How Do Y-Chromosomes Modulate Genome-Wide Epigenetic States: Genome Folding, Chromatin Sinks, and Gene Expression

Francisco, Flávio de Oliveira; Lemos, Bernardo

doi:10.7150/jgen.8043

Cited by 78 publications

(83 citation statements)

References 97 publications

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“…Collectively, these results are in agreement with the notion that epistatic interactions between the Y chromosome and the genetic background are prevalent for components of male fitness (Johnson et al, 1992(Johnson et al, , 1993Chippindale and Rice, 2001;Sackton et al, 2011;Yee et al, 2015). Molecularly, a variety of mechanisms-involving both RNA mediators and non-coding DNA sequences-have been suggested for Y chromosome modulation of autosomal and X-linked gene expression that is, in turn, expected to modulate male fertility (reviewed in Francisco and Lemos, 2014).…”

Section: Introductionsupporting

confidence: 77%

“…Differences in the extensive blocks of heterochromatin are given by the kinds and quantities of satellite DNA and transposable elements. These elements are predicted to be key players in the phenomenon of YRV, and the mechanisms for their manifestation are likely to be varied (Francisco and Lemos, 2014). The three sister species in the D. simulans clade are able to intercross, but postzygotic incompatibilities such as hybrid male sterility are evident.…”

Section: Discussionmentioning

confidence: 99%

“…In addition to sex-ratio distortion, other phenotypes associated with reproductive isolation and hybrid incompatibilities may be modulated by interactions with genic and regulatory sequences of the Y chromosome. These phenotypes, including fertility and YRV, may emerge from nongenic elements on the Y chromosome heterochromatin and may be under selection Francisco and Lemos, 2014). The piRNA pathway is a candidate to mediate Y chromosome effects in hybrids (Castillo et al, 2011;Kelleher et al, 2012) and could reconcile the low polymorphism in Y-linked protein-coding sequences (Zurovcova and Eanes, 1999;Larracuente and Clark, 2013) with YRV.…”

Section: Discussionmentioning

confidence: 99%

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Interspecific Y chromosome variation is sufficient to rescue hybrid male sterility and is influenced by the grandparental origin of the chromosomes

Araripe

Tao

Lemos³

2016

Heredity

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Y chromosomes display population variation within and between species. Co-evolution within populations is expected to produce adaptive interactions between Y chromosomes and the rest of the genome. One consequence is that Y chromosomes from disparate populations could disrupt harmonious interactions between co-evolved genetic elements and result in reduced male fertility, sterility or inviability. Here we address the contribution of 'heterospecific Y chromosomes' to fertility in hybrid males carrying a homozygous region of Drosophila mauritiana introgressed in the Drosophila simulans background. In order to detect Y chromosome-autosome interactions, which may go unnoticed in a single-species background of autosomes, we constructed hybrid genotypes involving three sister species: Drosophila simulans, D. mauritiana, and D. sechellia. These engineered strains varied due to: (i) species origin of the Y chromosome (D. simulans or D. sechellia); (ii) location of the introgressed D. mauritiana segment on the D. simulans third chromosome, and (iii) grandparental genomic background (three genotypes of D. simulans). We find complex interactions between the species origin of the Y chromosome, the identity of the D. mauritiana segment and the grandparental genetic background donating the chromosomes. Unexpectedly, the interaction of the Y chromosome and one segment of D. mauritiana drastically reduced fertility in the presence of Ysim, whereas the fertility is partially rescued by the Y chromosome of D. sechellia when it descends from a specific grandparental genotype. The restoration of fertility occurs in spite of an autosomal and X-linked genome that is mostly of D. simulans origin. These results illustrate the multifactorial basis of genetic interactions involving the Y chromosome. Our study supports the hypothesis that the Y chromosome can contribute significantly to the evolution of reproductive isolation and highlights the conditional manifestation of infertility in specific genotypic combinations.

