Host pathways mediating changes in immune states elicited by intestinal microbial colonization are incompletely characterized. Here we describe alterations of the host immune state induced by colonization of germ-free zebrafish larvae with an intestinal microbial community or single bacterial species. We show that microbiota-induced changes in intestinal leukocyte subsets and whole-body host gene expression are dependent on the innate immune adaptor gene myd88. Similar patterns of gene expression are elicited by colonization with conventional microbiome, as well as mono-colonization with two different zebrafish commensal bacterial strains. By studying loss-of-function myd88 mutants, we find that colonization suppresses Myd88 at the mRNA level. Tlr2 is essential for microbiota-induced effects on myd88 transcription and intestinal immune cell composition.

In the version of our paper originally published online on July 9, 2015, under the Experimental Procedures subsection ''Derivation of AG-haESCs,'' we included the line, ''Each embryo was transferred into one well of a 96-well plate seeded with ICR embryonic fibroblast feeders in ESC medium supplemented with 20% knockout serum replacement, 1,500 U/ml LIF, 3 M CHIR99021, and 1 M PD0325901.'' However, the concentrations of CHIR99021 and PD0325901 should have been written as 3 mM CHIR99021 and 1 mM PD0325901, and both the online and print versions of the article now reflect this change. We apologize for any confusion this may have caused.

The asymmetric C–H annulation of O-pivaloyl 1-indolehydroxamic acid with donor/acceptor diazo compounds has been achieved for the first time, to the best of our knowledge, by using a rhodium catalyst embedded in a chiral binaphthyl backbone. This protocol constitutes a straightforward route for the synthesis of a new family of 1,2-dihydro-3H-imidazo­[1,5-a]­indol-3-one derivatives having a quaternary carbon stereocenter in high yields and excellent enantioselectivity (up to 98:2 er).