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. 2017 Jul 10;15(1):5–7. doi: 10.1038/cmi.2017.55

Figure 1.

Figure 1

A novel mechanism of lncKdm2b-mediated transcriptional regulation implicated in maintaining ILC3 proliferation and function. (a) lncKdm2b is required for the activation of Zfp292 expression. lncKdm2b directly binds to Satb1, which subsequently recruits the NURF complex comprising Bptf and Snf2l. This RNA/protein complex further binds to the Zfp292 promoter to activate Zfp292 expression in ILC3s of wild-type mice. (b) Loss of lncKdm2b abrogates the recruitment of Satb1 and NURF complex comprising Bptf and Snf2l on the Zfp292 promoter, resulting in impaired number and function of ILC3s. Consequently, Vav-Cre-directed lncKdm2b conditional knockout mice are susceptible to Citrobacter rodentium infection compared to wild-type mice.