sequoia controls the type I>0 daughter proliferation switch in the developing Drosophila nervous system
2016 (English)In: Development, ISSN 0950-1991, E-ISSN 1477-9129, Vol. 143, no 20, 3774-3784 p.Article in journal (Refereed) Published
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.
Place, publisher, year, edition, pages
The Company of Biologists Ltd , 2016. Vol. 143, no 20, 3774-3784 p.
Lineage tree, Cell cycle, Asymmetric division, Combinatorial control, Notch
Cell and Molecular Biology Biochemistry and Molecular Biology Cell Biology Medical Biotechnology
IdentifiersURN: urn:nbn:se:liu:diva-132739DOI: 10.1242/dev.139998ISI: 000393452500013PubMedID: 27578794OAI: oai:DiVA.org:liu-132739DiVA: diva2:1048761
Funding agencies: Swedish Research Council (Vetenskapsradet); Knut and Alice Wallenberg Foundation (Knut och Alice Wallenbergs Stiftelse); Swedish Cancer Foundation (Cancerfonden)2016-11-222016-11-222017-03-14Bibliographically approved