Lo Sasso, GiuseppeRyu, DongryeolMouchiroud, LaurentFernando, Samodha CAnderson, Christopher LKatsyuba, ElenaPiersigilli, AlessandraHottiger, Michael OSchoonjans, KristinaAuwerx, Johan2014-08-292014-08-292014-08-29201410.1371/journal.pone.0102495https://infoscience.epfl.ch/handle/20.500.14299/106310WOS:000339378400099Dysfunction of Paneth and goblet cells in the intestine contributes to inflammatory bowel disease (IBD) and colitis-associated colorectal cancer (CAC). Here, we report a role for the NAD+-dependent histone deacetylase SIRT1 in the control of anti-bacterial defense. Mice with an intestinal specific Sirt1 deficiency (Sirt1int-/-) have more Paneth and goblet cells with a consequent rearrangement of the gut microbiota. From a mechanistic point of view, the effects on mouse intestinal cell maturation are mediated by SIRT1-dependent changes in the acetylation status of SPDEF, a master regulator of Paneth and goblet cells. Our results suggest that targeting SIRT1 may be of interest in the management of IBD and CAC.Gene Expression RegulationNeoplastictext::journal::journal article::research article