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

Spermatogenic failure in male mice lacking H–Y antigen

Nature ◽  
1986 ◽  
Vol 320 (6058) ◽  
pp. 170-172 ◽  
Author(s):  
Paul S. Burgoyne ◽  
Elaine R. Levy ◽  
Anne McLaren
Keyword(s):  
Male Mice ◽  
Spermatogenic Failure

scholarly journals Human Spermatogenic Failure Purges Deleterious Mutation Load from the Autosomes and Both Sex Chromosomes, including the Gene DMRT1

PLoS Genetics ◽  
2013 ◽  
Vol 9 (3) ◽  
pp. e1003349 ◽  
Author(s):  
Alexandra M. Lopes ◽  
Kenneth I. Aston ◽  
Emma Thompson ◽  
Filipa Carvalho ◽  
João Gonçalves ◽  
...  
Keyword(s):  
Sex Chromosomes ◽  
Deleterious Mutation ◽  
Mutation Load ◽  
Spermatogenic Failure

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.

The role of unpaired sex chromosomes in spermatogenic failure*

Andrologia ◽  
2009 ◽  
Vol 24 (1) ◽  
pp. 17-20 ◽  
Author(s):  
P. S. Burgoyne ◽  
M.J. Sutcliffe ◽  
S. K. Mahadevaiah
Keyword(s):  
Sex Chromosomes ◽  
Spermatogenic Failure

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.

Ultrastructural Lesions Produced by Alcohol and Sucrose in the Heart and Liver of C57BL Mice

1970 ◽  
Vol 28 ◽  
pp. 208-209
Author(s):  
K.K. SEKHRI ◽  
C.S. ALEXANDER ◽  
H.T. NAGASAWA
Keyword(s):  
Osmium Tetroxide ◽  
Male Mice ◽  
Alcohol Group ◽  
Group Iii ◽  
Group I ◽  
C57bl Mice ◽  
Group Ii

C57BL male mice (Jackson Lab., Bar Harbor, Maine) weighing about 18 gms were randomly divided into three groups: group I was fed sweetened liquid alcohol diet (modified Schenkl) in which 36% of the calories were derived from alcohol; group II was maintained on a similar diet but alcohol was isocalorically substituted by sucrose; group III was fed regular mouse chow ad lib for five months. Liver and heart tissues were fixed in 2.5% cacodylate buffered glutaraldehyde, post-fixed in 2% osmium tetroxide and embedded in Epon-araldite.

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