Same-Sex Twin Pair Phenotypic Correlations are Consistent with Human Y Chromosome Promoting Phenotypic Heterogeneity

Díaz-Castillo, Carlos

doi:10.1007/s11692-018-9454-y

Cited by 4 publications

(10 citation statements)

References 98 publications

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“…In recent years it has been proposed that the jDNA genomic content itself is an important element driving the spatiotemporal and evolutionary dynamics of natural populations [35][36][37].…”

Section: Junk Dna-driven Genetic Diversification and Cell Specializationmentioning

confidence: 99%

“…The heterochromatic jDNA (hjDNA)-based capacitance model spans organization levels to explain how the inherent ability of jDNA to vary within natural populations results in phenotypic heterogeneity, and how the ultimately hjDNA-based phenotypic heterogeneity permits natural populations better enduring variable environments and modulates genetic variation phenotypic exposure [35][36][37]. Very briefly, the idea that hjDNA genomic content promoting phenotypic heterogeneity in natural populations ultimately relies on four lines of evidence.…”

Section: Junk Dna-driven Genetic Diversification and Cell Specializationmentioning

confidence: 99%

“…Fourth, there is an ample phenomenology showing that the variation in hjDNA correlates with the variation in expression of many genes along the genome [56,[64][65][66][67][68][69]. Based on all this knowledge, the hjDNA-based capacitance model proposes how the inherent variation in hjDNA within natural populations results proximately in a variation in chromatin dynamics early in embryogenesis which is ultimately manifested as a gene expression and phenotypic heterogeneity, even in the absence of genetic variation within the coding portion of the genome [35][36][37].…”

Section: Junk Dna-driven Genetic Diversification and Cell Specializationmentioning

confidence: 99%

“…The hjDNA-based capacitance model also proposes that hjDNA-based phenotypic heterogeneity can drive the spatiotemporal dynamics of natural populations in two ways [35][36][37]. First, hjDNAbased phenotypic heterogeneity in natural populations might be important for them to thrive in variable environments.…”

Section: Junk Dna-driven Genetic Diversification and Cell Specializationmentioning

confidence: 99%

“…In particular, the utility of the junk DNA (jDNA) concept, the one among these concepts spanning the larger spectrum of elements, has been frequently called into question because of the stark heterogeneity of the elements it encompasses and the difficulty in definitely assessing the lack of function of any genetic element [28]. In spite of the debates on how to define jDNA or even the utility of this concept, it is widely acknowledged that jDNA elements act as evolutionary facilitators by directly participating in the causation of genetic changes, being exapted into new genes or regulatory elements, or tuning the expression gene expression [29][30][31][32][33][34][35][36][37].…”

Section: Introductionmentioning

confidence: 99%

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Regeneration: Why junk DNA might matter

Díaz-Castillo

2018

Preprint

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The ability of certain natural species to restore or regenerate missing structures has been a recurrent source of inspiration to forge our collective knowledge, from being used to adorn mythological figures with superhuman powers to permitting controlled reproducible observations that help setting the bases of entire research fields such as experimental biology and regenerative medicine. In spite of being one of the oldest natural phenomena under study, what makes certain species able or unable to regenerate missing parts is still largely a mystery. Recent advancements towards the highly detailed characterization of the sequence, the spatial organization, and the expression of genomes is offering a new standpoint to address the study of the natural variation in regenerative responses. An intriguing observation that has not yet conveniently pursued is that species with remarkable regenerative abilities tend to have genomes loaded with junk DNA (jDNA), i.e., genetic elements presumed to be useless for the benefit of the individual, whereas species for taxa with limited regenerative abilities tend to have jDNA-poor genomes. Here, I use existing knowledge on the role of jDNA as genome evolution facilitator and its non-random chromosome and nuclear distributions to speculate about two non-excluding ways through which the variation in jDNA genomic content might end up enhancing or limiting regenerative responses. The present piece aims to go beyond the confines of correlational studies between biological variables and to lay sensible conceptual grounds for future hypothesis-driven attempts to substantiate the genomic determinants of the natural variation of regenerative responses.

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“…In recent years it has been proposed that the jDNA genomic content itself is an important element driving the spatiotemporal and evolutionary dynamics of natural populations [35][36][37].…”

Section: Junk Dna-driven Genetic Diversification and Cell Specializationmentioning

confidence: 99%

Section: Junk Dna-driven Genetic Diversification and Cell Specializationmentioning

confidence: 99%

Section: Junk Dna-driven Genetic Diversification and Cell Specializationmentioning

confidence: 99%

Section: Junk Dna-driven Genetic Diversification and Cell Specializationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Regeneration: Why junk DNA might matter

Díaz-Castillo

2018

Preprint

Self Cite

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Endocrine disruption persistence through development and across generations can be mediated by environmental perturbations of the heterochromatin/euchromatin compartmentalization

Díaz-Castillo

Chamorro-García

2023

Environmental Contaminants and Endocrine Health

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Transgenerational Self-Reconstruction of Disrupted Chromatin Organization After Exposure To An Environmental Stressor in Mice

Díaz-Castillo

Chamorro-García

Shioda

et al. 2019

Sci Rep

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Exposure to environmental stressors is known to increase disease susceptibility in unexposed descendants in the absence of detectable genetic mutations. The mechanisms mediating environmentally-induced transgenerational disease susceptibility are poorly understood. We showed that great-great-grandsons of female mice exposed to tributyltin (TBT) throughout pregnancy and lactation were predisposed to obesity due to altered chromatin organization that subsequently biased DNA methylation and gene expression. Here we analyzed DNA methylomes and transcriptomes from tissues of animals ancestrally exposed to TBT spanning generations, sexes, ontogeny, and cell differentiation state. We found that TBT elicited concerted alterations in the expression of “chromatin organization” genes and inferred that TBT-disrupted chromatin organization might be able to self-reconstruct transgenerationally. We also found that the location of “chromatin organization” and “metabolic” genes is biased similarly in mouse and human genomes, suggesting that exposure to environmental stressors in different species could elicit similar phenotypic effects via self-reconstruction of disrupted chromatin organization.

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Same-Sex Twin Pair Phenotypic Correlations are Consistent with Human Y Chromosome Promoting Phenotypic Heterogeneity

Cited by 4 publications

References 98 publications

Regeneration: Why junk DNA might matter

Regeneration: Why junk DNA might matter

Endocrine disruption persistence through development and across generations can be mediated by environmental perturbations of the heterochromatin/euchromatin compartmentalization

Transgenerational Self-Reconstruction of Disrupted Chromatin Organization After Exposure To An Environmental Stressor in Mice

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