The XY Body of the Cat (Felis catus): Structural Differentiations and Protein Immunolocalization

2017 ◽  
Vol 152 (3) ◽  
pp. 137-147 ◽  
Author(s):  
Roberta B. Sciurano ◽  
Geraldine De Luca ◽  
I. Mónica Rahn ◽  
Alberto J. Solari
Keyword(s):  
Sex Chromosome ◽  
Structural Characteristics ◽  
Domestic Cat ◽  
Xy Body ◽  
Meiotic Sex Chromosome Inactivation ◽  
Y Chromosomes ◽  
Extreme Degree ◽  
Special Location ◽  
Pairing Region

The heteromorphic X and Y chromosomes behave in a special way in mammalian spermatocytes; they form the XY body and synapse only partially. The aim of this article was to study the origin and the role of the special differentiations in the XY pair of the domestic cat during pachytene by analyzing its fine structural characteristics and the immunolocalization of the main meiotic proteins SYCP3, SYCP1, SYCE3, SMC3, γ-H2AX, BRCA1, H3K27me3, and MLH1. The cat XY body shows particularly striking structures: an extreme degree of axial fibrillation in late pachynema and a special location of SYCP3-containing fibrils, bridging different regions of the main X axis, as well as one bridge at the inner end of the pairing region that colocalizes with the single mandatory MLH1 focus. There are sequential changes, first bullous expansions, then subdivision into fibrils, all involving axial thickening. The chromatin of the XY body presents the usual features of meiotic sex chromosome inactivation. An analysis of the XY body of many eutherians and metatherians suggests that axial thickenings are primitive features. The sequential changes in the mass and location of SYCP3-containing fibers vary among the clades because of specific processes of axial assembly/disassembly occurring in different species.

scholarly journals Deficiency of SYCP3-related XLR3 Disrupts the Initiation of Meiotic Sex Chromosome Inactivation in Mouse Spermatogenesis

2021 ◽  
Author(s):  
Michael John O'Neill ◽  
Natali Sobel Naveh ◽  
Robert Foley ◽  
Katelyn DeNegre ◽  
Tristan Evans ◽  
...  
Keyword(s):  
Sex Chromosomes ◽  
Transcriptional Repression ◽  
Sex Chromosome ◽  
Chromosome Inactivation ◽  
Nuclear Compartment ◽  
Xy Body ◽  
Meiotic Sex Chromosome Inactivation ◽  
Y Chromosomes ◽  
Multiple Clusters ◽  
Sex Chromosome Inactivation

In mammals, the X and Y chromosomes share only small regions of homology called pseudo-autosomal regions (PAR) where pairing and recombination in spermatocytes can occur. Consequently, the sex chromosomes remain largely unsynapsed during meiosis I and are sequestered in a nuclear compartment known as the XY body where they are transcriptionally silenced in a process called meiotic sex chromosome inactivation (MSCI). MSCI mirrors meiotic silencing of unpaired chromatin (MSUC), the sequestration and transcriptional repression of unpaired DNA observed widely in eukaryotes. MSCI is initiated by the assembly of the axial elements of the synaptonemal complex (SC) comprising the structural proteins SYCP2 and SYCP3 followed by the ordered recruitment of DNA Damage Response (DDR) factors to effect gene silencing. However, the precise mechanism of how unsynapsed chromatin is detected in meiocytes is poorly understood. The sex chromosomes in eutherian mammals harbor multiple clusters of SYCP3-like amplicons comprising the Xlr gene family, only a handful of which have been functionally studied. We used a shRNA-transgenic mouse model to create a deficiency in the testis-expressed multicopy Xlr3 genes to investigate their role in spermatogenesis. Here we show that knockdown of Xlr3 in mice leads to spermatogenic defects and a skewed sex ratio that can be traced to MSCI breakdown. Spermatocytes deficient in XLR3 form the XY body and the SC axial elements therein, but are compromised in their ability to recruit DDR components to the XY body.

The role of sex chromosomes in black fly evolution

Genome ◽  
1989 ◽  
Vol 32 (4) ◽  
pp. 538-542 ◽  
Author(s):  
R. M. Feraday ◽  
K. G. Leonhardt ◽  
C. L. Brockhouse
Keyword(s):  
Sex Chromosomes ◽  
Sex Chromosome ◽  
Chromosome Rearrangements ◽  
Black Flies ◽  
Black Fly ◽  
Adaptive Process ◽  
Y Chromosomes

Sex chromosomes have been repeatedly implicated in the process of speciation of black flies and other nemotocerans. Arguments are presented here against the case that frequent differences between species in their sex chromosomes are based on (i) different average rates of differentiation of sex-linked and autosomal loci or (ii) the fact that the X and Y chromosomes are less numerous than autosomal chromosomes and so are more subject to the effects of drift and the random fixation of chromosome rearrangements. The argument is made that speciation in black flies and many other groups is an adaptive process and that differentiated sex-chromosome systems play a role in this process.Key words: black flies, sex chromosomes, speciation, evolution.

