Asset Details
Do you wish to reserve the book?
Smarcad1 mediates microbiota-induced inflammation in mouse and coordinates gene expression in the intestinal epithelium
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Smarcad1 mediates microbiota-induced inflammation in mouse and coordinates gene expression in the intestinal epithelium
Do you wish to request the book?
Smarcad1 mediates microbiota-induced inflammation in mouse and coordinates gene expression in the intestinal epithelium
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Smarcad1 mediates microbiota-induced inflammation in mouse and coordinates gene expression in the intestinal epithelium
2020
Overview
Background
How intestinal epithelial cells interact with the microbiota and how this is regulated at the gene expression level are critical questions. Smarcad1 is a conserved chromatin remodeling factor with a poorly understood tissue function. As this factor is highly expressed in the stem and proliferative zones of the intestinal epithelium, we explore its role in this tissue.
Results
Specific deletion of
Smarcad1
in the mouse intestinal epithelium leads to colitis resistance and substantial changes in gene expression, including a striking increase of expression of several genes linked to innate immunity. Absence of Smarcad1 leads to changes in chromatin accessibility and significant changes in histone H3K9me3 over many sites, including genes that are differentially regulated upon
Smarcad1
deletion. We identify candidate members of the gut microbiome that elicit a Smarcad1-dependent colitis response, including members of the poorly understood TM7 phylum.
Conclusions
Our study sheds light onto the role of the chromatin remodeling machinery in intestinal epithelial cells in the colitis response and shows how a highly conserved chromatin remodeling factor has a distinct role in anti-microbial defense. This work highlights the importance of the intestinal epithelium in the colitis response and the potential of microbial species as pharmacological and probiotic targets in the context of inflammatory diseases.
Publisher
BioMed Central,Springer Nature B.V,BMC
Subject
