Misexpression of genes lacking CpG islands drives degenerative changes during aging

Jun Yeong Lee; Ian Davis; Elliot H.H. Youth; Jonghwan Kim; Gary Churchill; James Godwin; Ron Korstanje; Samuel Beck

doi:10.1126/sciadv.abj9111

Misexpression of genes lacking CpG islands drives degenerative changes during aging

Jun Yeong Lee, Ian Davis, Elliot H.H. Youth, Jonghwan Kim, Gary Churchill, James Godwin, Ron Korstanje, Samuel Beck

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8 Scopus citations

Abstract

Cellular aging is characterized by disruption of the nuclear lamina and its associated heterochromatin. How these structural changes within the nucleus contribute to age-related degeneration of the organism is unclear. Genes lacking CpG islands (CGI- genes) generally associate with heterochromatin when they are inactive. Here, we show that the expression of these genes is globally activated in aged cells and tissues. This CGI- gene misexpression is a common feature of normal and pathological aging in mice and humans. We report evidence that CGI- gene up-regulation is directly responsible for age-related physiological deterioration, notably for increased secretion of inflammatory mediators.

Original language	English
Article number	eabj9111
Journal	Science advances
Volume	7
Issue number	51
DOIs	https://doi.org/10.1126/sciadv.abj9111
State	Published - Dec 2021

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title = "Misexpression of genes lacking CpG islands drives degenerative changes during aging",

abstract = "Cellular aging is characterized by disruption of the nuclear lamina and its associated heterochromatin. How these structural changes within the nucleus contribute to age-related degeneration of the organism is unclear. Genes lacking CpG islands (CGI- genes) generally associate with heterochromatin when they are inactive. Here, we show that the expression of these genes is globally activated in aged cells and tissues. This CGI- gene misexpression is a common feature of normal and pathological aging in mice and humans. We report evidence that CGI- gene up-regulation is directly responsible for age-related physiological deterioration, notably for increased secretion of inflammatory mediators.",

author = "Lee, {Jun Yeong} and Ian Davis and Youth, {Elliot H.H.} and Jonghwan Kim and Gary Churchill and James Godwin and Ron Korstanje and Samuel Beck",

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T1 - Misexpression of genes lacking CpG islands drives degenerative changes during aging

AU - Lee, Jun Yeong

AU - Davis, Ian

AU - Youth, Elliot H.H.

AU - Kim, Jonghwan

AU - Churchill, Gary

AU - Godwin, James

AU - Korstanje, Ron

AU - Beck, Samuel

PY - 2021/12

Y1 - 2021/12

N2 - Cellular aging is characterized by disruption of the nuclear lamina and its associated heterochromatin. How these structural changes within the nucleus contribute to age-related degeneration of the organism is unclear. Genes lacking CpG islands (CGI- genes) generally associate with heterochromatin when they are inactive. Here, we show that the expression of these genes is globally activated in aged cells and tissues. This CGI- gene misexpression is a common feature of normal and pathological aging in mice and humans. We report evidence that CGI- gene up-regulation is directly responsible for age-related physiological deterioration, notably for increased secretion of inflammatory mediators.

AB - Cellular aging is characterized by disruption of the nuclear lamina and its associated heterochromatin. How these structural changes within the nucleus contribute to age-related degeneration of the organism is unclear. Genes lacking CpG islands (CGI- genes) generally associate with heterochromatin when they are inactive. Here, we show that the expression of these genes is globally activated in aged cells and tissues. This CGI- gene misexpression is a common feature of normal and pathological aging in mice and humans. We report evidence that CGI- gene up-regulation is directly responsible for age-related physiological deterioration, notably for increased secretion of inflammatory mediators.

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SN - 2375-2548

VL - 7

JO - Science advances

JF - Science advances

IS - 51

M1 - eabj9111

ER -

Misexpression of genes lacking CpG islands drives degenerative changes during aging

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