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Review
. 2020 Aug:38:100925.
doi: 10.1016/j.molmet.2019.12.005. Epub 2019 Dec 27.

Chromatin dynamics and histone modifications in intestinal microbiota-host crosstalk (VSports注册入口)

Rachel Fellows  1 , Patrick Varga-Weisz  2
Affiliations
Review

Chromatin dynamics and histone modifications in intestinal microbiota-host crosstalk

Rachel Fellows et al. Mol Metab. 2020 Aug.

VSports app下载 - Abstract

Background: The microbiota in the human gut are an important component of normal physiology that has co-evolved from the earliest multicellular organisms. Therefore, it is unsurprising that there is intimate crosstalk between the microbial world in the gut and the host VSports手机版. Genome regulation through microbiota-host interactions not only affects the host's immunity, but also metabolic health and resilience against cancer. Chromatin dynamics of the host epithelium involving histone modifications and other facets of the epigenetic machinery play an important role in this process. .

Scope of review: This review discusses recent findings relevant to how chromatin dynamics shape the crosstalk between the microbiota and its host, with a special focus on the role of histone modifications V体育安卓版. .

Major conclusions: Host-microbiome interactions are important evolutionary drivers and are thus expected to be hardwired into and mould the epigenetic machinery in multicellular organisms. Microbial-derived short-chain fatty acids (SCFA) are dominant determinants of microbiome-host interactions, and the inhibition of histone deacetylases (HDACs) by SCFA is a key mechanism in this process. The discovery of alternative histone acylations, such as crotonylation, in addition to the canonical histone acetylation reveals a new layer of complexity in this crosstalk V体育ios版. .

Keywords: Acylations; Chromatin; Crotonylation; Histone modifications; Microbiome; Microbiota. VSports最新版本.

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Figures

Figure 1
Figure 1
The structure of the small intestine and colon epithelium. The intestine has a large surface area to enable efficient absorption of dietary nutrients. It is comprised of pocket-like crypts containing stem cells that generate all of the necessary cell types for the intestinal epithelium. Cells develop as they move up the crypt walls before being lost by anoikis (apoptosis induced by loss of cell contact) into the gut lumen. In the small intestine, cells are lost at the top of the villi, which are finger-like projections that further increase the surface area. There are many cell types in the intestine, and the absorptive enterocytes and mucus-secreting goblet cells are the most abundant. Transit-amplifying cells are proliferative and lineage committed to become enterocytes. Enteroendocrine cells secrete hormones, tuft cells secrete prostanoids and opioids, and Paneth cells secrete anti-microbial peptides and support the stem cells. Label-retaining cells are quiescent Paneth cell precursors [90]. The small intestine contains a single diffuse layer of mucus that is not attached to the epithelium and contains some bacteria. The colon contains inner and outer mucus layers. The inner mucus layer is compact and attached to the epithelium and is normally free from bacteria. The outer mucus layer is diffuse with an undefined border and provides a habitat for intestinal bacteria. The colon microbiota is larger and more diverse than that of the small intestine [91]. The lamina propria is a thin layer of connective tissue that supports the epithelial cell niche. Intestinal-associated immune cells, lymphatic vessels, and capillaries are not shown. The muscularis mucosae, a thin layer of muscle, separates the lamina propria from the underlying submucosa (not shown). The epithelium, lamina propria, and muscularis mucosa together make up the mucosal layer [92].
Figure 2
Figure 2
Microbial metabolites influence host function. A non-exhaustive list of microbial generated molecules and their effects on cellular and organismal function. Some of the bacteria species that generate the specified metabolites are listed on the arrows. References for (A) [34,35,[93], [94], [95], [96], [97], [98]], (B) [36,99], (C) [100,101], (D) [30,102], (E) [[103], [104], [105], [106], [107], [108]], (F) [[109], [110], [111], [112], [113], [114]], (G) [115,116], (H) [99,[117], [118], [119], [120], [121]], (I) [[122], [123], [124], [125]], (J) [122,123,[126], [127], [128]], (K) [37,38,[40], [41], [42],[122], [123], [124],129,[129], [129], [130], [131], [132], [133]], and (L) [28,29,134].
Figure 3
Figure 3
Current model of how microbial-derived SCFA affect histone acetylation and crotonylation. The intestinal microbiota digests fibre present in dietary components, such as apples and brown bread, into SCFA. Butyrate is the main SCFA taken up by intestinal epithelial cells. Butyrate inhibits class I HDACs to reduce the removal of acetylation and crotonylation from the histone. It might also promote histone crotonylation and acetylation by metabolic conversion to acetyl-CoA and crotonyl-CoA precursors to be transferred to histones by p300/CBP.
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