Journal article

The Scalloped and Nerfin-1 Transcription Factors Cooperate to Maintain Neuronal Cell Fate

Joseph HA Vissers, Francesca Froldi, Jan Schroder, Anthony T Papenfuss, Louise Y Cheng, Kieran F Harvey

CELL REPORTS | CELL PRESS | Published : 2018


The ability of cells to stably maintain their fate is governed by specific transcription regulators. Here, we show that the Scalloped (Sd) and Nervous fingers-1 (Nerfin-1) transcription factors physically and functionally interact to maintain medulla neuron fate in the Drosophila melanogaster CNS. Using Targeted DamID, we find that Sd and Nerfin-1 occupy a highly overlapping set of target genes, including regulators of neural stem cell and neuron fate, and signaling pathways that regulate CNS development such as Notch and Hippo. Modulation of either Sd or Nerfin-1 activity causes medulla neurons to dedifferentiate to a stem cell-like state, and this is mediated at least in part by Notch path..

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Awarded by NHMRC

Awarded by NHMRC Program Grant

Awarded by National Health and Medical Research Council of Australia

Funding Acknowledgements

We thank Andrea Brand, Alex Gould, Claude Desplan, Kirsten Guss, Yuh-Nung Jan, Jin Jiang, Alexander Kuzin, Lei Zhang, Michael Lan, Helena Richardson, James Skeath, Tony Southall, Alexey Veraksa, the Vienna Drosophila RNAi Center, the Bloomington Drosophila Stock Centre, the Drosophila Genomics Resource Centre (DGRC), the Australian Drosophila Research Support Facility (, and the Developmental Studies Hybridoma Bank (DSHB) for fly stocks, antibodies, and plasmids. We thank Joke van Bemmel, Alexey Pindyurin, Owen Marshall, Tony Southall, Mark Dawson, Charles Bell, and Jose Polo for helpful discussions. We thank the Peter Mac Molecular Genomics and Flow Cytometry core facilities and the Centre for Advanced Microscopy and Histology. K.F.H. and A.T.P. are National Health and Medical Research Council (NHMRC) of Australia Senior Research Fellows (1078220 and 116955, respectively). The laboratories of K.F.H. and L.Y.C. were supported by project grants from the NHMRC (1080131 and 1103604). A.T.P. was supported by the Lorenzo and Pamela Galli Charitable Trust and by an NHMRC Program Grant (1054618). The research benefited from support from the Peter MacCallum Cancer Foundation, Victorian State Government Operational Infrastructure Support, and Australian Government NHMRC Independent Research Institute Infrastructure Support.