Aging in Mice Linked to Misexpression of Class of Genes
- sangwoo74
- 2022년 2월 6일
- 1분 분량
Genes lacking a particular structure known as CpG islands tend to go haywire in older cells, a study finds, potentially contributing to key facets of aging. But it’s not yet clear if the relationship is causal.
Aging is inevitable, and goes along with many changes in cells, tissues, and organs—including DNA damage, mitochondrial dysfunction, and telomere loss. But why we age in the first place and what drives these changes is still unknown. A study published December 15 in Science Advances suggests a possible answer, linking the increased activity of genes lacking long stretches of C and G bases with degeneration and aging.
As cells age, the architecture of chromatin, which packages DNA, unravels. Samuel Beck, a computational biologist at MDI Biological Laboratory, says he and his colleagues set out to explore whether these structural changes contribute to the degenerative changes also associated with aging. Specifically, the researchers focused on stretches of C and G bases called CpG islands (CGI). CGI are present in the promoters of around 60 percent of mammalian genes, termed CGI+ genes, but absent in the remaining 40 percent, called CGI- genes.
These CGI- genes typically lie silent in a densely-packed form of chromatin known as heterochromatin. Heterochromatin attaches to the nuclear lamina, which lines the inner nuclear membrane. As cells age, the nuclear lamina weakens and frees the heterochromatin, which loosens, allowing previously silenced genes to be expressed.
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