Epigenetic regulation of autosomal gene expression by sex chromosomes

Wijchers, Patrick J.; Festenstein, Richard

doi:10.1016/j.tig.2011.01.004

Cited by 142 publications

(120 citation statements)

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“…How a gene behaves can depend on the sex of the donor parent, with different consequences for offspring of each sex (Wijchers & Festenstein, 2011). Heterogamety could lead to a mismatch if paternal imprinting controls expression of telomere maintenance genes in one direction and maternal imprinting works in the reverse (Njajou et al, 2007).…”

Section: The Heterogametic Disadvantagementioning

confidence: 99%

Sex differences in telomeres and lifespan

2011

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SummaryMales and females often age at different rates resulting in longevity 'gender gaps', where one sex outlives the other. Why the sexes have different lifespans is an age-old question, still fiercely debated today. One cellular process related to lifespan, which is known to differ according to sex, is the rate at which the protective telomere chromosome caps are lost. In humans, men have shorter lifespans and greater telomere shortening. This has led to speculation in the medical literature that sex-specific telomere shortening is one cause of sex-specific mortality. However, telomere shortening may be a cause for and ⁄ or a consequence of the processes that govern survival, and to infer general principles from single-taxon studies may be misleading. Here, we review recent work on telomeres in a variety of animal taxa, including those with reverse sexual lifespan dimorphism (i.e., where males live longer), to establish whether sex-specific survival is generally associated with sex differences in telomere dynamics. By doing this, we attempt to tease apart the potential underlying causes for sex differences in telomere lengths in humans and highlight targets for future research across all taxa.

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Section: The Heterogametic Disadvantagementioning

confidence: 99%

Sex differences in telomeres and lifespan

2011

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“…Paternal imprinting of the bovine X chromosome could partly explain the upregulated expression of X-linked genes in normal female blastocysts, because parthenogenetic embryos, which carry two maternal X chromosomes, were found to have lower transcript levels of representative X-encoded genes, such as BEX1, CAPN6, BEX2, SRPX2, and UBE2A (Bermejo-Alvarez et al 2010). Moreover, the activity of the two X chromosomes in female blastocysts appears to affect the expression of autosomal genes, leading to gender-specific transcript differences (for a review, see Wijchers and Festenstein 2011). Female mouse embryonic stem cells with a deficiency of the DNMT3-like methyltransferase (DNMT3L 2/2 ) lose genomic DNA methylation patterns more rapidly than their male DNMT3L 2/2 embryonic stem cell counterparts (Ooi et al 2010).…”

Section: Recent Advances In Epigeneticsmentioning

confidence: 99%

Epigenetics and developmental programming of welfare and production traits in farm animals

Sinclair

Rutherford

Wallace

et al. 2016

Reprod. Fertil. Dev.

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Abstract. The concept that postnatal health and development can be influenced by events that occur in utero originated from epidemiological studies in humans supported by numerous mechanistic (including epigenetic) studies in a variety of model species. Referred to as the 'developmental origins of health and disease' or 'DOHaD' hypothesis, the primary focus of large-animal studies until quite recently had been biomedical. Attention has since turned towards traits of commercial importance in farm animals. Herein we review the evidence that prenatal risk factors, including suboptimal parental nutrition, gestational stress, exposure to environmental chemicals and advanced breeding technologies, can determine traits such as postnatal growth, feed efficiency, milk yield, carcass composition, animal welfare and reproductive potential. We consider the role of epigenetic and cytoplasmic mechanisms of inheritance, and discuss implications for livestock production and future research endeavours. We conclude that although the concept is proven for several traits, issues relating to effect size, and hence commercial importance, remain. Studies have also invariably been conducted under controlled experimental conditions, frequently assessing single risk factors, thereby limiting their translational value for livestock production. We propose concerted international research efforts that consider multiple, concurrent stressors to better represent effects of contemporary animal production systems.

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“…Because most of the genes responsible for this asymmetric response to androgens are autosomal (see next section), they must be transregulated in response to the XX versus XY sex chromosome karyotype. Transregulation can occur in many ways, but recent studies demonstrate that the sex chromosome karyotype alone, independent of sex hormones, epigenetically regulates many autosomal genes (reviewed in Wijchers and Festenstein 2011). Epigenetic modification (i.e., methylation, histone tail modifications, and nucleosome repositioning) is emerging as a pivotal factor controlling gene expression.…”

Section: Sex Hormone Differences Are Notmentioning

confidence: 99%

“…These data indicate that the XX/XY karyotype somehow influences (in trans) the expression of many genes during later embryo development (but before the testes start secreting T) in a manner that is independent of androgen signaling. Such XX/XY karyotype-specific transregulation is known to occur in adult humans (Wijchers and Festenstein 2011). For example, a gene on the human Y chromosome (TSPY) transregulates the level of expression of the X-linked androgen receptor in the adult germline (Akimoto et al 2010).…”

Section: Timing Of Xx/xy-induced Epi-marks That Canalize Sexual Develmentioning

confidence: 99%