Deficiency in transmitter release triggers homeostatic transcriptional changes that increase presynaptic excitability
Abstract
Weakening of synaptic transmission at the Drosophila larval neuromuscular junction triggers two forms of homeostatic compensation, one that increases the probability of glutamate release per action potential ( P r ) and another that increases motoneuron (MN) activity. We investigated the molecular changes in MNs that underlie the increase in MN activity. RNA sequencing (RNA-seq) analysis on MNs whose glutamate release is weakened by knockdown of components of the MN transmitter release machinery reveals a reduction in expression of a group of genes that encode potassium channels and their positive modulators. These results identify a mechanism of compensation for weakened synaptic transmission by MNs, which engages a transcriptional program in those cells to increase firing and, thereby, ensure sufficient locomotory drive.
Article Details
Journal Info
Proceedings of the National Academy of Sciences
National Academy of Sciences
Authors (7)
Caroline A. Cypranowska
Department of Molecular and Cell Biology, University of California Berkeley
Maya Feldthouse
Helen Wills Neuroscience Institute, University of California Berkeley
Yoon Gi Choi
Functional Genomics Laboratory, University of California Berkeley
Dariya Bakshinska
Helen Wills Neuroscience Institute, University of California Berkeley
Rachel Li
Department of Molecular and Cell Biology, University of California Berkeley
Zachary L. Newman
Department of Molecular and Cell Biology, University of California Berkeley
Ehud Y. Isacoff
Department of Molecular and Cell Biology, University of California Berkeley