Susie Doyle

Senior Research Scientist

About Susie

Susie Doyle

Susie holds a B.A. in Biology and Classic Civilization from Wellesley College, and a Master’s degree in Molecular Neuroscience from UniversitePierre-et-Marie-Curie (Paris 6). Her Ph.D. and postdoctoral work were done in the laboratory of Michael Menaker at the University of Virginia, where she studied circadian hormone and neurotransmitter rhythms in the mammalian retina and non-visual photoreception. Susie has a long-standing interest in biological timing, and in the Siegrist lab she is interested in exploring how extrinsic signalis integrate with stem cell intrinsic factors to control developmental timing.



Susie's Projects


Delta controls temporal patterning

Delta controls temporal patterning

During development, neural stem cells (NSCs) divide asymmetrically, sequentially expressing a series of intrinsic factors to generate a diversity of neuron types. After cycling through temporal programs, NSCs terminally differentiate or die, bringing an end to developmental neurogenesis.

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Imp, Syp and E93 regulate timing of neurogenesis

Imp, Syp and E93 regulate timing of neurogenesis

Most neurogenesis occurs during development, driven by the cell divisions of neural stem cells (NSCs). We use Drosophila to understand how neurogenesis terminates once development is complete, a process critical for neural circuit formation.

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Neuroblast niche positioning

Neuroblast niche positioning

Correct positioning of stem cells within their niche is essential for tissue morphogenesis and homeostasis. Yet how stem cells acquire and maintain niche position remains largely unknown. Here, we show that a subset of brain neuroblasts (NBs) in Drosophila utilize PI3-kinase and DE-cadherin to build adhesive contact for NB niche positioning.

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Notch signaling

Notch signaling

Stem cells enter and exit quiescence as part of normal developmental programs and to maintain tissue homeostasis during adulthood. We report that neural stem cells in Drosophila (neuroblasts) require the evolutionarily conserved Notch cell-cell signaling pathway to enter quiescence during development.

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Nutrient-regulated neural circuits and insulin signaling

Nutrient-regulated neural circuits and insulin signaling

In Drosophila, there are 14 neurosecretory neurons located in the pars intercerebralis (the fly hypothalamus) that synthesize and secrete 3 of the 8 Drosophila insulin-like peptides (Dilps). Dilps bind to and activate the single Insulin-like tyrosine kinase receptor, which leads to downstream activation of the evolutionarily conserved PI3-kinase growth signaling pathway.

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RNAi screening

RNAi screening

We continue to make use of Drosophila as a genetic model to identify genes required for termination of neurogenesis. Through screening, using UAS-RNAi lines generated by the Transgeneic RNAi Project (TRiP), we have identified 14 genes.

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Susie's Publications


Chhavi Sood, Md Ausrafuggaman Nahid, Matthew C. Pahl, Susan E. Doyle , Sarah E. Siegrist (2022) Delta-dependent Notch activation promotes neuroblast temporal patterning and timing of neurogenesis termination in Drosophila. -- Under review.

Cami N. Keliinui, Susan E. Doyle , Sarah E. Siegrist (2022) Neural Stem Cell Reactivation in Cultured Drosophila Brain Explants. Journal of visualized experiments:JoVE | PubMed | PDF

Chhavi Sood, Virginia T. Justis, Susan E. Doyle , Sarah E. Siegrist (2022) Notch signaling regulates neural stem cell quiescence entry and exit in Drosophila. Development 149 (4) | PubMed | PDF

Chhavi Sood, Susan E. Doyle , Sarah E. Siegrist (2020) Steroid hormones, dietary nutrients, and temporal progression of neurogenesis. Current Opinion in Insect Science 43, 70-77 | PubMed | PDF

Matthew C. Pahl, Susan E. Doyle , Sarah E. Siegrist (2019) E93 Integrates Neuroblast Intrinsic State with Developmental Time to Terminate MB Neurogenesis via Autophagy. Current Biology 29 (5), 750-762 | PubMed | PDF

Susan E. Doyle , Matthew C. Pahl, Karsten H. Siller, Lindsay Ardiff, Sarah E. Siegrist (2017) Neuroblast niche position is controlled by Phosphoinositide 3-kinase-dependent DE-Cadherin adhesion. Development 144, 820-929 | PubMed | PDF