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Section: Introductionsupporting

confidence: 77%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Interspecific Y chromosome variation is sufficient to rescue hybrid male sterility and is influenced by the grandparental origin of the chromosomes

Araripe

Tao

Lemos³

2016

Heredity

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“…Additionally, the sex chromosomes can reportedly affect epigenetic regulation of gene expression on the autosomes (53). In Drosophila , the large heterochromatic Y chromosome directly impacts autosomal gene expression through effects on the epigenetic status of other chromosomes (54–57). The heterochromatic inactive X may also bias autosomal expression (52,53).…”

Section: Explaining Sex Differencesmentioning

confidence: 99%

The genetics of pubertal timing in the general population

Cousminer

Widén

Palmert

2016

Current Opinion in Endocrinology, Diabetes &Amp; Obesity

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Purpose of review To overview advances in the genetics of puberty based on studies in the general population, describe evidence for sex-specific genetic effects on pubertal timing, and briefly review possible mechanisms mediating sexually dimorphic genetic effects. Recent findings Pubertal timing is highly polygenic, and many loci are conserved among ethnicities. A number of identified loci underlie both pubertal timing and related traits such as height and body mass index (BMI). It is increasingly apparent that understanding the factors modulating the onset of puberty is important because the timing of this developmental stage is associated with a wider range of adult health outcomes than previously appreciated. While most of the genetic effects underlying the timing of puberty are common between boys and girls, some effects show sex-specificity and many are epigenetically modulated. Several potential mechanisms, including hormone-independent ones, may be responsible for observed sex differences. Summary Studies of pubertal timing in the general population have provided new knowledge about the genetic architecture of this complex trait. Increasing attention paid to sex-specific effects may provide key insights into the sexual dimorphism in pubertal timing and even into the associations between puberty and adult health risks by identifying common underlying biological pathways.

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“…However, the inactivation state must continually be maintained (Csankovszki et al, 2001; Yang et al, 2015), and this places an ongoing demand on the epigenetic machinery in XX cells. Drosophila do not have X chromosome inactivation, but large portions of the Y chromosome are inactivated and this has been shown to affect the expression of autosomal genes (Francisco and Lemos, 2014), perhaps because elements of the epigenetic machinery (e.g., enzymes that place inactivating marks on the Y) are in limited supply. As of yet, sex differences in autosomal gene expression due to X chromosome inactivation have not been demonstrated in the mammalian brain, but could well be in the future (Wijchers et al, 2010).…”

Section: Role Of Epigeneticsmentioning

confidence: 99%

Cellular and molecular mechanisms of sexual differentiation in the mammalian nervous system

Forger

Strahan

Castillo‐Ruiz

2016

Frontiers in Neuroendocrinology

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Neuroscientists are likely to discover new sex differences in the coming years, spurred by the National Institutes of Health initiative to include both sexes in preclinical studies. This review summarizes the current state of knowledge of the cellular and molecular mechanisms underlying sex differences in the mammalian nervous system, based primarily on work in rodents. Cellular mechanisms examined include neurogenesis, migration, the differentiation of neurochemical and morphological cell phenotype, and cell death. At the molecular level we discuss evolving roles for epigenetics, sex chromosome complement, the immune system, and newly identified cell signaling pathways. We review recent findings on the role of the environment, as well as genome-wide studies with some surprising results, causing us to rethink often-used models of sexual differentiation. We end by pointing to future directions, including an increased awareness of the important contributions of tissues outside of the nervous system to sexual differentiation of the brain.

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How Do Y-Chromosomes Modulate Genome-Wide Epigenetic States: Genome Folding, Chromatin Sinks, and Gene Expression

Cited by 78 publications

References 97 publications

Interspecific Y chromosome variation is sufficient to rescue hybrid male sterility and is influenced by the grandparental origin of the chromosomes

Interspecific Y chromosome variation is sufficient to rescue hybrid male sterility and is influenced by the grandparental origin of the chromosomes

The genetics of pubertal timing in the general population

Cellular and molecular mechanisms of sexual differentiation in the mammalian nervous system

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