6; XYM, 24 ± 3.6 % lesion surface area; P<0.05). In the aortic sinus, atherosclerotic lesion surface area was significantly increased in XX mice, regardless of gonadal sex (FXX, 60.4 x 10 4 ± 3.6 x 10 4 ; FXY, 32.4 x 10 4 ± 3.8 x 10 4 μm 2 ; P<0.05; MXX, 67.1 x 10 4 ± 9.6 x 10 4 ; MXY, 36.2 x 10 4 ± 3.7 x 10 4 μm 2 ; P<0.05). Conclusion: Results demonstrate that an XX sex chromosome complement promotes diet-induced obesity, hypercholesterolemia and atherosclerosis regardless of gonadal sex. Future studies will identify the role of genes on the X or Y chromosome as mechanisms for these effects.

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