scholarly journals Sex chromosomes, sex ratios and sex gaps in longevity in plants

2021 ◽  
Author(s):  
Gabriel AB Marais ◽  
Jean-Francois Lemaitre
Keyword(s):  
Sex Chromosomes ◽  
Statistical Power ◽  
Sex Chromosome ◽  
Sex Ratios ◽  
Y Chromosomes ◽  
Adult Sex Ratio ◽  
Female Longevity ◽  
Males And Females ◽  
The Relationship

In animals, males and females can display markedly different longevity (also called sex gap in longevity, SGLs). Recent work has revealed that sex chromosomes contribute to establishing these SGLs. X-hemizygosity and toxicity of the Y chromosomes are two mechanisms that have been suggested to reduce male longevity (Z-hemizygosity and W toxicity in females in ZW systems). In plants, SGLs are known to exist but the role of sex chromosomes remains to be established. Here, by using adult sex ratio as a proxy for measuring SGLs, we explored the relationship between sex chromosome and SGLs across 43 plant species. Based on the knowledge recently accumulated in animals, we specifically asked whether: (i) species with XY systems tend to have female-biased sex ratios (reduced male longevity) and species with ZW ones tend to have male-biased sex ratios (reduced female longevity), and (ii) this patterns was stronger in heteromorphic systems compared to homomorphic ones. Our results tend to support these predictions although we lack statistical power because of a small number of ZW systems and the absence of any heteromorphic ZW system in the dataset. We discuss the implications of these findings, which we hope will stimulate further research on sex-differences in lifespan and ageing across plants.

scholarly journals Dynamic expression of long noncoding RNAs reveals their potential roles in spermatogenesis and fertility†

2017 ◽  
Vol 97 (2) ◽  
pp. 313-323 ◽  
Author(s):  
Lauren Wichman ◽  
Saigopal Somasundaram ◽  
Christine Breindel ◽  
Dana M. Valerio ◽  
John R. McCarrey ◽  
...  
Keyword(s):  
Expression Pattern ◽  
Noncoding Rna ◽  
Sex Chromosome ◽  
Sperm Count ◽  
Noncoding Rnas ◽  
Long Noncoding Rnas ◽  
Small Noncoding Rnas ◽  
Meiotic Sex Chromosome Inactivation ◽  
Y Chromosomes ◽  
Dynamic Expression

Abstract Mammalian reproduction requires that males and females produce functional haploid germ cells through complex cellular differentiation processes known as spermatogenesis and oogenesis, respectively. While numerous studies have functionally characterized protein-coding genes and small noncoding RNAs (microRNAs and piRNAs) that are essential for gametogenesis, the roles of regulatory long noncoding RNAs (lncRNAs) are yet to be fully characterized. Previously, we and others have demonstrated that intergenic regions of the mammalian genome encode thousands of long noncoding RNAs, and many studies have now demonstrated their critical roles in key biological processes. Thus, we postulated that some lncRNAs may also impact mammalian spermatogenesis and fertility. In this study, we identified a dynamic expression pattern of lncRNAs during murine spermatogenesis. Importantly, we identified a subset of lncRNAs and very few mRNAs that appear to escape meiotic sex chromosome inactivation, an epigenetic process that leads to the silencing of the X- and Y-chromosomes at the pachytene stage of meiosis. Further, some of these lncRNAs and mRNAs show a strong testis expression pattern suggesting that they may play key roles in spermatogenesis. Lastly, we generated a mouse knockout of one X-linked lncRNA, Tslrn1 (testis-specific long noncoding RNA 1), and found that males carrying a Tslrn1 deletion displayed normal fertility but a significant reduction in spermatozoa. Our findings demonstrate that dysregulation of specific mammalian lncRNAs is a novel mechanism of low sperm count or infertility, thus potentially providing new biomarkers and therapeutic strategies.

scholarly journals Extensive meiotic asynapsis in mice antagonises meiotic silencing of unsynapsed chromatin and consequently disrupts meiotic sex chromosome inactivation

2008 ◽  
Vol 182 (2) ◽  
pp. 263-276 ◽  
Author(s):  
Shantha K. Mahadevaiah ◽  
Déborah Bourc'his ◽  
Dirk G. de Rooij ◽  
Timothy H. Bestor ◽  
James M.A. Turner ◽  
...  
Keyword(s):  
Sex Chromosome ◽  
Male Meiosis ◽  
Chromosome Inactivation ◽  
Null Mouse ◽  
Dna Double Strand Breaks ◽  
Meiotic Silencing ◽  
Meiotic Sex Chromosome Inactivation ◽  
Y Chromosomes ◽  
Meiotic Dsbs ◽  
Sex Chromosome Inactivation

