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Background  WDR13 is a member of the WD repeat protein family and is expressed in several tissues of human and mice. Previous studies in our laboratory showed that the lack of this gene in mice resulted in mild obesity, hyperinsulinemia, enhanced beta cell proliferation and protection from inflammation. However, the molecular mechanism of WDR13 action is not well understood.    Methods  In the present study, we used AOM/DSS to induce colitis-mediated colorectal tumor after establishing expression of  Wdr13  gene in colon. Further, we have used human colon cancer cell lines, HT29 and COLO205, and mouse primary embryonic fibroblast to understand the molecular mechanism of WDR13 action.    Results  We observed that mice lacking  Wdr13  gene have reduced number of tumors and are more susceptible to DSS-induced colon ulcers. We also show that WDR13 is a part of multi protein complex c-Jun/NCoR1/HDAC3 and it acts as a transcriptional activator of AP1 target genes in the presence of JNK signal. Consistent with in vitro data, we observed reduced expression of AP1 target genes in colon after AOM/DSS treatment in  Wdr13  knockout mice as compared to that in wild type.    Conclusion  Mice lacking  Wdr13  gene showed reduced expression of AP1 target genes and protection from colitis-induced colorectal tumors.    Electronic supplementary material  The online version of this article (doi:10.1186/s12885-017-3118-7) contains supplementary material, which is available to authorized users.

WD-repeat protein WDR13 is a novel transcriptional regulator of c-Jun and modulates intestinal homeostasis in mice