SWI/SNF Chromatin Remodeling Complexes Regulate Stem Cell Asymmetric Division and Daughter Cell Fate Specification in Adult Drosophila Posterior Midgut. Xiankun Zeng¹, Xinhua Lin², Steven Hou¹. 1) The Mouse Cancer Gen Program, Frederick National Laboratory for Cancer Research, National Institutes of Health, Frederick, MD 21702; 2) Key Laboratory of Stem Cell and Developmental Biology Institute of Zoology, Chinese Academy of Sciences, Beijing 1 Beichen West Road, Chaoyang District Beijing 100101, P.R.China.

   The adult Drosophila posterior midgut is maintained by multipotent intestinal stem cells (ISCs). Asymmetric Notch signaling first regulates the transition of an ISC to an immature daughter cell enteroblast (EB) and then directs the differentiation of an EB to an enterocyte (EC) or a secretory enteroendocrine (ee) cell. However, it is not known what regulates the asymmetric Notch signaling and the signalings function in regulating daughter cell fate determination. In a screen for genes that regulate cell lineage determination in the posterior midgut, we identified the core components of SWI/SNF chromatin-remodeling factors Osa and Snr1. Mutations of osa and snr1 resulted in ISC expansion as well as ee reduction. We further demonstrated that the Osa and Snr1 regulate ISC asymmetric division by directly controlling Delta transcription and ee differentiation by controlling asense transcription. Therefore, our data suggest that SNF/SWI chromatin-remodeling complexes can regulate both ISC intrinsic asymmetric division and ISC daughter cell fate determination by controlling Delta and ase transcription, respectively.