Chromosome synapsis during zygotene is a prerequisite for the timely homologous recombinational repair of meiotic DNA double-strand breaks (DSBs). Unrepaired DSBs are thought to trigger apoptosis during midpachytene of male meiosis if synapsis fails. An early pachytene response to asynapsis is meiotic silencing of unsynapsed chromatin (MSUC), which, in normal males, silences the X and Y chromosomes (meiotic sex chromosome inactivation [MSCI]). In this study, we show that MSUC occurs in Spo11-null mouse spermatocytes with extensive asynapsis but lacking meiotic DSBs. In contrast, three mutants (Dnmt3l, Msh5, and Dmc1) with high levels of asynapsis and numerous persistent unrepaired DSBs have a severely impaired MSUC response. We suggest that MSUC-related proteins, including the MSUC initiator BRCA1, are sequestered at unrepaired DSBs. All four mutants fail to silence the X and Y chromosomes (MSCI failure), which is sufficient to explain the midpachytene apoptosis. Apoptosis does not occur in mice with a single additional asynapsed chromosome with unrepaired meiotic DSBs and no disturbance of MSCI.

scholarly journals The X and Y Chromosomes Assemble into H2A.Z, Containing Facultative Heterochromatin, following Meiosis

2006 ◽  
Vol 26 (14) ◽  
pp. 5394-5405 ◽  
Author(s):  
Ian K. Greaves ◽  
Danny Rangasamy ◽  
Michael Devoy ◽  
Jennifer A. Marshall Graves ◽  
David J. Tremethick
Keyword(s):  
Large Scale ◽  
Sex Chromosome ◽  
Round Spermatid ◽  
Sequential Process ◽  
Facultative Heterochromatin ◽  
Unique Role ◽  
Meiotic Sex Chromosome Inactivation ◽  
Y Chromosomes ◽  
Spermatogonia Stem Cells ◽  
Key Steps

ABSTRACT Spermatogenesis is a complex sequential process that converts mitotically dividing spermatogonia stem cells into differentiated haploid spermatozoa. Not surprisingly, this process involves dramatic nuclear and chromatin restructuring events, but the nature of these changes are poorly understood. Here, we linked the appearance and nuclear localization of the essential histone variant H2A.Z with key steps during mouse spermatogenesis. H2A.Z cannot be detected during the early stages of spermatogenesis, when the bulk of X-linked genes are transcribed, but its expression begins to increase at pachytene, when meiotic sex chromosome inactivation (MSCI) occurs, peaking at the round spermatid stage. Strikingly, when H2A.Z is present, there is a dynamic nuclear relocalization of heterochromatic marks (HP1β and H3 di- and tri-methyl K9), which become concentrated at chromocenters and the inactive XY body, implying that H2A.Z may substitute for the function of these marks in euchromatin. We also show that the X and the Y chromosome are assembled into facultative heterochromatic structures postmeiotically that are enriched with H2A.Z, thereby replacing macroH2A. This indicates that XY silencing continues following MSCI. These results provide new insights into the large-scale changes in the composition and organization of chromatin associated with spermatogenesis and argue that H2A.Z has a unique role in maintaining sex chromosomes in a repressed state.

scholarly journals Epigenetic Dysregulation of Mammalian Male Meiosis Caused by Interference of Recombination and Synapsis

Cells ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 2311
Author(s):  
Roberto de la Fuente ◽  
Florencia Pratto ◽  
Abrahan Hernández-Hernández ◽  
Marcia Manterola ◽  
Pablo López-Jiménez ◽  
...  
Keyword(s):  
Transcriptional Regulation ◽  
Sex Chromosomes ◽  
Sex Chromosome ◽  
Male Meiosis ◽  
Epigenetic Marks ◽  
Prophase I ◽  
Recombination Proteins ◽  
Meiotic Sex Chromosome Inactivation ◽  
Y Chromosomes ◽  
Genes Encoding

