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Motor Neuron Development and Circuitry

We are studying how the neural circuitry that is required for coordinated walking in adult flies is constructed during development, and how it functions in the adult.

Recent Publication

A variety of protein-DNA structures can form between Hox-Exd-DNA

Context matters

Judith F. Kribelbauer, Ryan E. Loker, Siqian Feng, Chaitanya Rastogi, Namiko Abe, H. Tomas Rube, Harmen J. Bussemaker, and Richard S. Mann

News

February 12, 2020

New paper: Selective loss TF-DNA complex binding as a consequence of compromising DNA shape recognition

In this paper, Judith Kribelbauer, who was a joint student with Harmen Bussemaker, significantly extended our understanding of how homeodomain protein complexes (Exd-Hox) bind to the correct binding sites in vivo. Judith generated an amazing amount of data for this paper: high-throughput SELEX-seq assays on wild type and mutant homeodomain proteins, ChIP-seq analyses of tagged homeodomain proteins from wing imaginal discs, and Hi-C data from wing discs to identify enhancer-promoter interactions.

November 29, 2019

What happens when animals are startled?

New paper from the lab that shows when flies are startled, the response to pause, which lasts only a few seconds, is mediated by a set of serotonergic neurons in the ventral nerve cord (VNC). Serotonergic release also serves as a constitutive break on walking speed and when this break is not functional, flies walk faster than normal, in a wide variety of situations. For example, when flies  are hungry they walk faster than normal, but they walk even faster when the serotonergic break is not functional.

Read the paper here

October 09, 2019

A role for low affinity binding sites in fine tuning the levels of transcription

Our most recent paper, published in PLOS Genetics, showing that low affinity binding sites for the Hox protein Ubx and its cofactors Exd/Hth are used to reduce the levels of Ubx transcription in the proximal compartment of the haltere. In transgenes, if these binding sites are killed, down regulation of Ubx does not occur, and if the affinity of these binding sites is increased, Ubx down regulation is even stronger.