title: sequoia controls the type I>0 daughter proliferation switch in the developing Drosophila nervous system.
abstract: Neural progenitors typically divide asymmetrically to renew themselves, while producing daughters with more limited potential. In the Drosophila embryonic ventral nerve cord, neuroblasts initially produce daughters that divide once to generate two neurons/glia (type I proliferation mode). Subsequently, many neuroblasts switch to generating daughters that differentiate directly (type 0). This programmed type I>0 switch is controlled by Notch signaling, triggered at a distinct point of lineage progression in each neuroblast. However, how Notch signaling onset is gated was unclear. We recently identified Sequoia (Seq), a C2H2 zinc-finger transcription factor with homology to Drosophila Tramtrack (Ttk) and the positive regulatory domain (PRDM) family, as important for lineage progression. Here, we find that seq mutants fail to execute the type I>0 daughter proliferation switch and also display increased neuroblast proliferation. Genetic interaction studies reveal that seq interacts with the Notch pathway, and seq furthermore affects expression of a Notch pathway reporter. These findings suggest that seq may act as a context-dependent regulator of Notch signaling, and underscore the growing connection between Seq, Ttk, the PRDM family and Notch signaling.
authors: Department of Clinical and Experimental Medicine, Linkoping University, Linkoping SE-58185, Sweden.
authors: Erika
authors: E
authors: Gunnar
authors: Department of Clinical and Experimental Medicine, Linkoping University, Linkoping SE-58185, Sweden.
authors: Caroline
authors: C
authors: Bivik
authors: Department of Clinical and Experimental Medicine, Linkoping University, Linkoping SE-58185, Sweden.
authors: Annika
authors: A
authors: Starkenberg
authors: Department of Clinical and Experimental Medicine, Linkoping University, Linkoping SE-58185, Sweden stefan.thor@liu.se.
authors: Stefan
authors: 0000-0001-5095-541X
authors: S
authors: Thor
mesh_terms: D000818:Animals; D049109:Cell Proliferation / Q000235:genetics / Q000502:physiology; D004268:DNA-Binding Proteins / Q000235:genetics / Q000378:metabolism*; D004330:Drosophila; D029721:Drosophila Proteins / Q000235:genetics / Q000378:metabolism*; D009154:Mutation / Q000235:genetics; D009419:Nerve Tissue Proteins / Q000235:genetics / Q000378:metabolism*; D009420:Nervous System / Q000166:cytology / Q000378:metabolism; D051880:Receptors, Notch / Q000235:genetics / Q000378:metabolism; D012097:Repressor Proteins / Q000235:genetics / Q000378:metabolism*; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism*
chemical_list: D004268:DNA-Binding Proteins; D029721:Drosophila Proteins; C497759:N protein, Drosophila; D009419:Nerve Tissue Proteins; D051880:Receptors, Notch; D012097:Repressor Proteins; D014157:Transcription Factors; C443103:seq protein, Drosophila; C075878:ttk protein, Drosophila
keywords: Asymmetric division; Cell cycle; Combinatorial control; Lineage tree; Notch