Vincent M. O'Connor

This study maps serotonin signalling pathways in Globodera pallida using immunohistochemistry and gene expression, revealing distinct serotonin distribution and neuronal identity.

This study uses C. elegans to investigate epigenetic modifiers linked to autism spectrum disorder, identifying behavioral and phenotypic changes related to sensory processing and development.

This paper identifies and characterizes an allatostatin C GPCR system in Octopus vulgaris, revealing two receptors with distinct potency in response to the same peptide.

This study identifies and functionally validates TRPV channels in Octopus vulgaris as polymodal nociceptors using in silico analysis and heterologous expression in model organisms.

This study identifies EAT-2 as a conserved nicotinic receptor in nematodes that regulates pharyngeal muscle function, suggesting it as a target to disrupt plant parasitic nematode infections.

The paper identifies potential nematicides targeting MOD-1, a 5-HT-gated chloride channel in nematodes, using a screening platform and validates their efficacy against plant parasitic nematodes.

The paper identifies 51 potential nociceptive genes in Octopus vulgaris using a bioinformatic pipeline and validates 18 in C. elegans through loss-of-function experiments.

The paper shows that modulating nicotinic acetylcholine receptor function in C. elegans can mitigate organophosphate poisoning through plasticity-promoting mechanisms.

The paper demonstrates that using co-CRISPR marker genes in C. elegans can lead to hidden genomic rearrangements that affect gene function, emphasizing the need for sequencing co-CRISPR genes after CRISPR editing.

The paper shows that cholinergic signaling at the body wall neuromuscular junction in C. elegans inhibits feeding by coupling with locomotion control.

This study investigates the role of neuroligin in social behavior in C. elegans by using CRISPR/Cas9 to edit an autism-associated mutation and shows its impact on social circuitry.

The paper investigates whether human tauopathies are associated with UPR activation and finds no significant changes in UPR markers across tauopathy samples compared to controls.

This study shows that C. elegans nlg-1 mutants are defective in food-induced pharyngeal pumping, despite normal chemotaxis, suggesting neuroligin regulates feeding circuits outside the pharynx.