neuroblasts are an excellent model for investigating how neuronal diversity is generated. Most brain neuroblasts generate a series of ganglion mother cells (GMCs) that each make two neurons (type I lineage), but 16 brain neuroblasts generate a series of intermediate neural progenitors (INPs) that each produce 4-6 GMCs and 8-12 neurons (type II lineage). Thus, type II lineages are similar to primate cortical lineages, and may serve as models for understanding cortical expansion. Yet the origin of type II neuroblasts remains mysterious: do they form in the embryo or larva? If they form in the embryo, do their progeny populate the adult central complex, as do the larval type II neuroblast progeny? Here, we present molecular and clonal data showing that all type II neuroblasts form in the embryo, produce INPs and express known temporal transcription factors. Embryonic type II neuroblasts and INPs undergo quiescence, and produce embryonic-born progeny that contribute to the adult central complex. Our results provide a foundation for investigating the development of the central complex, and tools for characterizing early-born neurons in central complex function.

The intestinal epithelium does not function in isolation, but interacts with many components including the Enteric Nervous System (ENS). Understanding ENS and intestinal epithelium interactions requires multidisciplinary approaches to uncover cells involved, mechanisms used, and the ultimate influence on intestinal physiology. This review is intended to serve as a reference for epithelial biologists interested in studying these interactions. With this in mind, this review aims to summarize the basic anatomy of the epithelium and ENS, mechanisms by which they interact, and techniques used to study these interactions. We highlight in vitro, ex vivo and in vivo techniques. Additionally, ENS influence on epithelial proliferation and gene expression within stem and differentiated cells as well as gastrointestinal cancer are discussed.

16Drosophila neuroblasts are an excellent model for investigating how neuronal diversity is 17 generated. Most brain neuroblasts generate a series of ganglion mother cells (GMCs) that each 18 make two neurons (type I lineage), but sixteen brain neuroblasts generate a series of intermediate 19 neural progenitors (INPs) that each produce 4-6 GMCs and 8-12 neurons (type II lineage). Thus, 20 type II lineages are similar to primate cortical lineages, and may serve as models for 21 understanding cortical expansion. Yet the origin of type II neuroblasts remains mysterious: do 22 they form in the embryo or larva? If they form in the embryo, do their progeny populate the adult 23 central complex, as do the larval type II neuroblast progeny? Here we present molecular and 24 clonal data showing that all type II neuroblasts form in the embryo, produce INPs, and express 25 known temporal transcription factors. Embryonic type II neuroblasts and INPs undergo 26 quiescence, and produce embryonic-born progeny that contribute to the adult central complex. 27 Our results provide a foundation for investigating the development of the central complex, and 28 tools for characterizing early-born neurons in central complex function. 29 30 31 KEY WORDS: neurogenesis, type II neuroblast, intermediate neural progenitors, INPs, temporal 32 patterning, Pdm, Castor, Grainy head, Dichaete, central complex 33 65 2015). Second, the temporal transcription factors Hunchback (Hb), Krüppel (Kr), Nubbin/Pdm2 66 (Pdm), Castor (Cas) and Grainy head (Grh) specify unique GMC identities within each neuroblast 67 3 lineage (Brody and Odenwald, Moris-Sanz et al., 2014). In contrast, much less is known 71 about type II neuroblasts. Only one of the eight type II neuroblasts has been identified in the 72 embryo (Hwang and Rulifson, 2011); the origin of the other type II neuroblasts has not been 73 reported in existing embryonic brain neuroblast maps (Urbach and Technau, 2003). It remains 74 unknown whether type II neuroblasts arise de novo from the neuroectoderm similar to type I 75 neuroblasts, or whether they arise from a type I > type II transition similar to the type I > type 0 76 neuroblast transitions (Baumgardt et al., 2014; Bertet et al., 2014). If type II neuroblasts form 77 during embryogenesis, it is unknown whether they utilize the same Hb > Kr > Pdm > Cas > Grh 78 temporal transcription factor cascade to generate neuronal diversity, or whether they make 79 embryonic born INPs that sequentially express Dichaete (D) > Grh > Eyeless similar to larval 80 INPs (Bayraktar and Doe, 2013). Furthermore, if type II neuroblast lineages are initiated in the 81 embryo, it would be interesting to know if their INPs undergo quiescence, similar to type I and II 82 neuroblasts; if so they would be the only cell type beyond neuroblasts known to enter quiescence 83 at the embryo/larval transition. Perhaps most importantly, identifying embryonic type II 84 neuroblasts is essential for subsequent characterization of their early-born progeny, which are 85 likely to gen...