Correa, Edgar [class:all]
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81 results (0.016 seconds)
- person: Edgar Correa University of Chicago; Chicago IL, United States of America
- paper:
Bessereau, Jean-Louis, Mialon, Morgane, Kratsios, Paschalis, Correa, Edgar, Pinan-Lucarre, Berangere, Zhou, Xin
[
International Worm Meeting,
2021] During nervous system development, it is critical for neurons to establish functional synapses. This process relies on the ability of a presynaptic neuron to synthesize, package, and release a specific neurotransmitter, and the ability of a postsynaptic neuron to present the correct neurotransmitter receptor. However, the molecular mechanisms that coordinate these distinct events, occurring at a pre- and a post-synaptic cell, are poorly understood. The nematode C. elegans represents a powerful model to study synapse development due to its known connectome, powerful genetics, and single-cell resolution analysis. The evolutionarily conserved transcription factor (TF) UNC-30/PITX1-3 has been shown to control neuronal communication between nerve cord GABAergic motor neurons (MNs) and body-wall muscle by directly activating the expression of GABA biosynthesis genes (e.g., unc-25/GAD, unc-46/LAMP, unc-47/VGAT) in the presynaptic side. Our preliminary data shows that animals lacking unc-30 gene activity display defects in GABA-Receptor (GABA-R) clustering in the postsynaptic side, although UNC-30 is not expressed in muscle. Intriguingly, the same GABA-R clustering defect is observed in animals lacking the short isoform of madd-4/Punctin (madd-4S), a secreted synaptic organizer produced by GABA MNs. Thus, we hypothesize that UNC-30 controls the establishment of functional synapses by activating GABA biosynthesis genes and madd-4S. We found that madd-4S expression is reduced in GABA MNs of unc-30 mutant animals. Chromatin immunoprecipitation followed by sequencing (ChIP-Seq) suggests UNC-30 controls madd-4S directly, a notion we confirmed by deleting the UNC-30 binding site in the context of the endogenous madd-4S locus. Besides acting as an activator of GABA synthesis genes and madd-4S, our preliminary data also suggests UNC-30 is required to prevent the adoption of alternative neuronal identities in GABA MNs. We found that several genes normally expressed in cholinergic MNs (e.g., madd-4L, glr-5, unc-53) become ectopically expressed in GABA MNs of unc-30 mutant animals. These findings together with ChIP-Seq data suggest an additional role for UNC-30 as direct repressor of alternative identities. Since these analyses rely on a null unc-30 allele that disrupts gene activity throughout all life stages, ongoing experiments will determine whether UNC-30 is continuously required to maintain proper gene expression in GABA MNs. Altogether, these findings suggest UNC-30/PITX1-3 is a transcriptional link for the coordination of synaptogenesis with cell identity features in C. elegans GABA MNs.
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