Meiosis involves a series of specific chromosome events, namely homologous synapsis, recombination, and segregation. Disruption of either recombination or synapsis in mammals results in the interruption of meiosis progression during the first meiotic prophase. This is usually accompanied by a defective transcriptional inactivation of the X and Y chromosomes, which triggers a meiosis breakdown in many mutant models. However, epigenetic changes and transcriptional regulation are also expected to affect autosomes. In this work, we studied the dynamics of epigenetic markers related to chromatin silencing, transcriptional regulation, and meiotic sex chromosome inactivation throughout meiosis in knockout mice for genes encoding for recombination proteins SPO11, DMC1, HOP2 and MLH1, and the synaptonemal complex proteins SYCP1 and SYCP3. These models are defective in recombination and/or synapsis and promote apoptosis at different stages of progression. Our results indicate that impairment of recombination and synapsis alter the dynamics and localization pattern of epigenetic marks, as well as the transcriptional regulation of both autosomes and sex chromosomes throughout prophase-I progression. We also observed that the morphological progression of spermatocytes throughout meiosis and the dynamics of epigenetic marks are processes that can be desynchronized upon synapsis or recombination alteration. Moreover, we detected an overlap of early and late epigenetic signatures in most mutants, indicating that the normal epigenetic transitions are disrupted. This can alter the transcriptional shift that occurs in spermatocytes in mid prophase-I and suggest that the epigenetic regulation of sex chromosomes, but also of autosomes, is an important factor in the impairment of meiosis progression in mammals.

scholarly journals Sex-chromosome evolution in frogs: what role for sex-antagonistic genes?

2021 ◽  
Vol 376 (1832) ◽  
pp. 20200094 ◽  
Author(s):  
Nicolas Perrin
Keyword(s):  
Sex Chromosomes ◽  
Turnover Rate ◽  
Evolutionary Dynamics ◽  
Chromosome Evolution ◽  
Sex Chromosome ◽  
Deleterious Mutations ◽  
Sex Chromosome Evolution ◽  
High Turnover ◽  
Y Chromosomes

Sex-antagonistic (SA) genes are widely considered to be crucial players in the evolution of sex chromosomes, being instrumental in the arrest of recombination and degeneration of Y chromosomes, as well as important drivers of sex-chromosome turnovers. To test such claims, one needs to focus on systems at the early stages of differentiation, ideally with a high turnover rate. Here, I review recent work on two families of amphibians, Ranidae (true frogs) and Hylidae (tree frogs), to show that results gathered so far from these groups provide no support for a significant role of SA genes in the evolutionary dynamics of their sex chromosomes. The findings support instead a central role for neutral processes and deleterious mutations. This article is part of the theme issue ‘Challenging the paradigm in sex chromosome evolution: empirical and theoretical insights with a focus on vertebrates (Part I)’.

105. MEIOTIC ACROBATS: MONOTREME SEX CHROMOSOME ORGANISATION DURING SPERMATOGENESIS

2010 ◽  
Vol 22 (9) ◽  
pp. 23
Author(s):  
F. Grutzner ◽  
A. Casey ◽  
T. Daish
Keyword(s):  
Sex Chromosomes ◽  
Meiotic Prophase ◽  
Sex Chromosome ◽  
National Academy Of Sciences ◽  
Prophase I ◽  
Meiotic Prophase I ◽  
Meiotic Sex Chromosome Inactivation ◽  
Y Chromosomes ◽  
Specific Order ◽  
Active Transcription

Monotremes feature an extraordinarily complex sex chromosome system which shares extensive homology with bird sex chromosomes but no homology to sex chromosomes of other mammals (1,2,3). At meiotic prophase I the ten sex chromosomes in platypus (nine in echidna) assemble in a sex chromosome chain. We previously identified the multiple sex chromosomes in platypus and echidna that form the meiotic chain in males (1,2,4). We showed that sex chromosomes assembly in the chain in a specific order (5) and that they segregate alternately (1). In secondary spermatocytes we observed clustering of X and Y chromosomes in sperm (6). Our current research investigates the formation of the synaptonemal complex, recombination and meiotic silencing of monotreme sex chromosomes. Meiotic sex chromosome inactivation (MSCI) has been observed in eutherian mammals, marsupials and birds but has so far not been investigated experimentally in monotremes. We found that during pachytene the X5Y5 end of the chain closely associates with the nucleolus and accumulates repressive chromatin marks (e.g. histone variant mH2A). In contrast to the differential accumulation of mH2A we observe extensive loading of the cohesin SMC3 on sex chromosomes in particular during the pachytene stage of meiotic prophase I. We have also used markers of active transcription and gene expression analysis to investigate gene activity in platypus meiotic cells. I will discuss how these findings contribute to our current understanding of the meiotic organisation of monotreme sex chromosomes and the evolution of MSCI in birds and mammals. (1) Grützner et al. (2004), Nature 432: 913–917.(2) Rens et al. (2007), Genome Biology 16;8(11): R243.(3) Veyrunes et al. (2008), Genome Research, 18(6): 995–1004.(4) Rens et al. (2004), Proceedings of the National Academy of Sciences USA. 101 (46): 16 257–16 261.(5) Daish et al. (2009), Reprod Fertil Dev. 21(8): 976–84.(6) Tsend-Ayush et al. (2009), Chromosoma 118(1): 53–69.

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