64. A novel role for mitochondria in regulating epigenetic modification in the nucleus

Smirgalia, Dominic J.; Kulawiec, Mariola; Bistulfi, Gaia; Ghoshal, Sampa; Singh, Keshav K.

doi:10.1016/j.mito.2008.12.058

Cited by 44 publications

(56 citation statements)

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“…These studies identified reversible or irreversible nature of nuclear DNA (nDNA) methylation profiles of the nuclear genome. Restriction Landmark Genomic Scanning analyses revealed that more than 10% of methylation-sensitive NotI restriction sites tested were differentially methylated in in cells depleted of mtDNA compared to their parental cell lines (Smiraglia et al, 2008). Repleting the mtDNA reversed some, but not all not all, of the methylation changes.…”

Section: Mitochondrial Modulation Of Nuclear Dna Methylationmentioning

confidence: 99%

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Mitoepigenetics: The different shades of grey

et al. 2015

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Section: Mitochondrial Modulation Of Nuclear Dna Methylationmentioning

confidence: 99%

“…Our (Minocherhomji et al, 2012;Smiraglia et al, 2008) studies have determined the epigenetic landscape of the nuclear genome as a consequence of depletion of mtDNA content. These studies identified reversible or irreversible nature of nuclear DNA (nDNA) methylation profiles of the nuclear genome.…”

Section: Mitochondrial Modulation Of Nuclear Dna Methylationmentioning

confidence: 99%

Mitoepigenetics: The different shades of grey

et al. 2015

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“…Future research in a large-animal system like cattle should also assess the potential of OT to affect paternal genome function and for more subtle phenotypic changes or transient effects [50][51][52].…”

Section: Further Perspectivesmentioning

confidence: 99%

Pronounced Segregation of Donor Mitochondria Introduced by Bovine Ooplasmic Transfer to the Female Germ-Line1

Ferreira

Burgstaller

Perecin

et al. 2010

Biology of Reproduction

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Ooplasmic transfer (OT) has been used in basic mouse research for studying the segregation of mtDNA, as well as in human assisted reproduction for improving embryo development in cases of persistent developmental failure. Using cattle as a large-animal model, we demonstrate that the moderate amount of mitochondria introduced by OT is transmitted to the offspring's oocytes; e.g., modifies the germ line. The donor mtDNA was detectable in 25% and 65% of oocytes collected from two females. Its high variation in heteroplasmic oocytes, ranging from 1.1% to 33.5% and from 0.4% to 15.5%, can be explained by random genetic drift in the female germ line. Centrifugation-mediated enrichment of mitochondria in the pole zone of the recipient zygote's ooplasm and its substitution by donor ooplasm led to elevated proportions of donor mtDNA in reconstructed zygotes compared with zygotes produced by standard OT (23.6% +/- 9.6% versus 12.1% +/- 4.5%; P < 0.0001). We also characterized the proliferation of mitochondria from the OT parents-the recipient zygote (Bos primigenius taurus type) and the donor ooplasm (B. primigenius indicus type). Regression analysis performed for 57 tissue samples collected from the seven OT fetuses at different points during fetal development found a decreasing proportion of donor mtDNA (r(2) = 0.78). This indicates a preferred proliferation of recipient taurine mitochondria in the context of the nuclear genotype of the OT recipient expressing a B. primigenius indicus phenotype.

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“…In addition, ATP is important for folate metabolism and synthesis of the methyl donor SAM (Wallace 2010). Indeed, it has been shown that altered mitochondrial content results in significant changes in DNA methylation of a number of nuclear genes and may contribute to tumorigenesis (Smiraglia, Kulawiec et al 2008), suggesting that the mitochondrial function may modulate DNA methylation and histone modifications of the nuclear genome.…”

Section: Mitochondrial Dysfunctionmentioning

confidence: 99%

Does epigenetic dysregulation of pancreatic islets contribute to impaired insulin secretion and type 2 diabetes?

Dayeh

Ling

2015

Biochem. Cell Biol.

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β cell dysfunction is central to the development and progression of type 2 diabetes (T2D). T2D develops when β cells are not able to compensate for the increasing demand for insulin caused by insulin resistance. Epigenetic modifications play an important role in establishing and maintaining β cell identity and function in physiological conditions. On the other hand, epigenetic dysregulation can cause a loss of β cell identity, which is characterized by reduced expression of genes that are important for β cell function, ectopic expression of genes that are not supposed to be expressed in β cells, and loss of genetic imprinting. Consequently, this may lead to β cell dysfunction and impaired insulin secretion. Risk factors that can cause epigenetic dysregulation include parental obesity, an adverse intrauterine environment, hyperglycemia, lipotoxicity, aging, physical inactivity, and mitochondrial dysfunction. These risk factors can affect the epigenome at different time points throughout the lifetime of an individual and even before an individual is conceived. The plasticity of the epigenome enables it to change in response to environmental factors such as diet and exercise, and also makes the epigenome a good target for epigenetic drugs that may be used to enhance insulin secretion and potentially treat diabetes.

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64. A novel role for mitochondria in regulating epigenetic modification in the nucleus

Cited by 44 publications

References 0 publications

Mitoepigenetics: The different shades of grey

Mitoepigenetics: The different shades of grey

Pronounced Segregation of Donor Mitochondria Introduced by Bovine Ooplasmic Transfer to the Female Germ-Line1

Does epigenetic dysregulation of pancreatic islets contribute to impaired insulin secretion and type 2 diabetes?

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